Equine Clinical Nutrition Booklet - Dr Jennifer Stewart - Jenquine

Page 1

LINICAL NUT R EC

ON ITI

EQU IN

Dr Jennifer Stewart BVSc BSc PhD Dip BEP Equine Veterinarian & Consultant Nutritionist

BVSc, BSc, PhD


Introducing Dr Jennifer Stewart After obtaining a veterinary degree & PhD, Dr Jen Stewart spent 40 years in equine practice, including 10 years as the equine nutritionist with Mitavite. During this time, Jen started developing premium formulas for studs, trainers & feed companies in Australia & around the world. She regularly consults to leading International studs & trainers in New Zealand, Australia, South Africa, Japan & India. Jen has spent a fair bit of time researching & being involved in nutritional management of developmental orthopedic diseases, colic, tying-up, laminitis, performance problems, post-surgery & other conditions.

Dr Jennifer Stewart - Australia’s only practicing Equine Veterinarian & Clinical Nutritionist

Combining all of Jen’s experience & wanting to bring science to your feed bin Jenquine was created, where the best evidence-based nutrition supported by veterinary & scientific research is provided. Jenquine is at the cutting edge & provides quality ethical products which have been tested with extensive clinical field trials by veterinarians & horses owners. Our products are formulated & produced in Australia in APVMA licensed & ISO accredited facilities. Jenquine also offer veterinary clinical diet-analysis, support & seminars to equine practitioners & their clients. Our skilled team are passionate about helping horse owners in equine clinical nutrition. A key responsibility for equine veterinarians is education of horse owners, which makes for healthier horses. Dr Stewart makes this easier with Jenquines formulated range of quality products that have been tried & trusted by many veterinarians. Our promise is to continue to BRING SCIENCE TO YOUR FEED BIN.

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LOW IN STARCH, SUGAR

NSC & IRON High in Amino Acids, Antioxidants, Omega 3 & Biotin DR JENNIFER STEWART’S ®

®

all-4-feet ALL-IN-ONE NUTRIENT-DENSE FEED REPLACER VETERINARY FORMULA 10kg PELLETS

®

A UNIQUE COMBINATION OF

For all horses, especially those grazing pastures with soluble & insoluble oxalates.

LINICAL NUT R EC

ON ITI

EQU IN

ORGANIC & INORGANIC CALCIUM

BVSc, BSc, PhD

18kg BLOCKS

Contact us for advice on Equine Equine Nutrition Nutrition & Equine Equine Clinical Clinical Nutrition Nutrition Available Avva A aiila lab blle Australia-wide Au Au ust strra st aliiaa-wi wd de e ask ask sk your yo ou ur local ur locca lo loc al produce prro p od du d uce store uc uce stor sst to orrre e & vet vve et clinic clin cl niicc to to order orrd der er some som ome in n if if they the th ey y don’t do on n’’tt already alr lrea ead dy y stock sto tock c it. it. t.

0419 04 419 19 121 12 211 314 314 4


The Importance of Equine Clinical Nutrition With Dr Jennifer Stewart

We are aware that nutrition in horses plays a part in health, welfare, behaviour & recovery from clinical conditions. That’s why it’s important to understand the importance of getting your horse’s nutrition right. There has been extensive research into feeding horses - much is accurate & applicable, but some is not. Generally, it needs to be combined with other information for it to be usable. The traditional diet analysis offered by nutritionists has limitations because much of the advice is based on data provided by feeding experiments in other species to arrive at minimum feeding standards. No consideration is given for weather, climate, individual requirements & veterinary clinical conditions. The minimum requirement is just that, calculated according to the amount required to prevent clinical signs of deficiencies. Equine clinical nutrition goes beyond minimum recommended intakes & standard feeding guides - taking into account recent veterinary & scientific studies, effects of growth, clinical conditions, performance problems etc, as well as the current diet. Horses that suffer from colic, especially if recurrent, should have their history & diet reviewed & analysed. For horses that are overweight, induction of weight loss is necessary to promote a return to insulin-sensitivity & reduce the risk of sub-clinical & clinical laminitis. 4

Clinical nutrition goes beyond mathematical calculations, minimum recommended intakes & diet analysis To be clinically applicable & meet ‘best practice’, nutritional advice requires veterinary knowledge, understanding of biochemistry, epigenetics, physiology, pathophysiology & the clinical assessment of health, growth, performance & veterinary conditions.


Alterations to the diet & feeding management begin with a full diet analysis to support veterinary medical management. Diet analysis is the only way to determine total daily nutrient intake, set realistic goals & manage weight loss. Computer calculations alone don’t reflect the complexity of requirements for a wide range of veterinary clinical conditions. Many nutritional recommendations change as new research expands our knowledge. Estimates of an individual horse’s requirements can be found on feeding guides, but to be clinically applicable & ‘best practice’, nutritional

advice requires veterinary knowledge & understanding. Horses that benefit from in-depth dietary analysis include: pregnant mares & growing horses, those at risk for or affected by veterinary clinical conditions such as arthritis, behavioural issues, body composition concerns, colic, convalescence, Cushings disease (PPID), dental conditions, developmental orthopaedic diseases (DOD), diarrhoea, EGUS, endocrine problems, EPSM, injuries, insulin resistance (IR), lack of muscle & topline, laminitis, orphan foals, poor hoof quality, performance problems, PSSM, post-surgery, tying-up (RER) & skin conditions.

Feeding horses is an art & a science. At Jenquine, we have progressed the standard, spreadsheet-based diet analysis to develop scientifically sound applied equine clinical nutrition.

HOW TO GET YOUR HORSES DIET ANALYSIS Get your horses Diet Analysis by Australia’s only practicing Equine Veterinarian & Clinical Nutritionist Dr Jennifer Stewart

1. Email or call us to discuss your needs info@jenquine.com 0419 121 314

3. You will receive your personalised diet analysis that has been completely undertaken & reported by Dr Jennifer Stewart

2. We will send you a diet request form to fill in. Please return with your payment receipt.

4. You will have a 1 on 1 30 min phone consultation with Dr Jennifer Stewart, to discuss your new diet analysis

To learn more about Equine Clinical Ntrition, Diet Analysis & our products, please contact us: info@jenquine.com or 0419 121 314 5


NEW PRODUCT Ask your local produce store or Vet clinic to order some.

Equine Clinical Nutrition

Magnesium

PLUS

Vitamins B 1,6 and E LOW IN DR JENNIFER STEWART’S

STARCH, SUGAR NSC & IRON High in Amino Acids, Antioxidants, Omega 3 ® & Biotin

EzyMAG + all-4-feet DR JENNIFER STEWART’S

®

SUPPLEMENT FOR ALL HORSES

YOUR ALL-IN-ONE NUTRIENT-DENSE FEED FOR MUSCLES REPLACER - JUST ADDAND FIBREMIND +/- EXTRA FOR / ADMINISTRATION IN FEED ENERGY SALT AS NEEDED VETERINARY FORMULA

10kg NETT FOR ANIMAL USE ONLY

1 & 2.5kg NETT FOR ANIMAL USE ONLY


DR JENNIFER STEWART’S

all-4-feet

®

YOUR ALL-IN-ONE NUTRIENT DENSE FEED REPLACER - JUST ADD FIBRE +/- EXTRA ENERGY / SALT AS NEEDED all-4-feet® has been developed by veterinarians & nutritionists to help protect growth, performance, health & soundness through improved nutrition. It is a concentrated feed for all horses & ponies & their FEET. It is especially suitable for those with or at risk of inflammatory conditions & whenever a low starch/sugar/NSC diet is indicated. all-4-feet® removes the need to feed multiple supplements (except on veterinary advice), & can replace manufactured feeds or be added to any roughage/grain-based diet.

