Ryszard Amarowicz1, Yi Gong2, and Ronald B. Pegg2
1 Division of Food Science, Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, ul, Poland
2 Department of Food Science and Technology, College of Agricultural and Environmental Sciences, University of Georgia, USA
Consumers tend to underestimate tree nuts as a nutritious and healthful snack; they put them into the same category as potato chips, nachos, and Cheetos. Nuts, including peanuts which are in fact a legume, are often viewed as high‐fat food items with too many calories that should be eaten only sparingly to avoid weight gain. Emerging research from epidemiological studies and clinical trials is demonstrating that tree nuts, as part of a balanced diet, promote satiety and weight maintenance and in fact are not culprits of body weight gain. Moreover, tree nuts contain a plethora of nutrients and bioactive compounds (e.g. phytochemicals and phytosterols), which are now being recognized for bestowing health benefits. As will be discussed in this chapter, tree nuts have been associated with improving heart health, lowering low‐density lipoprotein cholesterol levels, improving cognitive function and endothelial compliance, reducing inflammation, and even lowering cancer risks. The strongest evidence that tree nuts are cardioprotective comes from (i) epidemiological observations indicating a consistent and well‐defined inverse association between the frequency of nut consumption and development of coronary heart disease, and (ii) several short‐term clinical trials demonstrating the beneficial effects of nut intake on lipid profiles as well as other intermediate markers of heart disease. From the nutrient perspective, tree nuts are a nutrient‐dense food that supplies heart‐healthy mono‐ and polyunsaturated fats, high‐quality vegetable protein, dietary fiber as well as important vitamins and minerals. For example, just two Brazil nuts can provide the daily requirement of selenium, an important mineral for improving the body’s antioxidant defense mechanisms.
Tree nuts are convenient, nutritious, and tasty snacks that can easily be incorporated into our busy lifestyles. They are generally eaten whole, either raw or roasted with added salt or flavorings, but also are found in confectionery and bakery products. Because of their health‐promoting attributes, tree nuts have been referred to as a natural functional food. The mechanism of their actions likely is due to synergistic interactions amongst the many bioactive constituents within the nutmeat, which may favorably influence human physiology. One might say that these year‐round nutritional powerhouse are truly Mother Nature’s gift.
Tree nuts are considered as an excellent energy source. Many efforts have been made in studying compositional information of major tree nuts. The proximate compositions of all tree nuts are summarized in Table 11.1, with triacylglycerols being the predominant component; the lipid contents in tree nuts vary from 53.5% in almonds to 75.1% in pine nuts (Miraliakbari & Shahidi 2008). This high lipid‐containing nature has marked them as an excellent energy source. Nuts are generally low in available carbohydrate and glycemic index, ranging from 27.5 to 28.0 g/100 g in pistachios to 12.3 g/100 g in Brazil nuts. Tree nuts are also a rich source of protein, with the highest content found in peanuts, walnuts, almonds, pistachios, and cashews. Brazil nuts, hazelnuts, and pine nuts possess a low amount of protein with the lowest found in pecans and macadamia nuts (Brufau et al. 2006).
Table 11.1 Proximate composition of tree nuts (g/100 g nutmeat, fw).
| Nutrients | Almond | Brazil nut | Cashew | Chestnut | Hazelnut | Hickory nut | Macadamia | Pecan | Pine nut | Pistachio | Walnut |
| Moisture Lipids Proteins Ash Carbohydrates Dietary fiber |
3.1–9.5 43.3–50.6 19.5–23.3 2.5–4.6 19.7–27.0 11.8–13.0 |
3.1–3.5 66.4–67.1 13.9–14.3 3.3–3.5 12.3 7.5 |
4.4–8.0 42.8–43.9 18.2–20.9 2.5–2.8 24.1–30.2 1.4–3.3 |
45.3–52.0 45.3–52.0 1.6–7.4 1.0–2.9 44.2–62.3 2.3–3.7 |
4.0–5.3 59.8–61.5 14.1–20.6 2.0–2.3 10.0–16.7 3.4–9.7 |
2.7 64.4 12.7 2.0 18.3 6.4 |
1.4–2.1 66.2–75.8 7.9–8.4 1.1–1.2 13.8 8.6 |
3.5–7.4 66.2–72.0 7.5–9.2 1.5–1.9 13.9 9.6 |
1.5–2.3 61.7–68.4 13.1–13.7 2.5–2.6 13.1 3.7 |
3.9–5.7 44.4–45.4 19.8–20.6 3.0–3.2 27.5–28.0 10.3 |
2.7–4.7 64.5–65.2 13.5–15.2 1.8 13.7 6.7 |
References: Ruggeri et al. (1998); Venkatachalam & Sathe (2006); Çağlarırmark (2003); Çağlarırmark and Batkan (2005); De Leon and Delores (2004); USDA National Nutrient Database for Standard Reference, Release 27.
Similar to many other plants, the quality of tree nut proteins is considered to be suboptimal, as their amino acid profiles are incomplete (Table 11.2). According to the FAO/WHO, a pattern of indispensable (“essential” is an antiquated term) amino acids are recommended for children between the ages of two and five years. Tryptophan is the first limiting amino acid for a majority of tree nut proteins, with the exception being macadamias, which are limited by lysine. The predominant amino acids in tree nut proteins are aspartic and glutamic acids. For adults, on the other hand, the proteins of tree nuts contain adequate amounts of indispensable amino acids except for almonds, which are deficient in methionine and cysteine (Alasalvar & Shahidi 2009).
Table 11.2 Amino acids in tree nuts (g/100 g of portion).
| Amino acid | Almond | Brazil nut | Cashew | Chestnut | Hazelnut | Macadamia | Pecan | Pine nut | Pistachio | Walnut |
| Tryptophan Threonine Isoleucine Leucine Lysine Methionine Cysteine Phenylalanine Tyrosine Valine Arginine Histidine Alanine Aspartic acid Glutamic acid Glycine Proline Serine |
0.211 0.601 0.751 1.473 0.568 0.157 0.215 1.132 0.450 0.855 2.465 0.539 0.999 2.639 6.206 1.429 0.969 0.912 |
0.135 0.365 0.518 0.190 0.490 1.124 0.306 0.639 0.416 0.760 2.140 0.409 0.609 1.325 3.190 0.733 0.706 0.676 |
0.287 0.688 0.789 1.472 0.928 0.362 0.393 0.951 0.508 1.094 2.123 0.456 0.837 1.795 4.506 0.937 0.812 1.079 |
0.027 0.086 0.095 0.143 0.143 0.057 0.077 0.102 0.067 0.135 0.173 0.067 0.161 0.417 0.312 0.124 0.127 0.121 |
0.193 0.497 0.545 1.063 0.420 0.221 0.277 0.663 0.362 0.701 2.211 0.432 0.730 1.679 3.710 0.724 0.561 0.735 |
0.067 0.370 0.314 0.602 0.018 0.023 0.006 0.665 0.511 0.363 1.402 0.195 0.388 1.099 2.267 0.454 0.468 0.419 |
0.093 0.306 0.336 0.598 0.287 0.183 0.152 0.426 0.215 0.411 1.177 0.262 0.397 0.929 1.829 0.453 0.363 0.474 |
0.107 0.370 0.542 0.991 0.540 0.259 0.289 0.524 0.509 0.687 2.413 0.341 0.684 1.303 2.926 0.691 0.673 0.835 |
0.271 0.667 0.893 1.542 1.142 0.335 0.355 1.054 0.412 1.230 2.012 0.503 0.914 1.803 3.790 0.946 0.805 1.216 |
0.170 0.596 0.625 1.170 0.424 0.236 0.208 0.711 0.406 0.753 2.278 0.391 0.696 1.829 2.816 0.816 0.706 0.934 |
Reference: USDA National Nutrient Database for Standard Reference, Release 27.
Most tree nut proteins are rich in arginine, ranging from 2.47 g/100 g fresh weight (fw) nutmeat in almonds to 1.40 g/100 g fw nutmeat in macadamias, while the lowest arginine content of 0.173 g/100 g fw nutmeat was reported for chestnuts. Arginine can be metabolized to nitric oxide (NO), an important signaling molecule and a potent vasodilator, by endothelial NO synthase (Förstermann & Sessa 2012). Nut proteins generally have a lower lysine/arginine ratio than proteins from animal sources. This ratio is reportedly associated with a significantly lower risk of developing hypercholesterolemia and atherosclerosis, which also decreases the risk of cardiovascular diseases (Brufau et al. 2006).
