Iron - Nutrition - Revision history

Bara at 08:09, 11 May 2016

2016-05-11T08:09:44Z

Bara: Text replacement - "Category:To Do - Nutrition" to "Category:To_Do_-_Nutrition"

2016-05-10T19:07:41Z

Text replacement - "Category:To Do - Nutrition" to "Category:To_Do_-_Nutrition"

Bara at 13:58, 1 June 2015

2015-06-01T13:58:45Z

Bara: /* Recognised Syndromes Related to Iron Deficiency */

2015-05-22T08:01:07Z

Recognised Syndromes Related to Iron Deficiency

Bara: /* References */

2015-05-19T12:48:28Z

References

Bara: /* Dietary Sources */

2015-05-19T12:47:47Z

Dietary Sources

Bara: /* Cat: */

2015-05-19T12:44:14Z

Cat:

Bara: /* Dog: */

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Dog:

Bara: /* Roles in the Body */

2015-05-19T12:37:59Z

Roles in the Body

Bara: /* Why is it Important? */

2015-05-19T12:33:31Z

Why is it Important?

← Older revision		Revision as of 08:09, 11 May 2016
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	[[Category:Minerals in Nutrition]]		[[Category:Minerals in Nutrition]]
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 [[Category:Minerals in Nutrition]]
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 ==References==
 <references/>
 [[Category:Minerals in Nutrition]]
 [[Category:To Do - Nutrition]]
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 Reports of iron deficiency in dogs and cats are consistent with its involvement in haemoglobin function. The symptoms of iron deficiency are very similar for the two species. Although naturally-occurring dietary iron deficiency is rare, nursing puppies and kittens may have an inadequate intake due to the low iron concentration in milk<ref name="Naigamwalla"/>.
 ====Recognised Syndromes Related to Iron Deficiency====
-#'''Haematological changes:''' Weanling puppies and kittens showed suboptimal blood haemoglobin concentration and low [[Packed Cell Volume|haematocrit]] values when fed diets containing less than 80 mg/kg iron on a dry matter (DM) basis<ref>Chausow, D, Czarnecki-Maulden, G. (1987). “Estimation of dietary iron requirement for the weanling puppy and kitten”. J. Nutr. 117:928-932.</ref>. Other haematological changes reported in dogs include [[Regenerative and Non-Regenerative Anaemias|anaemia]] and low saturation of plasma transferrin – a beta-globulin acting as a carrier of iron<ref name="Harvey">Harvey, J (1998). “Iron deficiency anaemia in dogs and cats”.Proc. N. Am. Vet. Conf. Florida 12:336-338.</ref>.
+#'''Haematological changes:''' Weanling puppies and kittens showed suboptimal blood haemoglobin concentration and low [[Packed Cell Volume|haematocrit]] values when fed diets containing less than 80 mg/kg iron on a [[Nutrition Glossary#Dry Matter Basis|dry matter (DM) basis]]<ref>Chausow, D, Czarnecki-Maulden, G. (1987). “Estimation of dietary iron requirement for the weanling puppy and kitten”. J. Nutr. 117:928-932.</ref>. Other haematological changes reported in dogs include [[Regenerative and Non-Regenerative Anaemias|anaemia]] and low saturation of plasma transferrin – a beta-globulin acting as a carrier of iron<ref name="Harvey">Harvey, J (1998). “Iron deficiency anaemia in dogs and cats”.Proc. N. Am. Vet. Conf. Florida 12:336-338.</ref>.
 #'''Other clinical signs:''' The same researcher<ref name="Harvey"/> also reported clinical signs of iron deficiency in dogs and cats that included poor growth, pale mucous membranes, lethargy and [[Diarrhoea|diarrhoea]]. Haematochezia and melaena were also observed – both are signs of blood loss from the intestine, usually seen as blood in the faeces.

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 [[Category:Minerals in Nutrition]]
 [[Category:To Do - Nutrition]]
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 ==Dietary Sources==
-'''Animal products are rich sources of iron''', and typically manufactured dog and cat foods include materials containing organic iron in the form of haem, such as meat meals, meat and bone meals, fish meals and blood meals. Nevertheless some mineral supplements such as ground limestone and calcium phosphate can contain high amounts of iron. Supplemental sources of iron commonly added to dog and cat foods include salts such as ferrous sulphate or fumarate. Iron can exist in two oxidation states, ferrous (Fe<sup>2+</sup>) and ferric (Fe<sup>3+</sup>), and the ferrous salts in general (especially the sulphate) have higher bio-availability. In contrast, ferric oxide has a very low bio-availability and is unsuitable as a dietary source. These differences in bio-availability are reflected in their [[Iron - Nutrition#Toxicity|degree of toxicity]].
+'''Animal products are rich sources of iron''', and typically manufactured dog and cat foods include materials containing organic iron in the form of haem, such as meat meals, meat and bone meals, fish meals and blood meals. Nevertheless, some mineral supplements such as ground limestone and calcium phosphate can contain high amounts of iron. Supplemental sources of iron commonly added to dog and cat foods include salts such as ferrous sulphate or fumarate. Iron can exist in two oxidation states, ferrous (Fe<sup>2+</sup>) and ferric (Fe<sup>3+</sup>), and the ferrous salts in general (especially the sulphate) have higher bio-availability. In contrast, ferric oxide has a very low bio-availability and is unsuitable as a dietary source. These differences in bio-availability are reflected in their [[Iron - Nutrition#Toxicity|degree of toxicity]].
 ==References==