LOW IN

STARCH, SUGAR NSC & IRON High in Amino Acids, Antioxidants, Omega 3 & Biotin

ANALYSIS (per kg)

Energy (DE) 10MJ NSC 9.5% Starch 2.1% It is a fundamental principle of nature that every horse & pony Sugar 3% requires the same basic nutrients. The total amount required varies Crude Protein 25% with age, breed, body weight, clinical conditions, exercise intensity, Fibre 8% growth & reproductive status – but the essential nutrients are the Salt 1.5% same. Horses in work require the same nutrients as spelling or Oil 12% growing horses, broodmares, convalescing or aged horses & ponies Omega 3 Oil 7% but in larger amounts. It is also a fundamental principle that the more Calcium 25g a horse eats, the more nutrients they take in. Pregnant mares & Phosphorus 10g growing, hard-working horses simply need to be fed more of the same Magnesium nutrients to ensure that their increased requirements are met. 27g 630mg Copper all-4-feet® has been formulated for all horses, ponies & their feet, 1957mg Zinc It can also: 5mg Selenium • be used as a feed replacer 6.85mg Iodine • remove the need to use multiple supplements 1740mg Manganese • be added to existing commercial feed diets when recommended 80mg Biotin daily intakes are not being met 30g Lysine • be added to existing diet when horses have increased needs Methionine • be added to any roughage, grain-based or pasture diets GUARANTEED ANALYSIS 26g 26KIU • used for & is especially suitable for horses with veterinary clinical Vitamin A 360g/kg Magnesium conditions Vitamin D60000iu/kg12KIU Vitamin E 4000mg Vitamin E 80g/kg Thiaminrochloride (B1) ®

®

Correct nutrition is important for the management & preventionPyridoxine hydrochloride (B6) 50g/kg of a range of veterinary clinical conditions including Cushings Sodium 60g/kg (PPID), equine metabolic syndrome (EMS), insulin-resistance (IR),Chloride 63g/kg laminitis, obesity, developmental orthopaedic disease (DOD), PSSM, RER & tying-up. It has a correspondingly vital role FORMULATED AND MADE IN AUSTRALIA as an adjunct to optimise clinical outcomes for many veterinary medical & surgical treatments.

PO Box 541, Richmond NSW 2753 FORMULATED & MADE IN AUSTRALIA by Dr Jennifer Stewart BVSc, BSc, PhD, Equine Veterinarian & Consultant Nutritionist For more information email info@jenquine.com, call 0419 121 314 or www.jenquine.com

Phone 0419 121 314

www.jenquine.com 7


Equine Clinical Nutrition

Magnesium

PLUS

Vitamins B 1,6 &E DR JENNIFER STEWART’S

EzyMAG+ ®

SUPPLEMENT FOR ALL HORSES FOR MUSCLES & MIND FOR ADMINISTRATION IN FEED

1 & 2.5kg NETT FOR ANIMAL USE ONLY


DR JENNIFER STEWART’S

EzyMAG+

®

SUPPLEMENT FOR MUSCLES & MIND FOR ALL HORSES Magnesium has a role in the management or prevention of several equine clinical conditions, including behavioural problems (nervousness & excitability), Cushings disease (PPID), equine metabolic syndrome (EMS), insulin resistance, laminitis, muscle problems & osteochondrosis. Magnesium requirements are also increased in ageing horses; on lush, rapidly growing pasture; during exercise & training; in lactating & cycling mares, & with travel & transport. Behaviour: The combination of magnesium & thiamine has been shown to be equal to acepromazine in reducing excitability, reactivity & heart rate during stressful events. Muscles: In show jumpers, 3-day event, dressage & 4-in-hand horses, Olympic veterinarians reported that magnesium supplementation reduced skin sensitivity, ‘hot’ attitudes, unexplained hindleg lameness (muscular in origin), tying-up, irritability, weakness, stiffness & elevated muscle enzymes (AST & CK). Some mares & fillies are more prone to twitchiness, flighty behaviour, muscle pain & tying up when in-season & this has been associated with an hormone-induced fall in blood magnesium levels. Muscle pain, nervousness & tying-up can all occur in horses with a subclinical magnesium deficiency, & any horse that ties-up can benefit from extra magnesium in their diet. Bone: Young horses, especially those growing rapidly, are at risk of developmental bone disorders. Known as DOD, this syndrome mostly occurs with fast, rapid growth. Recent research in Europe looked at the influence of Mg supplementation on the incidence of osteochondrosis (OC). They concluded that supplements containing magnesium reduced OC incidence. Insulin-resistance & EMS: There are reports of magnesium supplementation improving insulin resistance, reducing & softening crest neck fat & lowering EMS-laminitis risk. It is advisable to ensure that diets for insulin-resistant horses & ponies at least meet the maintenance requirements & many veterinarians recommend 10g of magnesium per day. Immunity: There are important interactions between magnesium, Vitamin E & the immune system, especially in pregnant mares where they increase the quality of the colostrum, & in older horses, where they repair some of the age-related changes in the immune system & increase killing capacity of white blood cells. EzyMAG+® is intended to address subclinical deficiencies, the diagnosis of which is often difficult & requires urine clearance tests— but the clinical signs are recognisable. As with any nutritional deficiency, there are individual variations but most equine diets are deficient in magnesium & most horses benefit from supplementation. NOTE: EzyMAG+® does not include tryptophan. Although studies in rats & mice show a reduction in anxiety, current research in horses shows that tryptophan can cause stimulation & excitement 2–4 hours after dosing; does not change reactive behaviour & that long-term use may have detrimental effects (reduced endurance capacity & acute haemolytic anaemia).

ANALYSIS (per kg) 360g Magnesium 60000iu Vitamin E 80g Thiamine hydrochloride (B1) 50g Pyridoxine hydrochloride (B6) 60g Sodium 63g Chloride

FORMULATED & MADE IN AUSTRALIA

PO Box 541, Richmond NSW 2753 Phone 0419 121 314 www.jenquine.com

FORMULATED & MADE IN AUSTRALIA by Dr Jennifer Stewart BVSc, BSc, PhD, Equine Veterinarian & Consultant Nutritionist For more information email info@jenquine.com, call 0419 121 314 or www.jenquine.com

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Recommended by Veterinarians

A UNIQUE COMBINATION OF

ORGANIC & INORGANIC CALCIUM For all horses especally, those grazing pastures with soluble & insoluble oxalates

DR JENNIFER STEWART’S

BONE FORMULA

®

FORTIFIED CALCIUM FORTE SUPPLEMENT FOR HORSES FOR ADMINISTRATION IN FEED

5kg & 10kg NETT FOR ANIMAL USE ONLY


A UNIQUE COMBINATION OF

DR JENNIFER STEWART’S

BONE FORMULA

®

FORTE

FORTIFIED CALCIUM SUPPLEMENT FOR HORSES

ORGANIC & INORGANIC CALCIUM For all horses especally, those grazing pastures with soluble & insoluble oxalates

TWO types of oxalates = 2 serious veterinary clinical problems for horses SOLUBLE & INSOLUBLE OXALATES =the reason we need to feed inorganic & organic calcium. There are 2 types of oxalates: ones that are soluble & dissolve in the horse’s gut + ones (per that ANALYSIS are insoluble & don’t dissolve. Grasses like kikuyu, panic, setaria, buffel & other sub-tropical species contain oxalates. The oxalates in the plant are bound to minerals including sodium, potassium, magnesium & calcium. Sodium, potassium & magnesium oxalates are soluble & the minerals can be absorbed by the horse. Calcium-oxalate is insoluble & can’t be absorbed.

kg)

SOLUBLE OXALATES When the horse eats the grass, the sodium, potassium & magnesium oxalates (but not the calcium oxalate) dissolve in the horse’s stomach releasing the sodium, potassium, magnesium & oxalate. The horse can then absorb the free sodium, potassium, magnesium & oxalate into the blood. The horse uses the sodium, potassium & magnesium but it has no use for the oxalate. However once absorbed into the blood, the soluble oxalates will bind to the blood calcium. Both the free oxalate & the calcium oxalate in the blood are transported to the kidneys for excretion in the urine. Once in the kidneys, the oxalate forms crystals & stones that damage the kidney & cause renal failure. As well as being absorbed, soluble oxalates have a high affinity for calcium in the gut. Inorganic forms of calcium help prevent free oxalates binding calcium in the gut and oxalate absorption into the blood. Inorganic forms of calcium that can prevent oxalate poisoning include di- & mono-calcium phosphate & calcium carbonate. Jenquine Bone Formula Forte® & Calsorb Forte® provide inorganic forms of calcium to reduce the risk of soluble oxalate absorption & kidney damage. INSOLUBLE OXALATES Calcium-oxalate in the grass is insoluble in the horse’s gut. Because the calcium-oxalate cannot be dissolved to release the calcium, the diet can be calcium deficient. Providing an organic form of absorbable calcium helps prevent the free soluble plant oxalates from binding to the calcium in the diet. ®

ANALYSIS (per kg)

®

Jenquine Bone Formula Forte & Calsorb Forte include inorganic & a readily absorbable source of organic calcium.

