Copper, iron and zinc

Mean values for Cu, Fe and Zn concentrations in milk, meat and eggs (derived from McCance and Widdowson's The Composition of Food; Food Standards Agency 2002) are given in Table 2 together with a summary of the range of values reported in research publications, mainly from the last 10 years (see Supplementary Material for source references). In general, the ranges reported in the research studies agreed with the mean values from the Food Standards Agency (2002). However, while the ratio of the maximum to minimum values for different meats was approximately 10-fold, the maximum to minimum ratio for milk and eggs was less, approximately 2-fold. Although some of the variation in values for muscle meats is undoubtedly due to factors such as species, muscle type and age (Lawrie & Ledward Reference Lawrie and Ledward2006), this greater variation suggests that there might be scope for the manipulation of meat Cu, Fe and Zn concentrations.

Table 2.

Mean Cu, Fe and Zn concentrations for muscle meats, milk and eggs from the Food Standards Agency (2002) together with the range of values derived from recent literature (see Supplementary Material for details)

Copper

Copper homeostasis in mammals is largely achieved by an uptake of Cu into the liver and the excretion of excess Cu into bile (Sharp Reference Sharp2004). The ability to excrete Cu varies between species and is correlated with the risk of Cu deficiency in the species. Thus ruminants, particularly sheep, which habitually encounter Cu deficiency, accumulate more Cu in the liver and are correspondingly more susceptible to Cu toxicity (Underwood & Suttle Reference Underwood and Suttle1999). Thus, liver Cu concentrations reflect dietary status and vary widely, particularly in ruminants (e.g. 60–450 mg/kg liver in sheep; Woolliams et al. Reference Woolliams, Suttle, Wiener, Field and Woolliams1982) and are 100–1000-fold greater than muscle (Table 2). In contrast to liver concentrations, most supplementation studies have not increased the Cu concentration of other livestock products. It therefore appears that muscle Cu is unresponsive to increasing dietary Cu (Scientific Committee for Animal Nutrition 2003). Studies not reported in the above support this conclusion: there were no differences in muscle Cu in sheep either when herbage with increased Cu concentration was fed (Wilkinson et al. Reference Wilkinson, Hill and Livesey2001), or when ewes were fed 12 or 20 mg Cu/kg diet (Woolliams et al. Reference Woolliams, Suttle, Wiener, Field and Woolliams1982). In pigs, recent studies have shown that muscle Cu does not decline until the Cu status of the pig becomes marginal (Hartmann et al. Reference Hartmann, Eder and Kirchgessner1994; Hernández et al. Reference Hernández, Pluske, D'Souza and Mullan2008).

In eggs, responses (Pesti & Bakalli Reference Pesti and Bakalli1998; Skrivan et al. Reference Skrivan, Skrivanova and Marounek2006b) have been reported in egg Cu at levels of supplementation (250 mg/kg) which approach the tolerable upper level for Cu for hens but not at lower levels of supplementation (Skrivan et al. Reference Skrivan, Skrivanova and Marounek2005). However, increases in Cu concentrations have been observed in the yolk and shell but not the white; thus, overall increases in the Cu concentration of edible egg were not statistically significant (Pesti & Bakalli Reference Pesti and Bakalli1998). In addition, increases in Cu concentration at high levels of supplementation are associated with increased Cu excretion into the environment (Leeson Reference Leeson2009).

For milk, evidence that milk Cu can be influenced by diet arises from surveys of the effects of heavy metal exposure (e.g. Patra et al. Reference Patra, Swarup, Kumar, Nandi, Naresh and Ali2008); no data on dietary Cu were available in these studies and the range in milk Cu concentration was small (0·05–0·15 mg/l).