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 ===Cat:===
-As with dogs, the reports of adverse effects of iron are limited to studies of the administration of acute doses. Hoppe et al<ref>Hoppe, J, Marcelli, G, Tainter,M (1955a). “An experimental study of the toxicity of ferrous gluconate”. Am. J. Med. Sci. 230:491-498.</ref> found that acute oral doses of ferrous sulphate or gluconate equivalent to 16 to 128 mg iron per kg BW resulted in [[Vomiting|vomiting]] within one hour of administration. The same researchers found that the median lethal dose of ferrous sulphate heptahydrate in cats was greater than 500 mg iron per kg BW<ref>Hoppe, J, Marcelli, G, Tainter,M (1955b). “Progress of medical science therapeutics: A review of the toxicity of iron compounds”. Am. J. Med. Sci. 230:558-571.</ref>. In relation to the degree of toxicity, these results are broadly in line with those from the dog studies.
+As with dogs, the reports of adverse effects of iron are limited to studies of the administration of acute doses. Hoppe ''et al''<ref>Hoppe, J, Marcelli, G, Tainter,M (1955a). “An experimental study of the toxicity of ferrous gluconate”. Am. J. Med. Sci. 230:491-498.</ref> found that acute oral doses of ferrous sulphate or gluconate equivalent to 16 to 128 mg iron per kg BW resulted in [[Vomiting|vomiting]] within one hour of administration. The same researchers found that the median lethal dose of ferrous sulphate heptahydrate in cats was greater than 500 mg iron per kg BW<ref>Hoppe, J, Marcelli, G, Tainter,M (1955b). “Progress of medical science therapeutics: A review of the toxicity of iron compounds”. Am. J. Med. Sci. 230:558-571.</ref>. In relation to the degree of toxicity, these results are broadly in line with those from the dog studies.
 ==Dietary Sources==

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 ==Toxicity==
 ===Dog:===
-There is little information on the toxic effects of excess iron in foods, however there are several reports of the adverse effects of iron when administered directly to dogs. D’Arcy and Howard<ref name="D'Arcy">D’Arcy, PF, Howard, EM (1962). “The acute toxicity of ferrous salts administered to dogs by mouth”. J. Pathol. Bacteriol. 83:65-72.</ref> found that a dose of ferrous sulphate supplying only 12 mg iron per kg bodyweight (BW) resulted in mild gastrointestinal damage. A higher dose of 600 mg iron per kg BW was fatal. Doses of ferrous sulphate as low as 200 mg iron per kg BW administered directly to the [[Jejunum - Anatomy & Physiology|jejunum]] were fatal within 6 hours<ref>Bronson, WR, Sisson, TRC (1960). “Studies on acute iron poisoning”. Amer.  J. Dis. Children 99:18-26.</ref> and ferrous sulphate supplying 250 mg iron per kg BW was fatal within 5 to 7 hours when administered by stomach tube<ref>Reissman, E, Coleman, T (1955). “Acute intestinal iron intoxication. II. Metabolic, respiratory and circulatory effects of absorbed iron salts”. Blood 46:46-51.</ref>. In contrast, ferrous carbonate did not produce any effects at 1.5 g iron per kg BW but did at 3 g iron per kg BW. Ferric oxide fed to dogs for 18 months at a dietary content of 1% produced no adverse effects<ref name="D'Arcy"/>. These variations in toxic effects are further examples of the differences in bio-availability of iron salts.
+There is little information on the toxic effects of excess iron in foods, however there are several reports of the adverse effects of iron when administered directly to dogs. D’Arcy and Howard<ref name="D'Arcy">D’Arcy, PF, Howard, EM (1962). “The acute toxicity of ferrous salts administered to dogs by mouth”. J. Pathol. Bacteriol. 83:65-72.</ref> found that a dose of ferrous sulphate supplying only 12 mg iron per kg bodyweight (BW) resulted in mild gastrointestinal damage. A higher dose of 600 mg iron per kg BW was fatal. Doses of ferrous sulphate as low as 200 mg iron per kg BW administered directly to the [[Jejunum - Anatomy & Physiology|jejunum]] were fatal within 6 hours<ref>Bronson, WR, Sisson, TRC (1960). “Studies on acute iron poisoning”. Amer.  J. Dis. Children 99:18-26.</ref> and ferrous sulphate supplying 250 mg iron per kg BW was fatal within 5 to 7 hours when administered by stomach tube<ref>Reissman, E, Coleman, T (1955). “Acute intestinal iron intoxication. II. Metabolic, respiratory and circulatory effects of absorbed iron salts”. Blood 46:46-51.</ref>. In contrast, ferrous carbonate did not produce any effects at 1.5 g iron per kg BW but did at 3 g iron per kg BW. Ferric oxide fed to dogs for 18 months at a dietary content of 1% produced no adverse effects<ref name="D'Arcy"/>. These variations in toxic effects are further examples of the differences in [[Nutrition Glossary#Bioavailability|bio-availability]] of iron salts.
 ===Cat:===
 As with dogs, the reports of adverse effects of iron are limited to studies of the administration of acute doses. Hoppe et al<ref>Hoppe, J, Marcelli, G, Tainter,M (1955a). “An experimental study of the toxicity of ferrous gluconate”. Am. J. Med. Sci. 230:491-498.</ref> found that acute oral doses of ferrous sulphate or gluconate equivalent to 16 to 128 mg iron per kg BW resulted in [[Vomiting|vomiting]] within one hour of administration. The same researchers found that the median lethal dose of ferrous sulphate heptahydrate in cats was greater than 500 mg iron per kg BW<ref>Hoppe, J, Marcelli, G, Tainter,M (1955b). “Progress of medical science therapeutics: A review of the toxicity of iron compounds”. Am. J. Med. Sci. 230:558-571.</ref>. In relation to the degree of toxicity, these results are broadly in line with those from the dog studies.