Sodium Calcium Manganese Copper Iodine

302g 3855mg 2010mg 34mg

Zinc Selenium Chloride Sodium

3601mg 6.6mg 90g 60g

FORMULATED & MADE IN AUSTRALIA

FORMULATED & MADE IN AUSTRALIA by Dr Jennifer Stewart BVSc, BSc, PhD, Equine Veterinarian & Consultant Nutritionist For more information email info@jenquine.com, call 0419 121 314 or www.jenquine.com

PO Box 541,Phone Richmond NSW 0419 1212753 314 Phone 0419 121 314 jenquine.com

www.jenquine.com 11


DR JENNIFER STEWART’S

CALSORB

®

FORTE

FORTIFIED CALCIUM BLOCK FOR HORSES

WE HAVE YOUR PROBLEM LICKED!

SO YOUR PASTURES ARE DEFICIENT.....


A UNIQUE COMBINATION OF

DR JENNIFER STEWART’S

CALSORB

ORGANIC & INORGANIC CALCIUM

®

FORTE

For all horses, especially those grazing pastures with soluble & insoluble oxalates.

FORTIFIED CALCIUM BLOCK FOR HORSES Recommended by Veterinarians

Bighead, calcium deficiency & osteoporosis are significant problems for horses on sub-tropical grasses - including buffel, panic, kikuyu & setaria. Oxalates in these grasses bind calcium - making it unavailable to the horse & increasing the risk of a dietary calcium deficiency. Clinical signs of calcium deficiency, osteoporosis & nutritional secondary hyperparathyroidism include intermittent lameness, stiffness, shortened stride, tendon & ligament weakness, dental problems, weight loss & fractures. Nutritional secondary hyperparathyroidism (Bighead & osteoporosis) has been reported in pastured & stabled horses. It can occur on grain, bran, hay & pasture diets — especially buffel, pangola, setaria, kikuyu, green panic & signal grasses. These grasses contain oxalates that bind to the calcium in the grass, hard feed & supplements —making the diet calcium deficient & unbalancing the calcium:phosphorus ratio. Grain & bran-based diets often have excess phosphorus & an unbalanced - Ca:P ratio. Calcium is essential for life itself (regulating heartbeat, nerve function, muscle contraction & blood clotting) & blood levels are tightly regulated by parathyroid hormone (PTH). PTH is released when diets are low in calcium — causing calcium to move out of the bones & into the blood, & leading to demineralisation of bones & osteoporosis. Mild cases are difficult to detect, manifesting as vague shifting lameness, shortened stride, soreness at ligament & tendon insertions, joint pain & swelling. In more severe forms, ligament & tendon injuries increase & there may be watery nasal discharge, poor coat, difficulty chewing, dental pain & swelling of the jaws, maxilla, mandible & nasal bones.

18kg NETT FOR ANIMAL USE ONLY

MANAGEMENT & PREVENTION The dietary calcium deficiency must be corrected. Organic MHA is a calcium salt of organic acid & a source of readily assimilable organic calcium. Providing inorganic calcium to help protect against soluble oxalates & organic calcium as a readily absorbale form of calcium, Calsorb Forte® is formulated for diets that are calcium-deficient due to phosphorus, oxalate or medications. Dr Jennifer Stewart’s Bone Formula Forte® & Calsorb Forte® contain organic & inorganic calcium PLUS essential bone trace minerals that are deficient in Australian soils, pastures, hays & grains.

ANALYSIS (per kg) Calcium Salt (NaCl) Manganese Copper

176g 300g 1940mg 1014mg

Iodine Zinc Selenium Methionine

17mg 1814mg 3.3mg 90g

Sodium

FORMULATED & MADE IN AUSTRALIA

PO Box 541, Richmond NSW 2753 Phone 0419 121 314

FORMULATED & MADE IN AUSTRALIA by Dr Jennifer Stewart BVSc, BSc, PhD, Equine Veterinarian & Consultant Nutritionist For more information email info@jenquine.com, call 0419 121 314 or www.jenquine.com

jenquine.com

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FOR VETERINARIANS - Published literature & research The science behind all-4-feet® Correct nutrition is important for healthy horses & also for the management & prevention of a range of veterinary clinical conditions including Cushings (PPID), equine metabolic syndrome (EMS), insulin-resistance (IR), laminitis, obesity, developmental orthopaedic disease (DOD), PSSM, RER & tying-up. It has an equally important role as an adjunct in many veterinary medical & surgical treatments.

Dietary restriction & exercise can improve insulin dysregulation in horses with EMS but may be less successful in horses with PPID & insulin dysregulation.[8] Even when ACTH has normalised, horses with advanced PPID & insulin dysregulation can be difficult to manage. In these cases, careful attention to nutrition is necessary.[9] Reductions in insulin sensitivity are associated with diets rich in non-structural carbohydrates (NSC), starch & sugar[10, 11] and using feeds low in starch, sugar & NSC is really important in minimising & managing IR.[12, 13] Levels of starch, sugar & NSC in various feeds are in Table 1. The laboratory-analysed levels of starch, sugar and NSC in Jenquine all-4-feet® are lower than other available feeds.

PPID & EMS predispose to, & may induce laminitis[1] with risks increased in the presence of regional adiposity & obesity through release of inflammatory cytokines & adipokines.[2] PPID is associated with pars intermedia hyperplasia, whereas EMS is both an endocrine & a metabolic disorder.[1, 3] A component of both is ‘insulin dysregulation’ (tissue IR, basal hyperinsulinaemia &/or postprandial hyperinsulinaemia).[4] Insulin dysregulation is believed to be the link between PPID & laminitis.[5] Although insulin dysregulation is the key feature of EMS,[6] not all horses with PPID are IR.[7]

All grains & starch/sugar feeds containing grain by-products such as millrun, bran, pollard, hominy meal should be eliminated.

Jenquine all-4-feet® is based on vegetable protein meals, oil & fibre, contains no grain or by-products and is low in starch, sugar & NSC.

Table 1. STARCH & CARBOHYDRATE CONTENT OF SOME FEEDS* FEED*

STARCH% WSC%

Jenquine all-4-feet®

0.20

6

Stance Cool Stance*

1

9.3

ESC%

TOTAL NSC%

9.1

10.3

9.00%

Omega Weight Gain*

9.8

6.4

4.9

16.2

Stance GoStance*

11.3

12.1

12.4

23.3

Barastoc Calm Performer*

25.1

5.6

5.5

30.7

Mitavite Economix*

23.2

8.3

5.3

31.5

Mitavite Xtra Cool*

25.5

7.5

4

33

Mitavite Gumnuts*

22.3

10.7

7.8

33

Horsepower Equestrian*

26.7

6.7

4.9

33.4

Nutririce Show & Competition*

28.7

6.7

6.2

35.4

Weightlifter Calm*

29.6

10.4

6.9

40

Mitavite Formula 3*

28.5

13.7

7

42.2

Pryde's EasiResult*

26.3

16.3

8.4

42.6

Barastoc Cool Command*

37.4

6

5.1

43.4

Mi-Feed EasiRider Cool Mix*

40.3

5.7

5

46

*Richards 2008 14

NSC fractions in forages (Table 2) can also induce laminitis[15, 16] & the levels vary with species, stage of growth, day length, sunlight & humidity.[17]