Iron

In contrast to Cu, there is no controlled route for Fe excretion and the main homeostatic mechanism is the control of absorption from the gastro-intestinal tract. This is mediated by hepcidin (Cairo et al. Reference Cairo, Bernuzzi and Recalcati2006), coupled with recycling of Fe from senescent erythrocytes (Fairweather-Tait Reference Fairweather-Tait2004) and storage in the liver as ferritin. Therefore, only a small fraction of dietary Fe is absorbed. Haem Fe is absorbed via a specific carrier protein (Cairo et al. Reference Cairo, Bernuzzi and Recalcati2006) which accounts for its higher bio-availability compared to non-haem Fe: this is relevant, because muscle Fe is mainly haem Fe (c. 0·85) in the form of myoglobin.

Given the tight control of Fe absorption, it is not surprising that tissue Fe concentration is largely unresponsive to manipulation by dietary means. In supplementation studies with cattle (Standish et al. Reference Standish, Ammerman, Simpson, Neal and Palmer1969), sheep (van Ravenswaay et al. Reference Van Ravenswaay, Henry and Ammerman2001) and pigs (Shaw et al. Reference Shaw, Rozeboom, Hill, Booren and Link2002; O'Sullivan et al. Reference O'Sullivan, Byrne, Stagsted, Andersen and Martens2002; Apple et al. Reference Apple, Wallis-Phelps, Maxwell, Rakes, Sawyer, Hutchison and Fakler2007), responses in muscle Fe were reported only when Fe was supplied (7 g FeSO₄/kg feed; O'Sullivan et al. Reference O'Sullivan, Byrne, Stagsted, Andersen and Martens2002) above the legal limit for inclusion in feed (750 mg/kg feeding stuff). Seo et al. (Reference Seo, Lee, Lee, Shin and Paik2008), however, reported a significant increase in poultry meat Fe (from 20 to 29 mg/kg muscle) through the use of Fe chelated to methionine (200 mg Fe/kg diet), rather than the FeSO₄ used in the above studies.

Differences in effectiveness between Fe supplied as FeSO₄ or chelated to methionine or other organic materials may also apply to eggs. While supplementation with 150 mg/kg FeSO₄ increased egg Fe by approximately 0·05-fold (Skrivan et al. Reference Skrivan, Skrivanova and Marounek2005), 100 mg/kg organic Fe gave greater (>0·10-fold) increases in egg Fe (Park et al. Reference Park, Namkung, Ahn and Paik2004; Paik et al. Reference Paik, Lee and Park2009).

For milk, the only report (Knowles et al. Reference Knowles, Grace, Knight, Mcnabb and Lee2006) of an increase in milk Fe has been by the subcutaneous injection of supplementary Fe, emphasizing the lack of response to dietary Fe.

Zinc

Zinc homeostasis is controlled at the level of the gastro-intestinal tract by absorption from the tract and by excretion in pancreatic secretions (King et al. Reference King, Shames and Woodhouse2000). Control at the cellular level (Cousins et al. Reference Cousins, Liuzzi and Lichten2006) is achieved through balancing the expression of Zn-transporters which control cellular Zn efflux and influx.

Muscle Zn is refractory to manipulation by dietary means. In depletion studies in pigs (Shaw et al. Reference Shaw, Rozeboom, Hill, Booren and Link2002; Hernández et al. Reference Hernández, Pluske, D'Souza and Mullan2008), muscle Zn concentrations remained unchanged, while liver and kidney Zn were depleted. Supplementation with varying forms of Zn in cattle (Malcolm-Callis et al. Reference Malcolm-Callis, Duff, Gunter, Kegley and Vermeire2000; Kessler et al. Reference Kessler, Morel, Dufey, Gutzwiller, Stern and Geyer2003), sheep (Lee et al. Reference Lee, Treloar and Grace1994; Rojas et al. Reference Rojas, McDowell, Cousins, Martin, Wilkinson, Johnson and Velasquez1995; Henry et al. Reference Henry, Littell and Ammerman1997) and chickens (Bou et al. Reference Bou, Guardiola, Tres, Barroeta and Codony2004, Reference Bou, Guardiola, Barroeta and Codony2005) had little effect. In sheep, one study (Lee et al. Reference Lee, Treloar and Grace1994) found a significant increase in muscle Zn in response to herbage Zn, while in another Henry et al. (Reference Henry, Littell and Ammerman1997) reported a decrease. Similarly, egg (Skrivan et al. Reference Skrivan, Skrivanova and Marounek2005) and milk Zn (Cope et al. Reference Cope, Mackenzie, Wilde and Sinclair2009) were unresponsive to dietary supplementation.