Tree nuts are plant‐based powerhouses packed with a combination of macronutrients, vitamins, and minerals. Studies have shown that tree nuts are rich in tocopherols (vitamin E), which is not surprising because of their high lipid values (Miraliakbari & Shahidi 2008). Vitamin contents of major nut types are summarized in Table 11.3. Four tocopherol isomers were reported in all tree nuts at various levels, while tocotrienols (data not shown) were found to a much lesser extent (Robbins et al. 2011). The predominant tocopherol homologue in tree nut oils is γ‐tocopherol, with the exception being almond and hazelnut lipids, which are high in α‐tocopherol. The levels of both the α‐ and γ‐isomers are similar in pine nut oil. α‐Tocopherol is widely considered as the most bioactive homologue because of its high affinity to the tocopherol transfer protein in the liver. However, the exceptional property of γ‐tocopherol is receiving much attention. Research has indicated that γ‐CEHC, the metabolite of γ‐tocopherol, might have an antiinflammatory effect as demonstrated by its downregulating capacity of cyclooxygenase‐2 (COX‐2) and 5‐lipoxygenase (5‐LOX) (Jiang & Ames 2003; Jiang et al. 2000, 2001).
Table 11.3 Vitamins in tree nuts (fw).
| Vitamin | Almond | Brazil nut | Cashew | Chestnut | Hazelnut | Macadamia | Pecan | Pine nut | Pistachio | Walnut |
| Vitamin C (mg/100 g) Thiamine (mg/100 g) Riboflavin (mg/100 g) Niacin (mg/100 g) Pantothenic acid (mg/100 g) Vitamin B6 (mg/100 g) Folate, total (mg/100 g) Vitamin A (IU/100 g) α‐Tocopherol (mg/100 g) β‐Tocopherol (mg/100 g) γ‐Tocopherol (mg/100 g) δ‐Tocopherol (mg/100 g) Vitamin K (μg/100 g) |
0.0 0.205 1.138 3.618 0.471 0.137 44 2 25.63 0.23 0.64 0.07 – |
0.7 0.617 0.035 0.295 0.184 0.101 22 – 5.65 0.01 9.56 0.63 – |
0.5 0.423 0.058 1.062 0.864 0.417 25 – 0.90 0.03 5.31 0.36 34.1 |
43.0 0.238 0.168 1.179 0.509 0.376 62 28 – – – – – |
6.3 0.643 0.113 1.800 0.918 0.563 113 20 15.03 0.33 0.00 0.00 14.2 |
1.2 1.195 0.162 2.473 0.758 0.275 11 – 0.54 – – – – |
1.1 0.660 0.130 1.167 0.863 0.210 22 56 1.40 0.39 24.44 0.47 3.5 |
0.8 0.364 0.227 4.387 0.313 0.094 34 29 9.33 0.00 11.15 0.00 53.9 |
5.6 0.870 0.160 1.300 0.520 1.700 51 415 2.30 0.00 22.60 0.80 – |
1.3 0.341 0.150 1.125 0.570 0.537 98 20 0.70 0.15 20.83 1.89 2.7 |
Reference: USDA National Nutrient Database for Standard Reference, Release 27.
Regarding mineral content (Table 11.4), in general, tree nuts are rich in magnesium, manganese, phosphorus, and potassium. Almonds and cashews are recognized as an excellent nondairy source of calcium and iron, respectively. It is important to mention that Brazil nuts have a considerably higher content of selenium than any other tree nut type. Selenium intake is strongly related to the redox status in the human body. While selenium itself does not act as an antioxidant directly, it functions as a catalyst for glutathione peroxidase, an important component in the endogenous antioxidant defense system in the human body (Battin & Brumaghim 2009).
Table 11.4 Mineral content in tree nuts portion (fw).
| Compound | Almond | Brazil nut | Cashew | Chestnut | Hazelnut | Macadamia | Pecan | Pine nut | Pistachio | Walnut |
| Calcium, Ca (mg/100 g) Iron, Fe (mg/100 g) Magnesium, Mg (mg/100 g) Phosphorus, P (mg/100 g) Potassium, K (mg/100 g) Sodium, Na (mg/100 g) Zinc, Zn (mg/100 g) Copper. Cu (mg/100 g) Manganese, Mn (mg/100 g) Selenium, Se (μg/100 g) |
269 3.71 270 481 733 1 3.12 1.031 2.179 4.1 |
160 2.43 376 725 659 3 4.06 1.743 1.223 1917.0 |
37 6.68 292 593 660 12 5.78 2.195 1.655 19.9 |
27 1.01 32 93 518 3 0.52 0.447 0.952 – |
114 4.70 163 290 680 0 2.45 1.725 6.175 2.4 |
85 3.69 130 188 368 5 1.30 0.756 4.131 3.6 |
70 2.53 121 277 410 0 4.53 1.200 4.500 3.8 |
16 5.53 252 575 597 2 6.45 1.324 8.802 0.7 |
105 3.92 121 490 1025 1 2.20 1.300 1.200 7.0 |
98 2.91 158 346 441 2 3.09 1.586 3.414 4.9 |
Reference: USDA National Nutrient Database for Standard Reference, Release 27.
Many studies have been carried out on tree nut fatty acids and minor lipid constituents. Although rich in lipid content, the beneficial action of tree nut consumption on maintaining body weight and glucose homeostasis has been validated by clinical trials and intervention studies conducted over the past decade or so (García‐Lorda et al. 2003; Griel & Kris‐Etherton, 2006; King et al. 2008; Mattes et al. 2008; Schwingshackl & Hoffmann 2012). The fact may seem paradoxical but the healthful fatty acid profiles of tree nuts are responsible for these protective effects. The fatty acid compositions of common tree nuts are summarized in Table 11.5. The lipids of tree nuts are generally high in unsaturated fats, with the exception of Brazil and cashew nut oils. Although tree nut oils differed considerably in their levels of individual fatty acids, oleic acid (C18:1 ω‐9) and linoleic acid (C18:2 ω‐6) are considered as the two predominant ones. The oleic acid (O) and linoleic acid (L) ratio (O/L) is an important factor related to the quality and stability of oil products. The O/L ratio is greatest in hazelnuts, while the lowest ratios were reported for pine nut and walnut oils. Of particular note is that walnuts are the only tree nut containing a significant amount of α‐linolenic acid (C18:3 ω‐3).
Table 11.5 Fatty acid composition of tree nuts (g/100 g oil).
| Nut type | C16:0 | C18:0 | C20:0 | C16:1 ω7 | C18:1 ω9 | C20:1 ω9 | C18:2 ω6 | C18:3 ω3 |
| Almond | 6.00–6.45 | 1.47–2.10 | – | 0.40–0.43 | 65.70–67.62 | – | 24.03–24.80 | Trace |
| Brazil nut | 12.63–14.71 | 9.79–11.63 | – | 0.29 | 29.76–38.36 | – | 36.84–45.17 | 0.074 |
| Cashew | 10.31–11.14 | 9.08–9.83 | 0.68–0.74 | 0.34 | 56.87–60.57 | 0.19 | 17.03–22.22 | 0.21 |
| Hazelnut | 5.02–5.78 | 1.89–2.36 | 0.12–0.18 | 0.16–0.19 | 79.57–79.64 | 0.15–0.16 | 11.78–12.72 | 0.08 |
| Macadamia | 8.04–8.78 | 2.34–3.74 | 1.96–2.88 | 17.95–20.8 | 54.1–60.08 | 2.62–2.53 | 2.32–3.74 | – |
| Pecan | 6.15 | 2.54 | – | – | 62.36 | – | 27.69 | 1.25 |
| Pine nut | 4.08–5.22 | 2.36–2.78 | 0.41–0.42 | 0.08 | 24.82–27.67 | 1.32–1.38 | 45.02–46.41 | 19.28 |
| Pistachio | 9.17–11.79 | 1.23–1.5 | – | 1.07 | 55.11–56.75 | – | 28.56–29.45 | 0.33–0.37 |
| Walnut | 6.00–7.11 | 2.00–2.72 | 0.07 | 0.07 | 14.80–16.96 | 0.19 | 58.64–63.10 | 11.67–13.43 |
References: Robbins et al. (2011); Zadernowski et al. (2009); Chandrasekara et al. (2011); Amaral et al. (2006); Crews et al. (2005a and 2005b). C16:0, palmitic acid; C18:0, stearic acid; C20:0 arachidic acid; C16:1 ω7, palmitoleic acid; C18:1 ω9, oleic acid; C20:1 ω9, gondoic acid; C18:2 ω6, linoleic acid; C18:3 ω3, α‐linolenic acid.