[14]


Table 2 Carbohydrates in some roughages: mean & (range) FEED

SUGAR %

STARCH %

NSC %

WSC %

Alfalfa Hay Alfalfa Pellets Barley Hay Beet Pulp (unmolassed) Brewers grain dry Carrots Copra (coconut meal) Cottonseed hulls Cottonseed whole Flax/linseed meal Grass Hay Grass Pasture Lucerne/clover pasture Oat Hay Rice Bran Sorghum Soybean Hulls Soybean Meal Straw Wheat Wheat Bran Wheat Middlings

8.90 7.20 14.90 10.70

1.9 (0.9 - 2.9) 2.3 (0.27 - 5.4) 5.80 1.4 (0 - 2.55) 7.8 (2.3 - 14.5) 3.2 (0 - 6.6)

11.3 (8.8 - 13.9) 9.30 20.4 (13 - 26) 12.3 (7 - 17.5) 7.4 - 15.1

9.15 (7.32 - 11) 8 (5.5 - 10)

11.10 10.30 16.00 6.20 1.4 (0.7 - 2.4) 4.30 14.30 11.70 7 (4 - 9.5) 10.10

4.2 (1 - 5) 0.3 2.9 (0.3 - 5.4) 2.9 (0.8 - 3.7) 2.56 (0.12 - 5) 1.9 (1 - 3) 6.3 (1.6 - 8.6) 22 ( 9 - 36) 74.5 (70 - 79) 1.4 (0.14 - 2.75) 2.1 (0.4 - 3.2) 2.33 (0 - 5.3) 62 (55 - 69) 23 (15 - 30) 26.2 (16 - 36)

The maximum safe NSC is 10-12% & a threshold of 0.3g/kg body weight NSC has been established.[16] The NSC content of hay will be very close to the pasture from which it was cut & soaking or steaming reduces the NSC & the insulinaemic response.[18, 19] It also results in significant mineral loss & appropriate mineral, Vitamin & amino acid balancing is important.[20, 21] Jenquine all-4-feet® is formulated to provide all nutrients lost during soaking. Teff hay is low in NSC,[22] however it can be high in manganese & oxalates. Iron intake also needs to be monitored as increased serum ferritin has been linked to hyperinsulinaemia & IR.[23-25] The effect of chromium (suggested intake 5-7mg/day) on insulin sensitivity is contradictory & inconsistent.[26, 27] Diets & feeds with a low glycaemic index are preferable for prevention & management of glucose intolerance.[23] Higher fat diets tend to induce lower insulinaemic

10.6 (6.6 - 14.7) 5.50 0.10 4.8 (3.9 - 5.7) 13.8 (9 - 18.4) 15 (8 - 21) 14.5 (11 - 18) 22.1 (15 - 29) 25 (16 - 34) 61.3 (39 - 83) 6.3 (3 - 9.4) 16.2 (12.3 - 18) 9.6 (3 - 16)

11 (6.5 - 15) 10.4 (5 - 16) 16.8 (9 - 25)

6.7 (1.4 - 12)

31.1 (22.8 - 39) 32.00

responses.[28] Caution is required when using micronized & extruded feeds due to increased small intestinal starch digestion.[29] These ‘cooking’ processes are undertaken to increase starch digestion in the small intestine and can increase enzymatic digestion in the small intestine by over 446%.[30] The extent varies between manufacturers.[31] Jenquine all-4-feet® is not heat-processed or cooked. For horses with PSSM (type 1 or 2) limiting NSC intake underpins management.[32-34] Chromium is contraindicated in PSSM horses.[35] In cases of recurrent or idiopathic chronic exertional rhabdomyolysis (ER), current recommendations are that less than 20% of energy intake comes from NSC; at least 20% from fat;[36] Vitamin E (1000-5000iu/day) & selenium intake above NRC recommendations.[35]

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Such diets produce lower glucose, insulin & cortisol responses & lower pre-exercise heart rates.[37] Jenquine all-4-feet® is low in NSC & provides current recommended levels of Vitamin E & selenium for horses with PSSM & RER. Adiposity & obesity Are associated with hyperinsulinaemia, hyperleptinaemia, dyslipidaemia, IR & increased inflammatory cytokine expression.[38,39] Some ponies & horses are obese with normal insulin sensitivity & some EMS horses & ponies have no external evidence of obesity. Neck circumference & cresty neck scores are negatively correlated with insulin sensitivity & are phenotypic markers for EMS.[38,40,41] Increased TNF-α protein expression has been found in visceral adipose tissue collected from IR horses & increased mRNA coding for interleukin-1β & IL-6 has been found in neck crest fat.[42] Weight management Reduction in postprandial hyperinsulinaemia through dietary control is central to the management of EMS[3] & requires removal of grains, pellets or mixes (including those containing grain by-products such as bran, pollard, millrun, hominy meal, mill mix etc) with NSC>12%. Forage only diets rarely provide adequate protein, minerals or Vitamins & it is recommended that 125-500g of a balancer comprising 25% quality protein be fed with a forage diet.[9] Grazing time should be limited to less than an hour twice a day & when NSC is lowest (typically 5am to 10am). Muzzles may be required. Horses & ponies with no pasture access should be fed a measured amount of soaked hay with an appropriate Vitamin-mineral-amino acid balancer pellet.[43] Body condition score (BCS)

14 16

is of limited use for weight management[44] & nomograms & weight tapes are more sensitive measures of weight loss.[45] Jenquine all-4-feet® is 25% protein & fed at 100-500g per day. Information on weight management, nomograms & weight tapes is available on our website www.jenquine.com Pregnant, young & old horses Exaggerated plasma glucose & insulin responses should also be avoided in pregnant mares >200 days gestation, horses under 12 months of age & older horses.[46] The maternal environment has a determinant role in osteoarticular status, post-natal conformation, immune response, energy homeostasis & thyroid & adrenocortical functions in foals.[47] Pregnant mares develop IR at around 28 weeks gestation,[48-50] increasing their risk for laminitis & altering insulin & glucose dynamics in their foals.[49,51,52] Hyperglycaemia &/or hyperinsulinaemia has been correlated with OCD in young horses. The response is more severe in horses <14 months old[53] & is associated with increased incidence of osteochondrotic changes in articular & growth plate cartilages.[54,55] The changes can occur within 3 months on starch/grain-rich feeds.[56] Aged horses Often exhibit hyperglycaemia & hyperinsulinaemia following a glucose challenge.[57] Exercise improves skeletal muscle insulin signalling[58] & when combined with a low NSC diet can help the EMS & the older horse control their glucose & insulin metabolism.[59] Obese & insulin resistant mares also improved their insulin sensitivity with exercise.[60,61]


Protein quality & quantity Are important for all horses. High quality protein is necessary because a deficiency of any single essential amino acid places a limit on tissue building. The dietary protein must contain the 10 essential amino acids. For muscle the most important are lysine, threonine & methionine. Muscle building is so specific that if the feed meets required levels of 9 essential amino acids, but has only half the tenth, body protein synthesis may be reduced by up to 50%. Just as the shortest plank in a barrel limits the amount of water the barrel contains, an essential amino acid deficiency places a limit on new cell creation.