In summary, since normal constituents of animal diets contain adequate amounts of Cu, Zn and Fe, homeostatic mechanisms are set to avoid the accumulation of these potentially toxic elements. Therefore, attempts to increase product concentration by dietary means have been largely unsuccessful. There do appear to be some differences between trace elements, with Zn being completely refractory to manipulation, while egg Cu and Fe could be increased. The fact that chicken muscle and egg Fe were increased by chelated Fe but not FeSO₄ suggests that the form of the element may be important.

Iodine and selenium

Table 3 summarizes the range of values for I and Se reported for livestock products in comparison with mean values from the Food Standards Agency (2002). The range of concentrations, approximately 100-fold, is greater than for Fe, Cu and Zn (Table 2), but it is not consistent across all livestock products reflecting the homeostatic mechanisms involved.

Table 3.

Mean I and Se concentrations for muscle meats, milk and eggs from the Food Standards Agency (2002) together with the range of values derived from recent literature (see Supplementary Material for details)

* Sheep consuming seaweed (Liu et al. Reference Lu, Suliman, Hansen and Feldmann2006).

Iodine

In contrast to the positively charged Cu, Fe and Zn, the negatively charged iodide ion is efficiently absorbed from the gastro-intestinal tract and the control of body levels is achieved by uptake into the thyroid gland and excretion of excess in urine. The limited evidence suggests that across species, supplementation with I produces moderate increases in muscle I. In cattle (Meyer et al. Reference Meyer, Weigel, Schone, Leiterer and Flachowsky2008), an increase in dietary I (from 0·8 to 8·3 mg/kg) increased muscle I from 24 to 115 μg/kg. Similarly, in several studies (Schone et al. Reference Schone, Zimmermann, Quanz, Richter and Leiterer2006; Franke et al. Reference Franke, Schone, Berk, Leiterer and Flachowsky2008b), pigs which were fed supplements ranging from 3 to 30 mg I/kg, elicited muscle I concentrations from 15 to 150 μg/kg. An extreme case relates to values given in Table 3 for sheep. These were for sheep grazing seaweed in North Ronaldsay, Orkney Isles (Lu et al. Reference Lu, Suliman, Hansen and Feldmann2006), which habitually consumed I at least 1000-fold more (c. 5600 mg/kg dry matter (DM) than the above studies); however, muscle I concentrations in these sheep were 300–450 μg/kg, less than 10-fold greater than the values reported in cattle and pig studies.

In contrast to the modest increases possible with muscle meats, more substantial increases are possible for egg and in particular milk I concentration. Milk is an alternative route of I excretion to urine and I is secreted in milk proportionate to the intake (Underwood & Suttle Reference Underwood and Suttle1999). For example, Schone et al. (Reference Schone, Leiterer, Lebzien, Bemmann, Spolders and Flachowsky2009) increased dietary I from 0·2 to 10·1 mg/kg feed DM and recorded an increase in milk I from 101 to 2762 μg/kg milk.

The I concentration of the hen's egg is relatively easy to manipulate and a number of I-enriched egg products are commercially available, some providing all the Recommended Daily Allowance (RDA) in one egg (Bourre & Galea Reference Bourre and Galea2006). Yalcin et al. (Reference Yalcin, Kahraman, Yalcin, Yalcin and Dedeoglu2004) noted a linear increase in egg I from 160 to 1300 μg/kg in response to increases in dietary I supplementation up to 24 mg/kg.