Analysis of the unsaponifiables indicated that β‐sitosterol is the most abundant sterol in all tree nut types, followed by stigmasterol and campesterol. Please see Table 11.6 for phytosterol distributions in tree nuts. Pistachio oil contains a significantly higher quantity of β‐sitosterol (260.5 mg/100 g of nut). Intake of rich amounts of phytosterols in tree nut oils can eventually lead to a reduction of serum low‐density lipoprotein (LDL) and total cholesterol levels (Sathe et al. 2009).
Table 11.6 Phytosterol composition of tree nuts (mg/100 g oil).
| Nut type/processing | Campesterol | Stigmasterol | β‐Sitosterol | Δ5‐Avenasterol | Δ7‐Avenasterol | Δ5,24‐Stigmastadienol |
| Almond | 5.50–10.58 | 5.17–6.59 | 207.2–322.2 | 43.91 | – | 9.24 |
| Brazil nut | 1.75 | 8.02 | 91.40 | 32.07 | – | – |
| Cashew | 19.37 | 1.57 | 250.0 | 16.89 | – | 5.65 |
| Hazelnut | 10.09–11.36 | 1.85–2.43 | 156.0–202.6 | 6.16–12.23 | 0.98 | 2.30 |
| Macadamia | 7.33–12.32 | 3.83 | 150.7–196.5 | 20.75 | – | 2.54 |
| Pecan | 8.20 | 3.28 | 167.0 | 10.00 | – | – |
| Pine nut | 32.07 | 2.75 | 197.8 | 66.18 | – | 6.64 |
| Pistachio | 21.68 | 3.82 | 441.0 | 44.58 | – | 6.32 |
| Walnut | 7.76–8.28 | 0.60–1.34 | 142.5–153.9 | 8.60–13.73 | 1.45 | 3.32 |
References: Robbins et al. (2011); Crews et al. (2005a,b); Maguire et al. (2004); Ryan et al. (2006).
Tree nuts are a rich source of phenolic compounds (Tables 11.7 and 11.8). Their antioxidant properties have been confirmed in numerous studies using varying experimental systems (Table 11.9).
Table 11.7 Content of total phenolics in tree nuts.
| Nuts | Total phenolics | Reference |
| Almond | 239 | Kornsteiner et al. 2006; values are expressed as mg gallic acid equivalents/100 g of nuts, fw (mg GAE/100 g) |
| Brazil nut | 112 | |
| Cashew | 137 | |
| Hazelnut | 291 | – |
| Macadamia | 46 | – |
| Peanut | 420 | – |
| Pecan | 1284 | – |
| Pine nut | 32 | – |
| Pistachio | 867 | – |
| Walnut | 1625 | – |
| Almond (Crude extract) | 16.1 ± 0.4 | Amarowicz et al. 2005; values are expressed as mg (+)‐catechin equivalents/g of crude extract (mg CE/g) |
| Almond (LMW fraction) | 7.14 ± 0.2 | |
| Almond (HMW fraction) | 80.4 ± 2.1 | – |
| Almond | 4.18 ± 0.84 | Wu et al. 2004; values are expressed as mg gallic acid equivalents/g of nuts, fw (mg GAE/g) |
| Brazil nut | 3.10 ± 0.96 | |
| Cashew | 2.74 ± 0.39 | – |
| Hazelnut | 8.35 ± 2.16 | – |
| Macadamia | 1.56 ± 0.29 | – |
| Peanut | 3.96 ± 0.54 | – |
| Pecan | 20.16 ± 1.03 | – |
| Pine nut | 0.68 ± 0.25 | – |
| Pistachio | 16.57 ± 1.21 | – |
| Walnut | 15.56 ± 4.06 | – |
HMW, high molecular weight; LMW, low molecular weight.
Table 11.8 Content of flavonoids according to USDA database (mg/100 g edible portion (f w)).a
| Nuts | Anthocyanidins | Catechins | Flavanones | Flavonols |
| Almonds Brazil nuts Cashew Hazelnuts Macadamias Pecans Pine nuts Pistachios Walnuts |
2.43 (0.00–4.40)b – – 6.71 (4.40–13.60) – 7.29 (4.47–11.07) – 7.33 (3.15–14.30) 2.71 (2.11–3.74) |
3.91 (1.97–4.25) – 1.98 (0.00–3.82) 5.93 (0.00–7.23) – 15.99 (4.89–25.83) 0.49 (0.00–0.75) 6.85 (2.62–18.07) – |
0.68 (0.03–1.62) – – – – – – – – |
3.03 (1.02–11.03) – – – – – – 1.56 (0.00–4.30) – |
The numbers in brackets are min/max values reported in the database.
a USDA Database for the Flavonoid Content of Selected Foods: http://www.ars.usda.gov/News/docs.htm?docid=6231.
b Flavonoids content are listed for their mean value, minimum and maximum values reported in the database.
Table 11.9 Antioxidant capacity of tree nuts.
| Nuts | Method | Activity | Unit | Reference |
| Yellow cashew | ABTS | 3.322 | mmol TE/100 g dw | Moo‐Huchin et al. 2015 |
| ABTS | 0.970 | mg vit. C/100 g dw | ||
| DPPH | 1.579 | mmol TE/100 g dw | – | |
| DPPH | 0.340 | mg vit. C/100 g dw | – | |
| Red cashew | ABTS | 3.050 | mmol TE/100 g dw | – |
| ABTS | 0.890 | mg vit. C/100 g dw | – | |
| DPPH | 1.593 | mmol TE/100 g dw | – | |
| DPPH | 0.343 | mg vit. C/100 g dw | – | |
| Almond (Crude extract) | TAA | 0.24 ± 0.02 | μmol Trolox/mg extract | Amarowicz et al. 2005 |
| Almond (LMW fraction) | TAA | 0.09 ± 0.01 | μmol Trolox/mg extract | – |
| Almond (HMW fraction) | TAA | 3.93 ± 0.31 | μmol Trolox/mg extract | – |
| Almond | H‐ORACFL | 42.82 ± 8.71 | μmol of TE/g fw | Wu et al. 2004 |
| Brazil nut | H‐ORACFL | 8.62 ± 2.06 | μmol of TE/g fw | – |
| Cashew | H‐ORACFL | 15.23 ± 2.04 | μmol of TE/g fw | – |
| Hazelnut | H‐ORACFL | 92.75 ± 17.78 | μmol of TE/g fw | – |
| Macadamia | H‐ORACFL | 14.43 ± 2.31 | μmol of TE/g fw | – |
| Peanut | H‐ORACFL | 28.93 ± 2.36 | μmol of TE/g fw | – |
| Pecan | H‐ORACFL | 175.24 ± 10.36 | μmol of TE/g fw | – |
| Pine nut | H‐ORACFL | 4.43 ± 1.11 | μmol of TE/g fw | – |
| Pistachio | H‐ORACFL | 75.57 ± 10.50 | μmol of TE/g fw | – |
| Walnut | H‐ORACFL | 130.57 ± 35.20 | μmol of TE/g fw | – |
ABTS ‐ 2,2′‐azinobis‐(3‐ethylbenzothiazoline)‐6‐sulfonic acid; DPPH ‐ 2,2′‐diphenyl‐1‐picrylhydrazyl radical; dw, dry weight; fw, fresh weight; ORAC, oxygen radical absorbance capacity; TE, trolox equivalents.