Once an essential amino acid runs out, the building of tissues that require that amino acid, ceases. Feed can’t be used to assess protein quality (amino acid profile) or quantity (grams per day) of protein in the diet. Many horses with PPID have difficulty maintaining muscle mass[62] due to atrophy of type 2A & 2B fibres, loss of type 2B myofibers & oxidative stress. Adjustment of amino acid intake & provision of antioxidants (Vitamin E, selenium & the

minerals upon which the antioxidant defence system relies) can reverse & delay muscle loss.[63] A study on mares[64] Found those on low quality protein had higher rates of early embryonic loss (35.7%) than mares on a good quality protein (7.3%) &, in growing horses, the amino acid profile of the feed determines body composition. Correctly fed yearlings achieve greater gains in wither height, reaching mature height earlier inlife - while depositing less fat. Jenquine all-4-feetŽ supplies quality protein & all essential amino acids. Quality protein is important for all horses regardless of discipline, work level or reproductive status. It affects hoof strength & integrity, work capacity, power-to-weight ratio, endurance & reproduction. Omega 3 fatty acids Also important in the diet for all horses are biotin & methionine & omega 3 fatty acids.[65] Omega 3 fatty acids control microinflammation[66] & have antithrombotic & immunoregulatory properties.[67] Omega 3 benefits mares,[68, 69] colostral[70] & semen quality;[71-74] ageing horses; insulin sensitivity,[46, 75] older breeding stallions[74,76]; showjumpers;[73] inflammatory conditions (including laminitis & arthritis);[77-79] immune function[80] & endurance horses.[81,82] It also delays exercised-induced decrease in erythrocyte membrane flexibility in athletic horses.[83] Immune support Is also provided by Vitamin E – including improved colostral IgG[84] & in older horses, response to vaccination.[85,86] Vitamin C has also been show to support immune function

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& plasma levels are reduced in horses with poor performance, in the postoperative & post-traumatic state, with wound infections, epistaxis, strangles, fever & pneumonia.[87] Vitamin C may be helpful in horses with such conditions.[88] The recommended dose of Vitamin C is 10-25grams per day[89] & it can be supplemented separately as required. In older horses the suggested Vitamin C intake is 25 grams twice daily & it is recommended that zinc, selenium, Vitamins A & E be double NRC minimum levels. Older horses do not require special ‘senior’ feeds however mistakes in feeding or feeding management should be corrected.[90,91] It is a fundamental principle of nature that all horses & ponies requires the same basic nutrients. Horses in work require the same nutrients as spelling or growing horses, broodmares, convalescing or aged horses & ponies - but in larger amounts. Feeding more of the same fundamental nutrients ensures that increased requirements are met. This is the science behind Jenquine all-4-feet®

The science behind EzyMAG+® Jenquine EzyMag+®: a magnesium, thiamine, Vitamin E & B6 supplement for all horses. Magnesium (Mg) is an essential mineral for reactions involving ATP, RNA & DNA. It has an important role in calcium channel function, neurotransmitter release, neuronal excitation, skeletal muscle contraction, vasomotor tone[92] & is an activator of over 325 metabolic enzymes.[93] Clinically, the dominant response in all animals to inadequate Mg intake is poor ‘performance’, bone weakness, increased disease risk & muscle weakness.[94] The most recent Nutrient Requirements for

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Horses (NRC)[95] has increased the recommended minimum daily intake to 0.03g/kg bodyweight (15g for a 500kg horse). Typical diets often do not meet Mg requirements[96] & ongoing research has identified several classes of horses that benefit from Mg supplementation. Bone & DOD Mg deficiency is linked to bone weakness[97] & recommended levels of intake are inadequate for horses in training.[98,99] Increased mineralisation of the cannon bone has been reported at levels 150% of NRC.[100] Other work has linked Mg deficiency with the incidence of orthopaedic diseases, particularly in growing horses[101] & in a recent study supplementing foals with 4g of Mg from birth to 12 months of age resulted in a 50% reduction in OC of the hock & fetlock at 5 months of age & a 14% reduction in stifle OC at 12 months of age.[102] During early lactation & for horses in moderate to intense exercise, Mg requirements increase 1.5 to 2 times beyond NRC maintenance.[103] At recommended feeding rates, Jenquine EzyMag+® meets the most recent recommended intakes of Mg for mares, growing & exercising horses. Nervous & immune systems- behaviour & immunity There is also an important interaction of Mg with the immune & nervous systems. Mg depletion is associated with an increase in pro-inflammatory cytokines & lipid peroxidation.[104] Through its involvement in monoamine neurotransmitter synthesis & receptor binding, Mg deficiency has been linked to behaviour.[105] A recent study in Canada compared the effect on heart rate during transport, stall neophobia, startle responses & unfamiliar objects in horses administered oral acepromazine (ACE) or a


Mg-thiamine supplement.[106]’ When given 30 minutes before the onset of a stress, the combination of Mg & thiamine was as effective as ACE in blunting stress-induced increases in heart rate. Conucted in Australia Another recently-published study compared the effect of Mg to ACE in horses undertaking a reaction speed test. When they received 10g of Mg/day for 7 days, the horses were less reactive than when sedated with ACE.[107] Studies on showjumpers in Germany found that supplementing horses with Mg at 20mg/kg bodyweight resulted in lower heart rates & extended diastole after 4 weeks of jumping training. The Mg showed a stronger effect on decreasing heart rate than training alone.[108] Jenquine EzyMag+® matches the intakes recommended in these studies. Insulin Mg also has an anti-inflammatory role & is important for insulin sensitivity.[23] Insulin-resistant (IR) horses can benefit from Mg & Vitamin B6 supplementation.[109] In addition, soaking or steaming hay to reduce starch & sugar intake causes a significant loss of Mg[20,110,111] & it is recommended that diets for IR horses at least meet recommended maintenance requirements.[103] When fed according to the suggested feeding guide, Jenquine EzyMag+® meets the amounts advised for IR horses & replaces Mg lost in soaked hay. Measuring Mg Blood Mg concentration is an insensitive indicator of intake whereas reduced renal excretion may reflect marginal or deficient Mg.[112] Lowered serum alkaline phosphatase concentrations can indicate a low, if not deficient status in horses.[113]

chain–breaking antioxidant providing antioxidant defence in cells & playing an important role in maintaining the integrity of cell membranes.[114] Supplementing Vitamin E is recommended for pregnant & lactating mares (especially when infection pressure is high);[115] growing horses;[88] in cases of myopathy & when the diet contains oil;[116] horses in hard training:[117, 118] aged horses;[85] & to improve cell-mediated & humoral immune function[119] & the response to vaccination.[120] • In exercising horses high intakes are necessary to maintain Vitamin E status.[121] For antioxidant effects, supplementation at 5 times the NRC (2007) minimum dietary inclusion, or about 5000 IU/day for an average 500 kg horse, is indicated[122] • For parturient mares, it is recommended to provide Vitamin E in the feed at a rate of 160 mg/kg DM. Doubling Vitamin E intake to 160mg/kg diet (2500iu/day for a 500kg mare) increased colostral immunoglobulin G (IgG) content as well as foal serum IgG concentration[115] & it is appropriate to supply growing horses as much Vitamin E as recommended for broodmares.[88] • When feeding oil additional Vitamin E (150iu/100ml oil) is needed.[88] PSSM horses on high oil diets need 1500-5000iu Vitamin E per day.[35] • In endurance horses, a Vitamin E intake of 1150 to 4700 IU/day (1.2 to five times higher than NRC minimum recommended levels) has a protective effect on muscle membrane permeability &/or injury.[123,124] In horses in training Vitamin E lowered creatine kinase (CK), aspartate aminotransferase (AST) & plasma concentrations of total glutathione &

Vitamin E in horses Vitamin E is the major lipid-soluble, 19


glutathione peroxidase. Elevated blood levels of muscle enzymes & signs of tying up can also be caused by magnesium deficiency.[125] Thiamine Is highly involved in carbohydrate metabolism & particularly important for nervous system function. Synthesis occurs in the anterior part of the large colon, however production & absorption may be insufficient under some circumstances.[88] In addition, NRC (2007) minimum recommended intakes may not be adequate. It is advised to double the intake to 0.12mg/kg body weight or 60mg for a 500kg horse.[88] Mg is required for conversion of thiamine into its active form & a Mg deficiency could potentially induce a secondary thiamine deficiency. Tryptophan Jenquine EzyMag®+ does not contain tryptophan. There is some evidence that the desired effect may be evident for a few hours after dosage but tryptophan supplementation can have both sedative & excitatory effects on physiological stress measurements. It did not change reactive behaviour in this study.[126,127] Low doses can cause mild excitement, whereas high doses can reduce endurance capacity, & cause acute haemolytic anaemia if given orally[128] due to a toxic hindgut metabolite.[129] As with any nutritional deficiencies there are individual variations in sensitivity & response to supplementation.