Selenium

The chemical form of dietary Se has marked effects on its absorption and utilization, with the main difference being between inorganic (selenite or selenate) or organic (principally seleno-methionine, Se-Met) forms. In contrast to Cu, Fe and Zn, there appears to be no homeostatic control of Se absorption, with an absorption coefficient in non-ruminants of about 0·80 for inorganic Se (Rayman et al. Reference Rayman, Infante and Sargent2008), while Se-Met is actively absorbed via the methionine transport system. In ruminants, the availability of Se is lower, probably because of the reduction of selenite and the catabolism of Se-Met within the rumen. Human Se status widely varies with geographical location (Rayman Reference Rayman2008), reflecting the underlying Se concentration of the soil. In the case of livestock, diets are usually supplemented to avoid Se deficiencies and some countries, for example, Finland, mandate the inclusion of Se in fertilizers, with consequent improvements in the Se status of the human population (Reilly Reference Reilly2004).

Most reports of Se supplementation concern the addition of selenite or organic Se in the form of selenized yeast, which contains predominantly Se-Met. In general, there are consistent responses to supplementation in the Se concentration of all livestock products. Supplementation with Se-Met rather than inorganic Se usually results in greater Se deposition, probably via the non-specific incorporation of Se-Met into protein in place of methionine. There are also differences in the Se species that accumulate; supplementation with Se-Met favours the accumulation of Se-Met rather than seleno-cysteine, particularly at higher inclusion rates (Bierla et al. Reference Bierla, Dernovics, Vacchina, Szpunar, Bertin and Lobinski2008; Juniper et al. Reference Juniper, Phipps, Ramos-Morales and Bertin2008).

Selenium supplementation of poultry products has been summarized by Surai (Reference Surai2006). In one study typical of a number of similar experiments (Sevcikova et al. Reference Sevcikova, Skrivan, Dlouha and Koucky2006), poultry fed diets with no added Se had a breast meat Se concentration of 0·05 mg/kg, compared with 0·22 mg/kg from birds fed Se-Met at 0·3 mg/kg diet, a 4-fold increase in Se. Egg and egg products have been enhanced with varying levels of Se, with commercial products now available in many countries in the world. Typical responses to supplementation are those obtained by Payne et al. (Reference Payne, Lavergne and Southern2005), who observed an increase from 0·25 to 0·67 μg Se/kg when 0·6 mg/kg was included in the diet as Se-Met (from yeast), compared to an increase from 0·25 to 0·33 μg/kg for selenite, and by Skrivan et al. (Reference Skrivan, Simane, Dlouha and Doucha2006a) where increases from 0·14 to 0·25 and 0·14 to 0·39 mg Se/kg were recorded for 0·3 mg/kg selenite and Se-Met, respectively.

In pigs, feeding Se-yeast consistently increases Se deposition in muscle to a greater extent than selenite (Mahan & Parrett Reference Mahan and Parrett1996; Mahan et al. Reference Mahan, Cline and Richert1999; Pesut et al. Reference Pesut, Backovic and Sobajic2005; Zhan et al. Reference Zhan, Wang, Zhao, Li and Xu2007). The mean increase was 3·2-fold for Se-Met (to 0·3 mg/kg muscle) compared to 1·6-fold for selenite (to 0·16 mg/kg muscle). Supplementary Se ranged from 0·3 to 0·5 mg/kg diet. The increases in tissue Se were largely through the incorporation of dietary Se-Met.

In cattle, a 2·8-fold increase (from 0·06 to 0·16 mg/kg muscle) in muscle Se was found with 0·5 mg organic Se/kg (Juniper et al. Reference Juniper, Phipps, Ramos-Morales and Bertin2008). When feeding 0·3 mg Se/kg, a consistently greater response was noted to organic than inorganic Se and tissue deposition was again largely in the form of Se-Met. Finally, in sheep, a 2-fold increase in muscle Se (from 0·10 to 0·22 mg/kg; mainly as Se-Met) was found with 0·4 mg Se/kg diet (Bierla et al. Reference Bierla, Dernovics, Vacchina, Szpunar, Bertin and Lobinski2008), with responses to inorganic Se being smaller.