Extracts prepared from whole almond seeds and their brown skins showed antioxidant activity evaluated using a cooked comminuted pork model, a β‐carotene‐linoleate model, and a bulk stripped‐corn oil system. In the cooked comminuted pork model system, brown skin extracts inhibited the formation of 2‐thiobarbituric acid reactive substances (TBARS), total volatiles, and hexanal more effectively than the whole seed extract. RP‐HPLC analysis revealed the presence of caffeic, ferulic, p‐coumaric, and sinapic acids as the major phenolic acids in the extracts examined (Wijeratne et al. 2006). Phenolic compounds present in a crude extract of almonds and its fractions, after separation on a lipophilic Sephadex LH‐20 column, showed antioxidant and antiradical properties, as revealed following studies using a β‐carotene‐linoleate model system, the total antioxidant activity method, DPPH radical‐scavenging assay, and reducing power evaluation. Results of these assays showed the highest values of antioxidant activity for the tannin fraction. Another RP‐HPLC analysis of a crude extract from almond seeds revealed the presence of vanillic, caffeic, p‐coumaric, and ferulic acids (after basic hydrolysis), as well as quercetin, kaempferol, and isorhamnetin (after acidic hydrolysis), delphinidin and cyanidin (after n‐butanol‐HCl hydrolysis), and procyanidin B2 and B3 (Amarowicz et al. 2005).
Monagas et al. (2009) reported strong antioxidant capacity of roasted skins obtained from the industrial processing of peanuts, hazelnuts, and almonds as well as fractions containing low and high molecular weight bioactives. The total antioxidant capacity, ORACFL, DPPH radical‐scavenging test, and reducing power assays were employed in this study. Roasted peanut and hazelnut skins presented similar total phenolics contents, much higher than that of almond skins; yet their flavan‐3‐ol profiles, as determined by LC‐ESI‐MS and MALDI‐TOF‐MS, differed considerably. Peanut skins were low in monomeric flavan‐3‐ols (19%) in comparison to hazelnut (90%) and almond (89%) skins.
The phenolic compounds of crude extracts of hazelnut skin and their low molecular weight and tannin constituents exhibited strong antiradical activity against the ABTS radical cation and DPPH radical, as well as reducing power. These results suggest that hazelnut skins can be considered as a value‐added by‐product for use as dietary antioxidants (Alasalvar et al. 2009). The antioxidant activity of a crude hazelnut extract and its fractions was confirmed by the ABTS radical cation and DPPH radical‐scavenging assays, reducing power, and β‐carotene‐linoleate model system. In the extract, five phenolic acids, namely gallic, caffeic, p‐coumaric, ferulic, and sinapic acids, were tentatively identified and quantified, among which gallic acid was the most abundant in both free and esterified forms (Alasalvar et al. 2006).
Anderson et al. (2001) observed that copper‐mediated LDL oxidation was inhibited by 84% in the presence of a walnut extract. During the same study, plasma TBARS formation was significantly inhibited by the walnut extracts. Almond‐pellicle flavonoids increased the resistance of copper‐mediated LDL oxidation in vitro and ex vitro and acted synergistically with vitamins C and E (Chen et al. 2005).
Consumption of hazelnuts (1 g/day/kg body weight) improved oxidative stress markers (e.g. malon(di)aldehyde levels in plasma and plasma antioxidant capacity) in human studies (Durak et al. 1999). In other human clinical trials, the consumption of walnuts, almonds, and almond oil did not affect LDL’s oxidizability (Hyson et al. 2002; Iwamoto et al. 2002).
Phenolic extracts from defatted pecan nutmeat have demonstrated strong antioxidant capacity against reactive radical species in vitro. Hudthagosol et al. (2011) conducted a randomized, placebo‐controlled, cross‐over trial with pecan consumption. Results showed increased γ‐tocopherol and proanthocyanidin (PAC) postprandial levels after pecan consumption. This study indicated that the bioactive constituents from pecans are absorbable and contribute to the postprandial antioxidant defenses in the human body. Robbins et al. (2014, 2015) investigated the antioxidant capacity of pecan phenolic extracts using in vitro methods, and compositional information of low and high molecular weight pecan fractions by RP‐HPLC‐MSn after their separation from a crude acetonic extract via a Sephadex LH‐20 column. The mass spectral results showed ellagic acid, its derivatives, and proanthocyanidins, mostly of two and three degrees of polymerization, to be prominent contributors.
It is now widely accepted that a healthy diet plays a vital role in reducing the risk of disease and achieving optimal health and development. A number of epidemiological studies and clinical trials in recent decades have revealed an inverse relationship between nut consumption and chronic diseases. The outcomes of these researches have led to a move towards issuing a health claim for nut products. Tree nuts are a unique package of healthful fats, plant protein, minerals, and vitamins. The combination of these beneficial nutrients is most likely responsible for their proposed health benefits. O’Neil et al. (2015) conducted a survey assessing the nutrient adequacy of tree nut consumers based on the National Health and Nutrition Examination data from 2005 to 2010. The results showed that tree nut consumers comprised a lower percentage (p <0.0001) of the population below the estimated average requirement (EAR) for vitamins A, E, and C, folate, calcium, iron, magnesium, and zinc and thus possessed better nutrient adequacy than nonconsumers.
It is common for consumers to believe that frequent consumption of high‐fat foods like nuts could have an antagonist effect on body weight maintenance and glucose homeostasis. However, epidemiological studies do not support this concern. Excellent reviews regarding the effect of nut intake on body weight control have been published by García‐Lorda et al. (2003), Sabaté (2003), Vadivel et al. (2012), Jackson & Hu (2014), and Tan et al. (2014). These review articles point out that nut incorporation into the diet is unlikely to promote weight gain, despite an expected increase of total caloric intake. On the contrary, regular nut consumption may aid in maintaining body weight balance. More detailed research on the bioactive constituents and long‐term feeding trials featuring tree nuts are nevertheless warranted to substantiate these purported findings.
Many studies have consistently suggested that frequent nut consumption might protect against and reduce the risk of coronary heart disease (CHD) and cardiovascular disease (CVD) by improving serum blood lipids (Kris‐Etherton 2014; Sabaté & Wien 2013). Some results from clinical investigations are summarized in Table 11.10. For instance, Hu and Stampfer (1999) estimated that substitution of fat from 0.0283 kg of nuts for equivalent energy from carbohydrate in an average diet was associated with a 30% reduction in CHD risk, and the substitution of nut fat for saturated fat was associated with 45% reduction in risk.
Table 11.10 Nut consumption and cardiovascular‐related diseases.
| Nuts | Conclusions | Reference |
| Baru almond (Dipteryx alata Vog.) | Dietary supplementation of mildly hypercholesterolemic subjects with baru almonds improved serum lipid parameters, so that this food might be included in diets for reducing the CVD risk | Bento et al. 2014 |
| Brazil nuts | Brazil nuts intake improved the lipid profile and microvascular function in obese adolescents, possibly due to their high level of unsaturated fatty acids and bioactive substances | Maranhão et al. 2011 |
| Macadamia nuts | Macadamia nuts can be included in a heart‐healthy dietary pattern that reduces lipid/lipoprotein CVD risk factors | Griel et al. 2008 |
| Peanut | Regular peanut consumption lowers serum TAG, augments consumption of nutrients associated with reduced CVD risk, and increases serum magnesium concentration | Alper & Mattes 2003 |
| Peanut | The results suggest that frequent nut and peanut butter consumption is associated with a significantly lower CVD risk in women with type 2 diabetes | Li et al. 2009 |
| Pistachio | Inclusion of pistachios in a healthy diet beneficially affects CVD risk factors in a dose‐dependent manner, which may reflect effects on plasma stearoyl‐CoA desaturase activity (SCD) | Gebauer et al. 2008 |
| Pistachio | A significant decrease in small and dense LDL (sdLDL) levels was observed following the two and one serving of pistachios per day. The inclusion of pistachios in a moderate‐fat diet favorably affects the cardiometabolic profile in individuals with an increased risk of CVD | Hooligan et al. 2014 |
| Walnut | The restructured meat products with added walnuts supplied in this study can be considered functional foods for subjects with high risk for CVD, as their regular consumption provokes a reduction in total cholesterol of 4.5% with respect to baseline values (mixed diet) and 3% with respect to the restructured meat without walnuts | Olmedilla‐Alonso et al. 2008 |
| Walnut | In experiments with rats, a diet containing walnuts prevented hyperleptinemia and decreased the total cholesterol compared with the control | Domínguez‐Avila et al. 2015 |
| Walnut | The results suggest that the walnut extract has a high antiatherogenic potential and a remarkable osteoblastic activity, an effect mediated, at least in part, by its major component ellagic acid. Such findings suggest the beneficial effect of a walnut‐enriched diet on cardioprotection | Papoutsi et al. 2008 |
| Walnut | Flow‐mediated vasodilation (FMD) of the brachial artery improved significantly from baseline when subjects consumed a walnut‐enriched diet as compared with the control diet | Katz et al. 2012 |
| Tree nuts | Two ounces of nuts daily as a replacement for carbohydrate foods improved serum lipids in type 2 diabetes | Jenkins et al. 2011 |
| Tree nuts | The consumption of nuts is associated with a marked decrease in CVD risk in large population‐based studies. Nut consumption is also associated with clinically relevant reduction in LDL cholesterol without adversely affecting HDL cholesterol or causing a significant amount of weight gain | Good et al. 2009 |
| Tree nuts | Prospective studies in non‐Mediterranean populations have consistently related increasing nut consumption to lower coronary heart disease mortality | Guasch‐Ferré et al. 2013 |
| Tree nuts | An increased risk of stroke was observed among participants who never consumed nuts compared with those consuming nuts | Di Giuseppe et al. 2015 |
| Tree nuts | Substitution of the carbohydrate and saturated fatty acids in an average diet with 28.35 g of nuts of equivalent energy was associated with a reduction in CHD | Hu & Stampfer 1999 |
| Tree nuts | Because of their unique nutrient profile, nuts can be part of a diet that features multiple heart‐healthy foods resulting in a cholesterol‐lowering response that surpasses that of cholesterol‐lowering diets typically used to reduce CVD risk | Griel & Kris‐Etherton 2006 |
| Tree nuts | Nut consumption is associated with clinically relevant reduction in LDL cholesterol (‐9% to ‐16%) without adversely affecting HDL cholesterol or causing a significant amount of weight gain | Good et al. 2009 |
CHD, coronary heart disease; CVD, cardiovascular disease; HDL, high‐density lipoprotein; LDL, low‐density lipoprotein; TAG, triglyceride.