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 ==Roles in the Body==
-Haemoglobin found in the [[Erythrocytes|red blood cells (erythrocytes)]] transports oxygen from the lungs to the tissues. Myoglobin is the primary oxygen transporter in muscle tissues As a component of cytochromes, such as cytochrome c and cytochrome oxidase, iron is also essential for the functioning of the electron transport chain and the production of energy in the form of adenosine triphosphate (ATP). After haem, the [[Liver - Anatomy & Physiology|liver]] contains the largest iron stores, as ferritin or haemosiderin, both of which are iron-containing proteins<ref name="Naigamwalla">Naigamwalla, DZ, Webb, JA, Giger, U (2012). “Iron deficiency anaemia”. Canad. Vet. J. 53:250-256.</ref>. Body stores of iron are tightly regulated to provide adequate supplies for nutritional requirements, while avoiding toxicity from excess. This is achieved primarily by regulating absorption. The biological availability of iron is affected by a number of factors, in particular the chemical form of the [[Iron - Nutrition#Dietary Sources|iron source]]. In addition, some minerals, especially [[Calcium - Nutrition|calcium]], can decrease the absorption of iron so if calcium supplements are being given to the animal it is particularly important to ensure that the dietary iron content is adequate.
+Haemoglobin found in the [[Erythrocytes|red blood cells (erythrocytes)]] transports oxygen from the lungs to the tissues. Myoglobin is the primary oxygen transporter in muscle tissues. As a component of cytochromes, such as cytochrome c and cytochrome oxidase, iron is also essential for the functioning of the electron transport chain and the production of energy in the form of adenosine triphosphate (ATP). After haem, the [[Liver - Anatomy & Physiology|liver]] contains the largest iron stores, as ferritin or haemosiderin, both of which are iron-containing proteins<ref name="Naigamwalla">Naigamwalla, DZ, Webb, JA, Giger, U (2012). “Iron deficiency anaemia”. Canad. Vet. J. 53:250-256.</ref>. Body stores of iron are tightly regulated to provide adequate supplies for nutritional requirements, while avoiding toxicity from excess. This is achieved primarily by regulating absorption. The biological availability of iron is affected by a number of factors, in particular the chemical form of the [[Iron - Nutrition#Dietary Sources|iron source]]. In addition, some minerals, especially [[Calcium - Nutrition|calcium]], can decrease the absorption of iron so if calcium supplements are being given to the animal it is particularly important to ensure that the dietary iron content is adequate.
 ==Consequences of Iron Deficiency==

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 ==Why is it Important?==
-Iron was recognised as an essential dietary component more than 100 years ago. Its primary role is to serve as a '''component of haemoglobin and myoglobin''' which are the key for the transport and movement of oxygen around the body. It also functions in a number of enzymes such as the cytochromes, that are key regulators in energy metabolism.
+Iron was recognised as an essential dietary component more than 100 years ago. Its primary role is to serve as a '''component of [[Erythrocytes#Function|haemoglobin]] and myoglobin''' which are the key for the transport and movement of oxygen around the body. It also functions in a number of enzymes such as the cytochromes, that are key regulators in energy metabolism.
 ==Roles in the Body==