Se levels in milk can similarly be increased by supplementing the ration of dairy cows. In keeping with other livestock products, selenized yeast provided the greatest response. A recent meta-analysis (Ceballos et al. Reference Ceballos, Sanchez, Stryhn, Montgomery, Barkema and Wichtel2009) of all studies involving Se supplementation of dairy cows reported an average increase in milk Se of 13 μg/l; organic Se, in keeping with data from meat and eggs, produced a substantially greater increase of 29 μg/l. In one UK study (Phipps et al. Reference Phipps, Grandison, Jones, Juniper, Ramos-Morales and Bertin2008), increases from 24 to 75 μg/l were observed with Se-yeast.

Thus, across species there is a 2- to 4-fold increase in muscle, milk and egg Se in response to supplementation with 0·3–0·5 mg Se/kg as organic Se. Lower responses are found with inorganic Se. Therefore, consistent nutritionally useful improvements in meat Se can be obtained by supplementing the feed of livestock; there may also be benefits to product oxidative stability as glutathione peroxidase activity increases in parallel with tissue Se.

Vitamins

In contrast to the trace minerals, microbial fermentation in the ruminant fore-stomach has marked effects on the quantities of vitamins entering the small intestine and available for absorption. Dietary water soluble B vitamins (including cobalamin and riboflavin) are degraded within the rumen and contribute only a small proportion to the amounts entering the small intestine (Schwab et al. Reference Schwab, Schwab, Shaver, Girard, Putnam and Whitehouse2006), most of which are derived from microbial synthesis within the rumen. In contrast, fat soluble vitamin supply is derived from the diet as it is either resistant (vitamin E; Weiss et al. Reference Weiss, Smith, Hogan and Steiner1995; Chikunya et al. Reference Chikunya, Demirel, Enser, Wood, Wilkinson and Sinclair2004) or partially resistant (vitamin A; Weiss et al. Reference Weiss, Smith, Hogan and Steiner1995; Ballet et al. Reference Ballet, Robert, Williams, Givens, Owen, Axford and Omed2000) to rumen degradation. Therefore, for water soluble vitamins, it is necessary to separately consider the ruminant from the monogastric animal.

Cobalamin, folate and riboflavin

Since these vitamins are extensively degraded within the rumen (Santschi et al. Reference Santschi, Berthiaume, Matte, Mustafa and Girard2005; Girard et al. Reference Girard, Santschi, Stabler and Allen2009) and the needs of the animal are usually met or exceeded by microbial synthesis within the rumen, dietary supplementation is not normally practised in ruminant nutrition. The exception to this may be the dairy cow in early lactation, in which there is some evidence that B vitamin supply may be sub-optimal (Girard & Matte Reference Girard and Matte2005). For cobalamin, it is necessary to ensure that sufficient cobalt is supplied in the diet to meet the needs for microbial cobalamin synthesis in the rumen. Opportunities to manipulate vitamin supply to the ruminant are limited, since the supply is dependent on microbial synthesis. Therefore, riboflavin supply expressed per unit feed fermented within the rumen is constant (Schwab et al. Reference Schwab, Schwab, Shaver, Girard, Putnam and Whitehouse2006) and the diet composition does not influence riboflavin supply. Cobalamin differs in that supply was negatively related to the starch concentration of the diet (Schwab et al. Reference Schwab, Schwab, Shaver, Girard, Putnam and Whitehouse2006). There is one report of the effect of supplementary cobalamin on milk cobalamin concentration. Graulet et al. (Reference Graulet, Matte, Desrochers, Doepel, Palin and Girard2007) reported an increase in milk cobalamin from 1·7 to 4·8 μg/l, but the efficiency of transfer from diet to milk was very low (c. 0·0002). Similarly, supplementary folate resulted either in no (Morel Reference Morel2007) or modest increases (15–20 μg/l; Girard et al. Reference Girard, Lapierre, Matte and Lobley2005; Graulet et al. Reference Graulet, Matte, Desrochers, Doepel, Palin and Girard2007) in milk folates. Similar to cobalamin, the efficiency of transfer from diet to milk was very low (0·0002–0·0004), probably because of extensive degradation within the rumen, and unlikely to be economic.