The results of research conducted by Fraser et al. (1992) strongly suggest that frequent consumption of nuts may protect against the risk of CHD events. The favorable fatty acid profile of many nuts is one possible explanation for such an effect. Subjects who consumed nuts frequently (e.g. more than four times per week) experienced substantially fewer fatal CHD events and definite nonfatal myocardial infarctions, compared to those who consumed nuts less than once a week.
In the etiology and development of atherosclerosis, plaque plays an important role in chronic inflammation. Activation of the vascular endothelium is an early inflammatory event in the development of atherosclerosis leading to endothelium dysfunction and its consequences (Hansson 2005). Nuts contain several active compounds/bioactives that exhibit antiinflammatory activity; these include ω‐3 polyunsaturated fatty acids (PUFA), dietary fiber, magnesium, L‐arginine, and some antioxidants (Salas‐Salvadó et al. 2008).
Jiang et al. (2006) examined associations between nut and seed consumption and C‐reactive protein (CRP), interleukin‐6, and fibrinogen in the Multi‐Ethnic Study of Atherosclerosis. This 2000 cross‐sectional analysis included 6080 USA participants aged 45 and 84 years old with adequate information on diet and biomarkers. The authors concluded that frequent nut and seed consumption was associated with lower levels of inflammatory markers.
In the study by Salas‐Salvadó et al. (2008) with a total of 339 men and 433 women aged between 55 and 80 years at high cardiovascular risk, the consumption of some typical Mediterranean foods (e.g. fruits, cereals, virgin olive oil, and nuts) was associated with lower serum concentrations of inflammatory markers, especially those related to endothelial function. Subjects with the highest consumption of nuts showed the lowest concentrations of vascular cell adhesion molecule (VCAM‐1) and intracellular adhesion molecule (ICAM‐1), IL‐6, and CRP.
Hshieh et al. (2015) conducted a prospective cohort study with 20 742 male physicians. The study investigated nut intake between 1999 and 2002 via a food‐frequency questionnaire and ascertained deaths through an endpoint committee. The results substantiated the inverse association between nut consumption and the risk of all‐cause and cardiovascular disease mortality amongst all subjects.
Compared to a placebo, supplementation of the diet of 20 mildly hypercholesterolemic subjects (total cholesterol = 5.8 ± 0.2 mmol/L) in a randomized, cross‐over, placebo‐controlled study with 20 g/day of baru almonds (Dipteryxalata Vog.; a native species of almond from Brazil) reduced total cholesterol by 8.1%, LDL cholesterol by 9.4%, and non‐high‐density lipoprotein (HDL) cholesterol by 8.1% (Bento et al. 2014). The improvement of the serum fatty acid profile was found to be dose dependent.
In a randomized, cross‐over clinical trial conducted by Nishi et al. (2014), 27 healthy hyperlipidemic subjects completed three one‐month dietary phases featuring two almond (full and half) and a control phase. Each phase was separated by a washout period lasting a minimum of two weeks. The study revealed that almond consumption favorably altered the serum fatty acids by increasing their total monounsaturated fatty acid (MUFA) content, most notably oleic acid. These changes in the fatty acid profile were postulated as being associated with a lower CHD risk.
In a randomized, placebo‐controlled clinical trial, the consumption of Brazil nuts improved the lipid profile and microvascular function in obese female adolescents (n = 17), possibly due to their high level of unsaturated fatty acids and bioactive substances (Maranhão et al. 2011).
Twenty‐one hypercholesterolemic adults participated in a double‐control sandwich model intervention with a single group and three isoenergetic diet periods for a total of 12 weeks (Orem et al. 2013). The findings indicated that a hazelnut‐enriched diet significantly improved flow‐mediated dilation (FMD) by 56.6%. Oxidized LDL, high sensitivity CRP, and soluble VCAM‐1 levels from the group ingesting the hazelnut diet were significantly lower compared to those of the control diet group. It was suggested that regular consumption of a hazelnut‐enriched diet can improve endothelial function and prevent oxidation of LDL. An improvement in the status of these biomarkers is thought to be responsible for the cardioprotective effects.
In a study with 6309 women with type 2 diabetes, frequent consumption of peanuts and peanut butter (i.e. five servings per week; 26 g nuts per serving and 16 g butter per serving) was inversely associated with total CVD risk in age‐adjusted analyses. Increased nut consumption was significantly associated with a more favorable plasma lipid profile, including lower LDL cholesterol, non‐HDL cholesterol, total cholesterol, and apolipoprotein‐B‐100 concentrations (Li et al. 2009).
In the study conducted by Alper and Mattes (2003), 15 normolipidemic adults participated in a 30‐week cross‐over intervention; the subjects were provided 500 kcal as peanuts during an eight‐week free feeding (FF) diet. The same quantity of peanuts was added during a three‐week addition (ADD) diet or replaced an equal amount of other fats in the diet during an eight‐week substitution (SUB) diet. Serum triacylglycerol concentrations were reduced by 24% during ADD, by 17% during SUB, and by 14% during four weeks of free feeding. In conclusion, regular peanut consumption was shown to lower serum triacylglycerols, augment consumption of nutrients associated with reduced CVD risk, and increase serum magnesium concentrations.
From a randomized, cross‐over, controlled feeding study with 28 subjects, a significant decrease in small and dense LDL (sdLDL) levels was observed after one and two servings of pistachios per day (comprising 30% and 34% of total fat). Furthermore, reductions in sdLDL levels were correlated with reduced TAG levels following the two servings versus the control group (Holligan et al. 2014). In a similar study involving 28 individuals with LDL cholesterol levels greater than or equal to 2.86 mmol/L, two servings/day of a pistachio diet (20% energy from pistachios) resulted in decreased total cholesterol (‐8%), LDL cholesterol (‐11.6%), non‐HDL cholesterol (‐11%), apo B (‐4%), apo B/apo A‐I (‐4%), and plasma of stearoyl‐CoA desaturase activity (SCD) (Gebauer et al. 2008).
In experiments by Domínguez‐Avila et al. (2015), a diet containing whole pecans prevented hyperleptinemia and decreased the content of total cholesterol in blood compared to that of the control. The high fat in the whole pecans (HF + WP) diet upregulated the hepatic expression of apolipoprotein B and LDL receptor mRNAs with respect to the high fat levels. Addition of pecan oil to the diet resulted in a reduced level of triacylglycerols in the blood compared with that of the control.