Magnesium has a role in the management & prevention of several equine clinical conditions

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The science behind Bone Formula Forte® & Calsorb Forte® Nutritional secondary hyperparathyroidism (NSH), induced by a diet with a persistent imbalance of calcium & phosphorus, causes generalised osteoporosis.[130-136] It has been described in unweaned foals,[137] stabled horses,[138,139] & grazing horses,[140, 141] in Australia,[139,140,142] Canada,[143] Ethiopia,[144] Hawaii,[145] Hong Kong,[138] Japan,[146,147] Netherlands,[148] New Zealand,[141] Panama,[149] Philippines,[150] South Africa,[151] Spain,[137] Thailand, [152] & the United States.[132,153] Soluble & insoluble oxalates Several tropical grasses & hays contain oxalates at levels that significantly interfere with calcium utilization by horses.[154-161] In the plants, oxalates bind to cations. Magnesium & potassium-oxalates are soluble in the gut but calcium-oxalate is insoluble & largely excreted in the manure.[162] The parathyroid glands respond rapidly to minimal changes in Ca2+ concentrations.[163,164] High phosphorus & low calcium diets induce parathyroid cell hyperplasia[130] & increased serum PTH concentrations.[148] Interaction of PTH with PTH receptors in the osteoblasts increases the synthesis & release of receptor activators & macrophage colony-stimulating factor (M-CSF) resulting in PTH-induced bone resorption, defective mineralisation & generalised osteoporosis.[157,164,165] Clinical & subclinical signs Clinical signs range from watery nasal discharge, mild swelling of the distal pasterns, facial distortion, sinusitis, upper


stomach tube, ill-thrift, lameness, swelling of the maxilla & mandible (found in ~20% of cases), hypocalcaemia & pregnancy tetany, increased incidence of spontaneous fractures, tendon & ligament injuries. Intermittent, insidious, shifting lameness occurs secondary to focal periosteal avulsion, torn or detached ligaments & tendons &/or subepiphyseal microfractures, & joint pain due to loss of underlying trabeculae & articular cartilage erosions.[132] The mineral content of the facial bones & mandible is replaced with osteoid & fibrous tissue (osteodytrophia fibrosa) & combined with resorption of the laminae dura, may result in problems with mastication. Bone loss in NSH peridontal disease is a forerunner to more severe manifestations such as vertebral & long bone fractures.[166] ‘Bighead’? Only 20% of affected horses show classical symptoms of ‘bighead’. In young growing horses, the skeletal calcium cannot be mobilized quickly enough to maintain a normal serum calcium level & the result is rapid development of clinically recognisable NSH (‘bighead’). In the adult the dietary deficiency can be compensated for by the parathyroids, & osteitis fibrosa occurs only in severe deficiency. NSH in adult horses is more frequently characterised by generalised osteoporosis due to increased bone apposition & even more accelerated bone resorption.[131,138,167] A high incidence of vertebral compression fractures may be the only manifestation of NSH in the adult horse & Caple et al (1982)[139] speculated that much of the lameness, tendonitis & spontaneous fractures in racehorses may be due to undetected NSH.

Pathology, radiography & nephropathy The most important pathological change is a generalised osteolytic resorption of the outer circumferential lamellae of long bones.[130,168,169] The periosteum becomes attached by the Sharpey’s fibres to the fibrous tissue which replaces the resorbed lamellae. It now yields to tension from tendons & ligaments & this is the most important cause of lameness. Any bone may be affected & temporary healing may explain the shifting lameness.[131] The earliest radiographic changes are progressive radiolucency, miliary mottling & ongoing loss of the laminae durae dentes.[130] The radiographic changes in the metacarpi include endosteal roughening, radiolucent linear striations in the cortex & coarse trabeculation of the spongy bone at the metaphyseal ends of the medullary cavity. Radiographic changes are insidious, appearing sooner & progressing faster in the maxilla & mandible than in the canon bones, but there is extreme porosity of the entire skeleton. Nephrosis With renal congestion, interstitial fibrosis, white granular deposits in the cortices, necrosis of the tubular epithelium & oxalate crystals in the lumen has been reported in horses grazing setaria.[135,157] Two cases of oxalate-induced nephrosis have occurred recently in Queensland (Stewart & Rupin – manuscript in preparation). Diagnosis Physical examination & diet analysis can be used to support a diagnosis for NSH, which should be based on history, clinical signs & diet analysis.[138,170] The pathophysiology, clinical signs & diagnosis of NSH have been reviewed.[171]

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Prevention & management Calcium supplementation is required. However, because the duration of oxalate ingestion is often unknown, plant levels vary widely & the degree of osteoporosis can only be confirmed with a bone biopsy, it is difficult to prescribe the exact amount of calcium that must be supplemented to an individual horse. The amount of daily Ca required to restore positive Ca balance in horses fed hazardous grasses lies between 45 & 84 mg/kg live weight/day.[172] Supplements Several methods of supplementation have been developed. A once weekly mixture of one kg of ground limestone plus dicalcium phosphate (1:2) in 1.5 kg molasses each week resulted in a reduction in clinical signs, but during the 6 months study period, 3 new cases occurred. The breakdown was thought to be due in part to inadequate dose. When the dose was doubled to 5kg a week & rock phosphate was added, no new cases occurred during the study period.[173,155] The authors concluded that the mixture may be adequate to prevent NSH in horses when the negative balances are of the order of about 20 mg Ca/kg live weight/day. However, negative balances with certain grasses including buffel, kikuyu & Kazungula setaria may exceed these values[174] & this weekly supplement may only delay the onset of clinical signs of NSH.[173] A once weekly dose delivers a high loading of Ca over a short time. There is a limit of approximately 20 mg Ca/kg live weight/ day which can be absorbed & negative balances can remain with once-weekly compared to daily supplementation. Greater weekly amounts or more frequent feeding may be necessary to prevent & cure NSH in grazing horses.[172]

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Adding calcium to the water supply A supplement for field use has to be inexpensive, of high Ca concentration, palatable on its own or by mixing with a suitable vehicle, consumed in sufficient quantity to promote storage when supplied regularly & safe in the long term. Sources of Ca suitable for inclusion in the drinking water were found not to fulfil these criteria.[172] Magnesium There is a perception that oxalates reduce Mg availability but whole body balance studies conducted in metabolism stalls have shown that Mg balance is little affected by oxalate consumption & Mg supplementation is not required.[174,175] Calcium MHA Is a calcium salt of organic acid & a readily assimilable organic calcium. It has 84% methionine activity & is 100 percent absorbed by the animal. There are also several clinical considerations in horses grazing oxalate-containing pastures:[157,176,177] 1. Soluble plant Mg & K-oxalates dissociate in the gut, releasing oxalate. The free oxalate can be absorbed & result in oxalate-induced nephrosis. 2. Soluble oxalates exert a variable effect on absorption of remaining calcium in grasses because free oxalate in the grass can bind calcium in the small intestine. 3. Soluble oxalates & acute toxicity[178] 4. Insoluble calcium-oxalates Because of the combined risks of soluble & insoluble oxalates a combination of inorganic & organic[179] calcium is required in the diet.


In some field situations, a combination of supplement methods may be required to meet management needs. Jenquine Bone Formula Forte® & Calsorb Forte® provide a combination of inorganic & organic calcium as a powder or self-administering block.