The few reports on muscle vitamin concentrations in the literature are in general agreement with Food Standards Agency (2002) (Table 4), with higher concentrations of cobalamin found in beef and lamb compared to pork and chicken. In cattle (Girard et al. Reference Girard, Berthiaume, Faucitano and Lafreniere2007), the negative effect of dietary starch intake on cobalamin supply was reflected in a reduction in muscle cobalamin concentration (from 11 to 9 μg/kg). Additionally, oxidative muscles (for example, rectus abdominis) had higher cobalamin concentrations (Ortigues-Marty et al. Reference Ortigues-Marty, Micol, Prache, Dozias and Girard2005) than glycolytic muscles (for example, semitendinosus).

Table 4.

Mean cobalamin, folate and riboflavin concentrations for muscle meats, milk and eggs from the Food Standards Agency (2002) together with the range of values derived from recent literature (see Supplementary Material for details)

ND, no data.

Pig diets normally include sufficient supplementary riboflavin, folate and cobalamin to meet the needs of the animal. Recently (Giguere et al. Reference Giguere, Girard and Matte2008), supplementation of pig diets with cobalamin (25 and 150 μg/kg) and folate (10 mg/kg) resulted in modest increases in muscle (longissimus dorsi) cobalamin (2·6–3·8 μg/kg) and folate (18–23 μg/kg). In poultry, McCann et al. (Reference McCann, McCracken, Hoey, Pentieva, McNulty and Scott2004) reported larger increases from 100 to 160 μg/kg in breast meat folate when up to 32 mg folate was added per kg of diet. The basal folate concentration in poultry meat (100–200 μg/kg; McCann et al. Reference McCann, McCracken, Hoey, Pentieva, McNulty and Scott2004) was notably greater than that reported in pig meat (20–30 μg/kg; Giguere et al. Reference Giguere, Girard and Matte2008). For riboflavin, both pig and poultry muscle concentrations appear to be resistant to dietary manipulation (Ang et al. Reference Ang, Jung, Benoff and Charles1984; Bohmer & Roth-Maier Reference Bohmer and Roth-Maier2007).

Similarly, although the cobalamin concentration of eggs can be readily increased nutritionally (4-fold), the responses to riboflavin are modest (Naber & Squires Reference Naber and Squires1993; Leeson & Caston Reference Leeson and Caston2003). There has been more interest in manipulating egg folate concentration. In most studies, maximum response has been to the inclusion of 4 mg folate/kg diet, resulting in an approximate doubling of egg folate concentration (House et al. Reference House, Braun, Ballance, O'Connor and Guenter2002; Hebert et al. Reference Hebert, House and Guenter2005; Roth-Maier & Bohmer Reference Roth-Maier and Bohmer2007; Bunchasek & Kachana Reference Bunchasak and Kachana2009). However, Hoey et al. (Reference Hoey, Mcnulty, McCANN, McCracken, Scott, Marc, Molloy, Graham and Pentieva2009) reported responses up to 16 mg/kg feed (increases from 650 to 1500 μg/kg egg) and attributed part of the difference between studies to whether the total folate or 5-methyltetrahydrofolate was measured.