Regular consumption of walnut‐enriched meat products for five weeks compared with restructured meat products devoid of added walnuts resulted in a decrease in total cholesterol by 12.8% in test subjects. Compared to baseline (mixed diet) data, meat products with walnuts decreased total cholesterol (17.1%), LDL cholesterol (13%), and increased γ‐tocopherol (16.8%) levels (Olmedilla‐Alonso et al. 2008). Daily ingestion of 56 g of walnuts improved endothelial function in overweight adults with visceral adiposity (Katz et al. 2012).
As the endothelial cell expression of adhesion molecules has been recognized as an early step in atherogenesis, Papoutsi et al. (2008) examined the effect of a methanolic extract of walnuts as well as ellagic acid, one of the walnut’s major polyphenolic components, on the expression of vascular cell adhesion molecule (VCAM‐1) and intracellular adhesion molecule (ICAM‐1) in human aortic endothelial cells. The walnut extract and ellagic acid significantly decreased the tumor necrosis factor (TNF)‐α‐induced endothelial expression of both VCAM‐1 and ICAM‐1. The acquired results suggest that the walnut extract possesses a high antiatherogenic potential.
The contents of MUFAs, PUFAs, dietary fiber, vegetable proteins, and polyphenols play an essential role in reducing risk factors for diabetes complications. Some of the findings to date are summarized in Table 11.11.
Table 11.11 Nut consumption and type 2 diabetes.
| Nuts | Conclusions | Reference |
| Almonds | For 22 postmenopausal women with type 2 diabetes, a diet with the addition of almonds has clinically beneficial effects on lipid‐ and lipoprotein‐mediated CVD risk | Richmond et al. 2013 |
| Hazelnuts | Incorporation of hazelnuts into the diet can prevent reduction of HDL‐C concentrations in patients with type 2 diabetes | Damavandi et al. 2013 |
| Tree nuts | Pooled analyses show a metabolic syndrome (MetS) benefit of tree nuts through modest decreases in fasting blood glucose | Mejia et al. 2014 |
| Tree nuts | Pooled analyses show that tree nuts improve glycemic control in individuals with type 2 diabetes, supporting their inclusion in a healthy diet | Viguiliouk et al. 2014 |
| Tree nuts | Consuming 56.7 g of nuts daily as a replacement for carbohydrate foods improved both glycemic control and serum lipids in type 2 diabetes | Jenkins et al. 2011 |
| Tree nuts | In two large, independent cohorts of nurses and other health professionals, the frequency of nut consumption was inversely associated with total and cause‐specific mortality, independently of other predictors of death | Bao et al. 2013a |
| Walnut | A walnut‐enriched ad libitum diet improves endothelium‐dependent vasodilation in type 2 diabetic individuals, suggesting a potential reduction in overall cardiac risk | Ma et al. 2010 |
| Walnut | The consumption of walnuts was inversely associated with risk of type 2 diabetes, and the associations were largely explained by Body Mass Index (BMI). The results suggest that higher walnut consumption is associated with a significantly lower risk of type 2 diabetes in women | Pan et al. 2013 |
| Walnut | Walnut methanolic extract showed a strong α‐glucosidase inhibitory activity with IC50 values of 80 μg/mL | Sancheti et al. 2011 |
CVD, cardiovascular disease; HDL‐C, high‐density lipoprotein cholesterol.
Viguiliouk et al. (2014) conducted a systematic review and meta‐analysis of randomized‐controlled trials to assess the effects of tree nuts on glycemic markers in individuals with diabetes. Pooled analyses show that tree nuts improve glycemic control in subjects with type 2 diabetes. Review articles published by Kendall et al. (2010a,b) suggested that nut consumption had minimum effects on rising postprandial blood glucose levels; instead, it can suppress the rise in blood glucose levels when consumed with other carbohydrate‐dense foods. Fasting blood glucose, as an effect of tree nut consumption, was also underlined by Mejia et al. (2014). Unfortunately, the number of clinical trials on the onset and prevalence of type 2 diabetes and tree nut consumption is limited.
In the Jenkins et al. (2011) study, a total of 117 type 2 diabetic subjects were randomized to one of three treatments for three months. Supplements were provided at 475 kcal per 2000 kcal diet as mixed nuts (75 g/day), muffins, or half portions of both. Improved glycemic control and serum lipids in type 2 diabetes subjects were observed with 0.0567 kg of nuts daily as a replacement for carbohydrate foods.
The association between nut consumption and the risk of type 2 diabetes was studied in a prospective cohort of 20 224 male participants (Kochar et al. 2010). While nut consumption was associated with a lower risk of type 2 diabetes in a model adjusted for age, this relation was attenuated upon additional controls for other confounders from the lowest to the highest category of nut consumption, respectively.
Twenty‐two postmenopausal women with type 2 diabetes consumed personalized diets, with the addition of 30 g/day of almonds. All food was supplied for two periods of three weeks, separated by a four‐week washout. The findings revealed that total and LDL cholesterol decreased significantly (Richmond et al. 2013).
In an eight‐week controlled, randomized parallel study of patients with type 2 diabetes, 50 eligible volunteers were assigned to either the control or intervention groups. The replacement of 10% of the total daily caloric intake with hazelnuts in the intervention group had no effect on fasting blood sugar levels (Damavandi et al. 2013).
The results of Pan et al. (2013) suggest a beneficial effect of walnut consumption. In the multivariable‐adjusted Cox proportional hazards model without body mass index (BMI), walnut consumption was associated with a lower risk of type 2 diabetes, and the HRs for participants consuming 1–3 servings/month (1 serving = 0.028 kg), 1 serving/week, and ≥2 servings/week of walnuts were compared with women who never or rarely consumed walnuts.
According to Ma et al. (2010), a walnut‐enriched diet improves endothelium‐dependent vasodilation in type 2 diabetic individuals, suggesting a potential reduction in overall cardiac risk. This study was a randomized, controlled, single‐blind, cross‐over trial. Twenty‐four participants with type 2 diabetes (mean age 58 years; 14 women and 10 men) were randomly assigned to one of two possible sequence permutations: to receive an ad libitum diet enriched with 0.056 kg (366 kcal) walnuts/day or an ad libitum diet without walnuts for eight weeks. A walnut extract also demonstrated strong α‐glucosidase inhibitory activity with IC50 value of 80 μg/mL (Sancheti et al. 2011).
Nuts can be served as a specific food option for diabetic patients to reduce carbohydrate intake. There is enough evidence to suggest that incorporating nuts, including peanuts, into daily diets can protect against type 2 diabetes and other metabolic syndromes associated with diabetes, even though the exact mechanisms are still unknown. However, the beneficial actions were likely attributed to the reduction in oxidative damage and inflammatory biomarkers in blood lipids. Further efforts are warranted on detailed phytochemical compositions and more interventional studies to elucidate the mechanism regarding the preventive potential of nuts.
Macronutrients, micronutrients, and bioactive compounds (e.g. phenolics, phytoestrogens) present in nuts can act in the prevention of cancer (Falasca et al. 2014; Papanastasopoulos & Stebbing 2013). Some studies of this potential are reported in Table 11.12.
Table 11.12 Nut consumption and cancer.