JENQUINE’S CLINICAL DIET ANALYSIS SERVICE Nutrition is an important part of equine veterinary practice. The Jenquine vision is to provide a world best-practice equine nutrition & equine clinical nutrition (ECN) service. Diet-analysis is frequently used by nutritionists, veterinarians & horse owners: There are a number of computer-based, diet-analysis software packages available. These programs simplify diet evaluation but should be primarily used as a guide, not the ultimate answer. Care must be taken in interpretation of their output. The main disadvantage of standard software is the use of minimum NRC (2007) values. These are minimum, average intakes to sustain life in an average healthy horse within the population - making the results applicable to less than 50% of horses. In reality requirements vary considerably & horses with a range of veterinary clinical conditions have increased or decreased requirements. The NRC values make no provision for special requirements. Other limitations include: • the assumption that body weight is linearly related to requirements • the use of values derived from data in other species • the emphasis placed on absolute values • the suitability & balance of the source of energy (carbohydrate, fibre & oil) which is critical for many horses in terms of clinical

health, growth (average daily gain & developmental orthopaedic diseases) or performance • lack of discrimination between the practical demands of different types of exercise, fitness, environmental conditions & terrain. • finally, the needs of miniature breeds, donkeys, extreme environments & animals with veterinary clinical conditions are not considered. Recognising the 'one-size-fits-all' approach does not work in every situation, we have progressed spreadsheet-based diet-analyses from the basic foundations to include our expanding knowledge of equine clinical nutrition, epigenetics, achieving genetic potential, avoiding growth disorders & supporting athletic performance. Jenquine incorporates NRC (2007) guidelines with research in the decade since the 2007 publication, results from the German Equine Feeding Standards, lnstitut National de la Recherches Agronomique INRA, & our own databases. Dr Jen Stewart combines 40 years experience as an equine veterinarian & over 20 years of international clinical, racing, stud & performance nutrition with all breeds to provide evidence-based, scientifically sound applied, practical nutrition & equine clinical nutrition. Horses that benefit from in-depth dietary analysis include: pregnant mares & growing horses, those at risk for or affected by veterinary clinical conditions such as arthritis, behavioural issues, body composition concerns, convalescence, Cushings disease (PPID), dental conditions, developmental orthopaedic diseases (DOD), diarrhoea, EGUS, endocrine problems, EPSM, injuries, insulin resistance (IR), lack of muscle & topline, laminitis, orphan foals, poor hoof quality, performance problems, PSSM, post-surgery & skin conditions. 23


REFERENCES 1. Tadros, E. & N. Frank, Endocrine disorders & laminitis. Equine veterinary education, 2013. 25(3): p. 152-162. 2. Suagee, J., et al., Relationships between body condition score & plasma inflammatory cytokines, insulin, & lipids in a mixed population of light‐breed horses. Journal of veterinary internal medicine, 2013. 27(1): p. 157-163. 3. Frank, N., et al., Equine metabolic syndrome. Journal of veterinary internal medicine, 2010. 24(3): p. 467-475. 4. Potter, S., et al., Prevalence of obesity & owners’ perceptions of body condition in pleasure horses & ponies in south‐eastern Australia. Australian veterinary journal, 2016. 94(11): p. 427-432. 5. Frank, N. & E. Tadros, Insulin dysregulation. Equine veterinary journal, 2014. 46(1): p. 103-112. 6. Karikoski, N., et al., Pathology of natural cases of equine endocrinopathic laminitis associated with hyperinsulinemia. Veterinary pathology, 2015. 52(5): p. 945-956. 7. McGowan, T., G. Pinchbeck, & C. McGowan, Prevalence, risk factors & clinical signs predictive for equine pituitary pars intermedia dysfunction in aged horses. Equine veterinary journal, 2013. 45(1): p. 74-79. 8. McGowan, C. Managing the endocrine aged horse with a focus on those at risk of laminitis. in Annual Convention of the American Association of Equine Practitioners. 2018. 9. Morgan, R., J. Keen, & C. McGowan, Treatment of equine metabolic syndrome: a clinical case series. Equine veterinary journal, 2016. 48(4): p. 422-426. 10. Pratt, S., R. Geor, & L. McCutcheon, Effects of dietary energy source & physical conditioning on insulin sensitivity & glucose tolerance in Standardbred horses. Equine veterinary journal, 2006. 38(S36): p. 579-584. 11. Stewart‐Hunt, L., et al., Dietary energy source & physical conditioning affect insulin sensitivity & skeletal muscle glucose metabolism in horses. Equine Veterinary Journal, 2010. 42: p. 355-360.

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12. Kronfeld, D., et al., Insulin resistance in the horse: Definition, detection, & dietetics. Journal of animal science, 2005. 83(suppl_13): p. E22-E31. 13. Nielsen, B.D., et al., Glycemic & insulinemic responses are affected by age of horse & method of feed processing. Journal of equine veterinary science, 2010. 30(5): p. 249-258. 14. Richards, N. THE NON-STRUCTURAL CARBOHYDRATE CONTENT OF SOME COMMERCIALLY AVAILABLE HORSE FEEDS IN AUSTRALIA in Aust. Equine Sc. Symp 2008. 15. Longland, A.C. & B.M. Byrd, Pasture nonstructural carbohydrates & equine laminitis. The Journal of nutrition, 2006. 136(7): p. 2099S-2102S. 16. Pollitt, C., et al., Equine laminitis: 49th Annual convention of the American Association of Equine Practioners. New Orleans, LA, 2003. 17. Hoffman, R., et al., Hydrolyzable carbohydrates in pasture, hay, & horse feeds: direct assay & seasonal variation. Journal of Animal Science, 2001. 79(2): p. 500-506. 18. Hoffman, R., et al., Nonstructural carbohydrate & glycemic response of feeds: how low is “low” starch? Journal of Equine Veterinary Science, 2009. 5(29): p. 379-380. 19. Carslake, H., et al., Insulinaemic & glycaemic responses to three forages in ponies. The Veterinary Journal, 2018. 235: p. 83-89. 20. Mack, S., et al., Impact of water-soaking on the nutrient composition of UK hays. Veterinary Record, 2014: p. etrec-2013-102074. 21. Longland, A., C. Barfoot, & P. Harris, The loss of water-soluble carbohydrate & soluble protein from nine different hays soaked in water for up to 16 hours. Journal of equine veterinary science, 2009. 5(29): p. 383-384. 22. Staniar, W.B., et al., Voluntary intake & digestibility of teff hay fed to horses. Journal of animal science, 2010. 88(10): p. 3296-3303. 23. Kellon, E. Dietary Management of the Insulin Resistant Horse VMD Equine Nutritional Solutions Co-Owner: Equine Cushing’s & Insulin Resistance Group 2005; Available from: www.drkellon.com. 24. Kellon, E.M. & K.M. Gustafson, Possible dysmetabolic hyperferritinemia in hyperinsulinemic horses.


25. Kellon, E.M. & E.N. Solutions, Iron status of hyperinsulinemic/insulin resistant horses. diabetes, 2006. 51(8): p. 2348-2354. 26. Chameroy, K., et al., Effects of a supplement containing chromium & magnesium on morphometric measurements, resting glucose, insulin concentrations & insulin sensitivity in laminitic obese horses. Equine veterinary journal, 2011. 43(4): p. 494-499. 27. Pagan, J., S.G. Jackson, & S.E. Duren. The effect of chromium supplementation on metabolic response to exercise in thoroughbred horses. in Proc. 14th Equine Nutrition & Physiology Symposium. 1995. 28. McGowan, C.M., Getting the Old Guys Back on Track, in AVA Annual Conference. 2018: Brisbane. 29. Julliand, V., A. De Fombelle, & M. Varloud, Starch digestion in horses: the impact of feed processing. Livestock science, 2006. 100(1): p. 44-52. 30. Richards, N., GRAIN PROCESSING: THE DOUBLE EDGED SWORD, in Aust. Equine Sc. Symp. 2006. p. 33. 31. Richards, N., MICRONISED & STEAM FLAKED GRAIN STARCH DIGESTIBILITY:VARIATION BETWEEN PROCESS & MANUFACTURER in AUSTRALASIAN EQUINE SCIENCE SYMPOSIUM. 2012. p. 39. 32. Lentz, L.R., et al., Myoplasmic calcium regulation in myotubes from horses with recurrent exertional rhabdomyolysis. American journal of veterinary research, 2002. 63(12): p. 1724-1731. 33. Johlig, L., et al., Epidemiological & genetic study of exertional rhabdomyolysis in a Warmblood horse family in Switzerland. Equine veterinary journal, 2011. 43(2): p. 240-245. 34. Valentine, B.A., et al., Role of dietary carbohydrate & fat in horses with equine polysaccharide storage myopathy. Journal of the American Veterinary Medical Association, 2001. 219(11): p. 1537-1544. 35. Valberg, S., Muscular System Chapter 4. Nutritional Management of Equine Diseases & Special Cases. 2017: John Wiley & Sons. 36. MacLeay, J.M., et al., Effect of ration & exercise on plasma creatine kinase activity & lactate concentration in Thoroughbred horses with recurrent exertional rhabdomyolysis. American