Vitamins A and E

Both vitamins A (retinol) and E (α-tocopherol) are, after luminal hydrolysis of esters, absorbed by facilitated diffusion from the small intestine into the enterocyte (Debier & Larondelle Reference Debier and Larondelle2005). Absorbed retinol is re-esterified, incorporated into chylomicrons and the majority of retinol taken up into the liver and stored therein. Blood retinol concentrations are tightly controlled and there is a well-established relationship between dietary and liver retinol concentrations (see e.g. Arnett et al. Reference Arnett, Dikeman, Daniel, Olson, Jaeger and Perrett2009). Muscle retinol was increased by dietary supplementation in chickens (from 90 to 180 μg/kg; Jensen et al. Reference Jensen, Jensen, Jakobsen, Engberg, Andersen, Lauridsen, Sorensen, Skibsted and Bertelsen1998) and in pigs (from 30 to 60 μg/kg; Olivares et al. Reference Olivares, Rey, Daza and Lopez-Bote2009), but these were 1000-fold less than increases in liver retinol (58–190 mg/kg for chicken and 62–430 mg/kg for pig) in the same experiments. Similarly, the net increase in egg retinol on supplementation was substantially greater (250 μg/kg; Leeson & Caston Reference Leeson and Caston2003) than muscle.

In contrast to retinol, absorbed α-tocopherol is not re-esterified in the enterocyte (Debier & Larondelle Reference Debier and Larondelle2005), does not accumulate in the liver and circulates in plasma, and is associated with lipoproteins from which it is readily available. As a consequence, concentrations of α-tocopherol in livestock products (Table 5) differ less between tissues than vitamin A, although values for chicken meat and eggs tend to be higher. Meat, milk and egg α-tocopherol concentrations all respond to increased dietary vitamin E: (Givens et al. Reference Givens, Allison and Blake2003; Leeson & Caston Reference Leeson and Caston2003; Bou et al. Reference Bou, Grimpa, Baucells, Codony and Guardiola2006; Cho & Ahn Reference Cho and Ahn2006; De La Fuente et al. Reference De La Fuente, Diaz, Alvarez, Lauzurica, Caneque and Perez2007; Morel et al. Reference Morel, Janz, Zou, Purchas, Hendriks and Wilkinson2008).

Table 5.

Mean retinol and α-tocopherol concentrations for muscle meats, milk and eggs from the Food Standards Agency (2002) together with the range of values derived from recent literature (see Supplementary Material for details)

NR, no value reported.

Summary of responses to dietary supplementation

Table 6 summarizes the responsiveness of livestock products to dietary supplementation. General conclusions are, firstly, egg trace element and vitamin concentrations were more responsive than milk or muscle meats. Secondly, the trace elements Cu, Fe and Zn and the vitamins riboflavin and retinol were largely unresponsive, albeit in some cases based on limited evidence. However, the summary in Table 6 is only useful when intakes of livestock products are taken into account. Table 7 gives estimates for the increase in human intakes (expressed as a percentage of the RNI) that could be achieved if the micro-nutrient concentration in livestock products was increased by the average response possible from feed supplementation. Caution should be attached to these estimates as some increases in nutrient concentration were based on one study (for that reason, beef and lamb are combined and reported as red meat in Table 7). From Table 7, it can be seen that either individually or combined, increasing the nutrient concentration of livestock products could supply a substantial proportion of the RNI (<0·5 in most cases) for I, Se and all vitamins except for riboflavin, but would have little or no effect on Fe, Cu and Zn intakes. Therefore, evidence that the concentrations of these micro-nutrients could be selected genetically will now be addressed.

Table 6.

Summary of the responsiveness of livestock product trace element and vitamin concentrations to dietary supplementation

O, no effect; + to +++, increasing response to supplementation; ND, no data; NA, not applicable, ruminant supply is determined by biosynthesis within the rumen rather than feed supply.

Table 7.

Estimates of the increase (expressed as a proportion of RNI for an adult male) that could be achieved if the nutrient concentration in livestock products was increased by the supplementation of animal feeds by the average value reported in the literature

Estimates were made after the calculation of micro-nutrient intakes from Henderson et al. (Reference Henderson, Irving and Gregory2002) and the Food Standards Agency (2002).