| Nuts | Conclusion | Reference |
| Fermented almonds, macadamias, hazelnuts, pistachios, and walnuts | This study presents the chemopreventive effects (reduction of tumor‐promoting deoxycholic acid, rise in chemopreventive short chain fatty acids, protection against oxidative stress) of different nuts after in vitro digestion and fermentation, and shows the potential importance of nuts in the prevention of colon cancer | Lux et al. 2012 |
| Tree nuts | Recent studies have suggested that nut consumption is associated with reduced cancer mortality | Falasca et al. 2014 |
| Tree nuts | There are numerous mechanisms of action by which the biological‐active compounds of nuts can intervene in the prevention of cancer, although they have not been fully elucidated | Falasca & Casari 2012 |
| Tree nuts | New epidemiological studies are required to clarify the possible effects of nuts on cancer, particularly prospective studies that make reliable and complete estimations of their consumption and which make it possible to analyze their effects independently of the consumption of legumes and seeds | González & Salas‐Salvadó 2006 |
| Tree nuts | Nuts consumed during adolescence were associated with reduced breast cancer risk | Liu et al. 2014 |
| Tree nuts | Frequent nut consumption is inversely associated with risk of pancreatic cancer in this large prospective cohort of women, independent of other potential risk factors for pancreatic cancer | Bao et al. 2013b |
| Tree nuts | These findings support the hypothesis that dietary intake of fiber and nuts during adolescence influences subsequent risk of breast disease and may suggest a viable means for breast cancer prevention | Su et al. 2010 |
| Walnuts | The results support an effect of walnut and its bioactive constituents on mammary epithelial cells and that multiple molecular targets may be involved | Vanden Heuvel et al. 2012 |
| Walnuts | Walnuts in the diet inhibit colorectal cancer growth by suppressing angiogenesis | Nagel et al. 2012 |
| Walnuts | Walnut phenolic extracts showed concentration‐dependent growth inhibition toward human kidney and colon cancer cells. The results strongly indicate that walnuts constitute an excellent source of effective natural antioxidants and chemopreventive agents | Carvalho et al. 2010 |
There are numerous supposed mechanisms of this action: scavenging of free radicals, regulation of differentiation, inhibition of chemical‐induced carcinogenesis, regulation of DNA damage, regulation of inflammatory response and immunological activity, induction of phase 2 metabolic enzymes, and regulation of hormone mechanisms (González & Salas‐Salvadó 2006). The number of epidemiological studies is limited. Sabaté and Ang (2009) emphasized that studies in the past two decades have examined only three tumor sites, and the benefits appear to be manifested only in women. Several authors concluded that further research is necessary (González & Salas‐Salvadó 2006; Jenab et al. 2004; Nagel et al. 2012; Sabaté & Ang 2009). One of the greatest difficulties in interpreting the results of such studies is that the consumption of nuts, legumes, and seeds is often investigated and reported together (González & Salas‐Salvadó 2006).
According to Falasca et al. (2014), recent studies have suggested that nut consumption is associated with reduced cancer mortality. This evidence reinforces the interest in investigating the chemopreventive properties of nuts, and it raises questions about the specific cancer type(s) and settings that may be affected by nut consumption, as well as the cellular mechanisms involved in this protective effect.
The results of the European Prospective Investigation into Cancer and Nutrition study – a large prospective cohort study involving 10 European countries – showed no association between higher intake of nuts and seeds and the risk of colorectal, colon, and rectal cancers in men and women combined; however, a significant inverse association was observed in subgroup analyses for colon cancer in women at the highest (>6.2 g/day) versus the lowest category of intake and for the linear effect of log‐transformed intake, with no associations in men (Jenab et al. 2004).
Grosso et al. (2015) conducted a systematic review and meta‐analysis of perspective studies that explored the effects of nut consumption on CVD and cancer mortality. The results showed that nut consumption was tightly associated with lower risk of cancer mortality when comparing highest and lowest nut intake categories although the author suggested that no dose effect was observed.
Inverse associations were found between intakes of dietary fiber, vegetable protein, vegetable fat, and nuts during adolescence and breast cancer risk, which persisted after controlling adult intakes (Liu et al. 2014).
Bao et al. (2013b) prospectively followed 75 680 women in the Nurses’ Health Study and examined the association between nut consumption and pancreatic cancer risk. Frequent nut consumption was inversely associated with risk of pancreatic cancer, independent of other potential risk factors for pancreatic cancer.
The findings of Su et al. (2010) support the hypothesis that dietary intake of fiber and nuts during adolescence influences subsequent risk of breast disease and may suggest a viable means for breast cancer prevention. Women consuming greater than or equal to two servings of nuts/week had a 36% lower risk than women consuming less than one serving/month.
The results from the pilot study of Jia et al. (2006) indicate that almond consumption has preventive effects on oxidative stress and DNA damage caused by smoking. The levels of two known biomarkers for DNA damage, urinary 8‐hydroxy‐2′‐deoxyguanosine (8‐OH‐dG) and single‐strand DNA breaks of peripheral blood lymphocytes, were measured by ELISA and Comet assays, respectively. The results showed lower levels of urinary 8‐OH‐dG and single‐strand DNA breaks in the two almond‐treated groups (84 g and 168 g of almonds each day, respectively for four weeks) compared with the control group.
The results of Vanden Heuvel et al. (2012) supported an effect of walnut and its bioactive constituents (α‐linolenic acid (ALA) and β‐sitosterol) on mammary epithelial cells. Lipids from walnuts decreased the proliferation of MCF‐7 cells, as did ALA and β‐sitosterol. An extract of walnut oil increased activity of the farnesoid X receptor (FXR) in the mouse breast cancer cell line TM2H.
Chemopreventive effects (reduction of tumor‐promoting deoxycholic acid, rise in chemopreventive short chain fatty acids (SCFA), protection against oxidative stress) of different nuts after in vitro digestion and fermentation, and their potential importance in the prevention of colon cancer were reported by Lux et al. (2012). Bioactive compounds from in vitro fermented almonds, macadamias, hazelnuts, and walnuts significantly reduced the growth of HT29 cells. DNA damage induced by H2O2 was significantly reduced by the compounds of fermented walnuts after 15 minutes co‐incubation of HT29 cells.
In the research study of Nagel et al. (2012), HT29 human colon cancer cells were injected into six‐week‐old female nude mice. The growth rate of tumors was slower in walnut‐fed compared to corn oil‐fed animals by 27%. Walnuts and their oil significantly reduced serum expression levels of angiogenesis factors, including vascular endothelial growth factor (by 30%), and approximately doubled total necrotic areas despite smaller tumor sizes.
The results obtained by Davis and Iwahashi (2001) suggest that almond consumption may reduce the risk of colon cancer. Six‐week‐old male rats were fed either whole almond‐, almond meal‐, almond oil‐containing or control diets, and were then given subcutaneous injections of azoxymethane twice one week apart. After 26 weeks the animals were injected with bromodeoxyuridine, after which colons were evaluated for aberrant crypt foci (ACF) and cell turnover (labeling index, LI). Whole‐almond ACF and LI were both significantly lower than the wheat bran and cellulose diet groups (−30 and −40%, respectively), while almond meal and almond oil ACF and almond meal LI declines were only significant versus cellulose.
Dietary walnut intake suppressed mammary gland tumorigenesis in mice (Hardman et al. 2011), when compared to a diet without walnuts. Consumption of walnuts significantly reduced tumor incidence (fraction of mice with at least one tumor), multiplicity (number of glands with tumor/mouse), and size. Gene expression analyses indicated that consumption of the walnut diet altered expression of multiple genes associated with the proliferation and differentiation of mammary epithelial cells.
Hardman and Ion (2008) performed a pilot study to determine whether consumption of walnuts could affect growth of MDA‐MB 231 human breast cancers implanted into nude mice. Tumor cells were injected into nude mice that were consuming a control diet with 10% corn oil. After the tumors reached a 3–5 mm diameter, the diet of one group of mice was changed to include ground walnuts, equivalent to 56 g per day in humans. The tumor growth rate from day 10, when tumor sizes began to diverge, until the end of the study was significantly less for the group that consumed walnuts than the group that did not. Tumor cell proliferation decreased, but apoptosis was not altered as a result of walnut consumption.
Reiter et al. (2013) investigated whether a standard mouse diet supplemented with walnuts reduced the establishment and growth of LNCaP human prostate cancer cells. The walnut‐enriched diet reduced the number of tumors and the growth of the LNCaP xenografts. Similarly, the xenografts in the walnut‐fed animals grew more slowly than those in the control diet mice. The final average tumor size in the walnut‐diet animals was roughly one‐fourth the average size of the prostate tumors in the mice that ate the control diet.
Aligning with the beneficial effects of nut consumption on cardio‐ and diabetes‐related diseases, scientific evidence has suggested an association between nut intake and cancer risk reduction. However, the types of cancer examined were limited, and the nuts were usually grouped with other seeds and legumes. Future research, in particular large prospective cohort studies, is needed to substantiate and reinforce the rationale of the effects of nut consumption on cancer risk.
Nutrient‐dense tree nuts and peanuts are an excellent addition to savory snacks for boosting energy or assuaging hunger. Food manufacturers have launched flavored tree nuts and peanut snacks along with their unflavored counterparts. The diversification of product lines can greatly increase consumer acceptance of nut snacks loaded with potential health beneficial properties. A novel spin‐off, such as polyphenol‐rich peanut skin‐fortified peanut butter, has been formulated and investigated (Ma et al. 2013). The proanthocyanidin‐rich red skin of peanuts is a major waste product from peanut‐processing plants. Incorporation of the skins up to 3.75% into peanut butters significantly increased the total phenolics content (TPC) compared with nonfortified counterparts, with minimum perceivable changes in physical texture of the product.
A high lipid‐bearing nature and heart‐healthy lipid profile have made tree nuts good candidates for specialty oils. Although the size of this niche market is relatively small, it has expanded remarkably over the last decade, as more health‐conscious consumers are demanding healthier alternatives with better taste. Tree nuts can be prepared for oil expression after adequate cleaning and shelling. The oil can either be mechanically pressed or extracted with a food‐grade solvent. Mechanically pressed oils are bottled directly after filtration and nitrogen flush to prevent oxidation. These premium‐priced products are commonly used in salad dressings or as dipping sauces to bring signature nutty flavors.
Several authors reported nuts as one of the main food groups causing allergic reactions (Crespo et al. 2006; Roux et al. 2003; Sathe et al. 2009). The concerns about peanut and tree nut allergy have increased along with their growing popularity in recent years, as the nutritional benefits of nut consumption have become more widely known. It is estimated that approximately 1% of the USA population is allergic to peanuts and/or tree nuts. Most of the peanut and tree nut allergens are caused by their storage proteins, which are resistant to heat treatment and complete digestion in the gastrointestinal (GI) tract.
Because of the prevalence of peanut allergies, their allergenicities are the most studied cases. Experimental investigations have shown that the majority of peanut allergens are resistant to digestion in vitro (Fu et al. 2002; Sathe et al. 2005). IgE immunoreactivity of purified Ara h 1 and Ara h 2 prepared from roasted peanuts was higher than that of their counterparts prepared from raw and boiled peanuts. The IgE‐binding capacity of purified Ara h 1 and Ara h 2 was altered by heat treatment, and in particular was increased by roasting. However, no significant difference in IgE immunoreactivity was observed between whole protein extracts from raw and roasted peanut products. The decrease in allergenicity of boiled peanuts results mainly from a transfer of low molecular weight allergens into the water during cooking (Mondoulet et al. 2005).
In the experiment of Schmitt et al. (2010), the soluble and insoluble fractions of peanuts that were boiled, fried, and roasted were subjected to electrophoresis and Western blot analysis using anti‐Ara h 1 and anti‐Ara h 2 antibodies and serum IgE from peanut‐allergic individuals. Overall, protein solubility is reduced with processing and IgE binding increases in the insoluble fractions, due mostly to the increase in the amount of insoluble proteins with increased time of heating in all processes tested. Therefore, it can be concluded that thermal processing of peanuts alters solubility, and the differences in protein solubility within various extract preparations may contribute to inconsistent skinprick test and immunoassay results, particularly when nonstandardized reagents are used.
The protein fractions of peanuts were altered to a similar degree by frying or boiling. Compared with roasted peanuts, the relative quantity of Ara h 1 was reduced in the fried and boiled preparations, resulting in a significant reduction of IgE‐binding intensity. In addition, there was significantly less IgE binding to Ara h 2 and Ara h 3 in fried and boiled peanuts compared with that in roasted peanuts, even though the protein amounts were similar in all three preparations (Beyer et al. 2001).
The findings of Chung and Champagne (2007) revealed that phytic acid formed complexes with the major peanut allergens (Ara h 1 and Ara h 2), which were insoluble in acidic and neutral conditions. Succinylation of the allergens inhibited complex formation, indicating that lysine residues were involved. A six‐fold reduction in IgE binding or allergenic potency of the peanut protein extract was observed after treatment with phytic acid. It was concluded that phytic acid formed insoluble complexes with the major peanut allergens, and resulted in a reduced allergenic potency. Application of phytic acid to a peanut butter slurry presented a similar result, indicating that phytic acid may find use in the development of hypoallergenic peanut‐based products.
The findings of Chung et al. (2004) indicate that peroxidase can help reduce roasted peanut allergens. In their experiments, protein extracts from raw and roasted defatted peanut meals at pH 8 were incubated with and without peroxidase in the presence of H2O2. Results showed that peroxidase treatment had no effect on raw peanuts with respect to protein cross‐linking. However, a significant decrease was evident in the levels of the major allergens, Ara h 1 and Ara h 2, in roasted peanuts after peroxidase treatment; moreover, polymers were formed. Despite this, a reduction in IgE binding was observed. It was concluded that peroxidase induced the cross‐linking of mainly Ara h 1 and Ara h 2 from roasted peanuts and that, due to peroxidase treatment, IgE binding was reduced.
Pomés et al. (2006) studied the effect of roasting on Ara h 1 quantification in peanuts by using a specific monoclonal antibody‐based ELISA. Ara h 1 levels were up to 22‐fold higher in roasted than in raw peanuts. Inhibition ELISA tests indicated that this increase was not due to conformational changes in the Ara h 1 monoclonal antibody epitopes; rather, these results suggest that roasting increases the efficiency of Ara h 1 extraction, and/or that the monoclonal antibody binding epitopes were more accessible in roasted peanuts.
The stability of amadin (14S legumine‐like protein of almonds) to thermal processes (e.g. blanching, roasting, and autoclaving) was confirmed by Roux et al. (2001). The authors used Western blots and almond‐allergic human serum. In the experiments of Venkatachalam et al. (2002), only prolonged roasting and microwave heating for three minutes significantly decreased the allergenic properties of almonds. In this investigation, antigenicity was measured with antialmond rabbit polyclonal antibodies, not human IgE.
Incidence of allergy after tree nut consumption covered almost all types of tree nuts, but current research efforts have only been extended to almonds, Brazil nuts, cashews, hazelnuts, and walnuts. Future work in identifying allergens of other tree nuts is ongoing. To date, a total number of 32 tree nut proteins showing IgE reactivity have been isolated.
Two types of allergens, Ana o 1 and 2, have previously been identified in the extractable protein of cashew nuts, which are defined as vicilin and anacardein, respectively (Wang et al. 2002, 2003). It is important to point out that greater than 50% of cashew‐allergic patients are reported to react with vicilin, even though it accounts for only 5% of the extractable proteins from cashew nuts.
Allergy cases stemming from Brazil nuts are less common in the USA than in the UK. A methionine‐rich 2S albumin protein, Ber e 1, has been identified as being responsible for the allergy reaction (Koppelman et al. 2005; Murtagh et al. 2003).
The hazelnut allergens are characterized by two reaction processes. Some patients are clinically allergic to hazelnuts via a tree pollen‐sensitizing mechanism. A hazelnut allergen, Cor a 1, was reportedly responsible for this type of allergy. However, the nonpollen‐related allergy to hazelnuts has not been well investigated. It is speculated that an 11S globulin, named Cor a 9, might be the cause for hazelnut allergic patients in the USA. Heat treatment at 100 °C for up to 90 minutes had no influence on the allergenicity of hazelnut proteins. The IgE binding activity of the main hazelnut allergens decreased after a 15‐minute heat treatment at temperatures between 100 °C and 185 °C, and was no longer detectable at 170 °C (Wigotzkia et al. 2000). A boiling treatment was reported to be able to decrease the allergenic potency of chestnut (Lee et al. 2005).
Several proteins isolated from walnuts have been confirmed as important allergens. While most of the allergic patients reacted with rJug r 1, a recombinant 2S albumin precursor, other allergens including Jug r 2, 3, 4, and Ara h 1 are also responsible for allergic symptoms.
Pecan antigens are also stable towards digestion. Multiple IgE‐reactive polypeptide bands isolated from pecan protein extracts have shown reactivity in pecan‐allergic patients (Venkatachalam et al. 2006). Sharma et al. (2011a,b) identified pecan 2S albumin, Car I I, Car I 4, and its isomers as major pecan allergens. However, human digestive enzymes were able to decrease the allergenic potency of chestnuts (Lee et al. 2005).
Tree nuts are rich in macronutrients, micronutrients, and bioactives. It is suggested that consuming nuts regularly as part of the diet is associated with better nutrient adequacy and quality. Nut lipids are generally low in saturated fats and high in mono‐ and polyunsaturated fats. The combination of healthful lipid constituents and the beneficial action of nut polyphenols is protective against the development of chronic diseases and cancers. Nuts can be formulated into nutritious snacks or used as food ingredients to serve as both an energy source and bioactive antioxidants; these will provide additional benefits to consumers.