journal of veterinary research, 2000. 61(11): p. 1390-1395. 37. MacLEAY, J.M., et al., Effect of diet on Thoroughbred horses with recurrent exertional rhabdomyolysis performing a standardised exercise test. Equine Veterinary Journal, 1999. 31(S30): p. 458-462. 38. Frank, N., et al., Physical characteristics, blood hormone concentrations, & plasma lipid concentrations in obese horses with insulin resistance. Journal of the American Veterinary Medical Association, 2006. 228(9): p. 1383-1390. 39. Vick, M., et al., Relationships among inflammatory cytokines, obesity, & insulin sensitivity in the horse. Journal of animal science, 2007. 85(5): p. 1144-1155. 40. Carter, R.A., et al., Apparent adiposity assessed by standardised scoring systems & morphometric measurements in horses & ponies. The Veterinary Journal, 2009. 179(2): p. 204-210. 41. Fitzgerald, D.M., et al., The cresty neck score is an independent predictor of insulin dysregulation in ponies. PloS one, 2019. 14(7). 42. Burns, T., et al., Proinflammatory cytokine & chemokine gene expression profiles in subcutaneous & visceral adipose tissue depots of insulin�resistant & insulin�sensitive light breed horses. Journal of veterinary internal medicine, 2010. 24(4): p. 932-939. 43. McGowan, C. Managing the waistline: Prevention & management of EMS. in AVA Annual Conference. 2018. Brisbane. 44. Dugdale, A.H., et al., Body condition scoring as a predictor of body fat in horses & ponies. The Veterinary Journal, 2012. 194(2): p. 173-178. 45. Dugdale, A., et al., Effect of dietary restriction on body condition, composition & welfare of overweight & obese pony mares. Equine veterinary journal, 2010. 42(7): p. 600-610. 46. Kronfeld, D., A. Rodiek, & C. Stull, Glycemic indices, glycemic loads, & glycemic dietetics. Journal of Equine Veterinary Science, 2004. 9(24): p. 399-404. 47. Peugnet, P., et al., Management of the pregnant mare & long-term consequences on the offspring. Theriogenology, 2016. 86(1): p. 99-109.

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48. Hoffman, R., et al., Glucose clearance in grazing mares is affected by diet, pregnancy, & lactation. Journal of animal science, 2003. 81(7): p. 1764-1771. 49. George, L., et al., Insulin sensitivity & glucose dynamics during pre-weaning foal development & in response to maternal diet composition. Domestic animal endocrinology, 2009. 37(1): p. 23-29. 50. Coverdale, J., C. Hammer, & K. Walter, HORSE SPECIES SYMPOSIUM: Nutritional programming & the impact on mare & foal performance. Journal of animal science, 2015. 93(7): p. 3261-3267. 51. Robles, M., et al., Maternal obesity increases insulin resistance, low-grade inflammation & osteochondrosis lesions in foals & yearlings until 18 months of age. PloS one, 2018. 13(1). 52. George, L.A., et al., Evaluation of the effects of pregnancy on insulin sensitivity, insulin secretion, & glucose dynamics in Thoroughbred mares. American journal of veterinary research, 2011. 72(5): p. 666-674. 53. Ralston, S., Hyperglycemia/hyperinsulinemia after feeding a meat of grain to young horses with osteochondritis dissecans (OCD) lesions. Pferdeheilkunde, 1996. 12: p. 320-322. 54. Glade, M. & T. Belling Jr, A dietary etiology for osteochondrotic cartilage. Journal of equine veterinary science, 1986. 6(3): p. 151-155. 55. Pagan, J.D., et al., The relationship between glycemic response & the incidence of OCD in Thoroughbred weanlings: A field study. Advances in Equine Nutrition III, 2005. 3: p. 433. 56. Glade, M.J., The control of cartilage growth in osteochondrosis: A review. Journal of Equine Veterinary Science, 1986. 6(4): p. 175-187. 57. Ralston, S., C. Nockels, & E. Squires, Differences in diagnostic test results & hematologic data between aged & young horses. American Journal of Veterinary Research, 1988. 49(8): p. 1387-1392. 58. Lacombe, V.A., K.W. Hinchcliff, & S.T. Devor, Effects of exercise & glucose administration on content of insulin-sensitive glucose transporter in equine skeletal muscle. American journal of veterinary research, 2003. 64(12): p. 1500-1506.

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59. Malinowski, K., et al., Effect of training on age‐related changes in plasma insulin & glucose. Equine veterinary journal, 2002. 34(S34): p. 147-153. 60. De Laat, M., et al., Sustained, low‐intensity exercise achieved by a dynamic feeding system decreases body fat in ponies. Journal of veterinary internal medicine, 2016. 30(5): p. 1732-1738. 61. Powell, D., et al., Effect of short‐term exercise training on insulin sensitivity in obese & lean mares. Equine veterinary journal, 2002. 34(S34): p. 81-84. 62. Mid & R.E. Centre. Equine Topline Evaluation Scoring (TES) Chart. 20.1.20]; Available from: https://www.midriversequine.com/equine-topline-evaluation-scoring-tes-chart/. 63. Aleman, M., et al., Myopathy in horses with pituitary pars intermedia dysfunction (Cushing’s disease). Neuromuscular disorders, 2006. 16(11): p. 737-744. 64. Van Niekerk, F. & C. Van Niekerk, The effect of dietary protein on reproduction in the mare. VII. Embryonic development, early embryonic death, foetal losses & their relationship with serum progestagen. Journal of the South African Veterinary Association, 1998. 69(4): p. 150-155. 65. Munsterman, A.S., et al., Effects of the omega-3 fatty acid, α-linolenic acid, on lipopolysaccharide-challenged synovial explants from horses. American journal of veterinary research, 2005. 66(9): p. 1503-1508. 66. Serhan, C.N., et al., Novel functional sets of lipid-derived mediators with antiinflammatory actions generated from omega-3 fatty acids via cyclooxygenase 2–nonsteroidal antiinflammatory drugs & transcellular processing. The Journal of experimental medicine, 2000. 192(8): p. 1197-1204. 67. De Caterina, R., R. Madonna, & M. Massaro, Effects of omega-3 fatty acids on cytokines & adhesion molecules. Current atherosclerosis reports, 2004. 6(6): p. 485-491. 68. Swanson, T., Effects of Dietary Supplementation of Flaxseed & Metabolizable Protein on Reproduction in Mares & Ewes. 2014, North Dakota State University.


69. Jacobs, R.D., Dietary Supplementation of Omega-3 Fatty Acids Influences the Equine Maternal Uterine Environment & Embryonic Development. 2015, Virginia Tech. 70. Hodge, L.B., Effect of omega-3 fatty acid supplementation to gestating & lactating mares on milk IgG & fatty acid composition, mare & foal blood concentrations of IgG, fatty acid composition, insulin & glucose, & placental efficiency. 2015: Mississippi State University. 71. Rodrigues, P.G., et al., Dietary polyunsaturated fatty acid supplementation improves the quality of stallion cryopreserved semen. Journal of equine veterinary science, 2017. 54: p. 18-23. 72. Schmid-Lausigk, Y. & C. Aurich, Influences of a diet supplemented with linseed oil & antioxidants on quality of equine semen after cooling & cryopreservation during winter. Theriogenology, 2014. 81(7): p. 966-973. 73. Oliveira, K., et al., Functional capacity of jumping horses supplemented with linseed. Arquivo Brasileiro de Medicina Veterinária e Zootecnia, 2014. 66(2): p. 497-504. 74. Brinsko, S.P., et al., Effect of feeding a DHA-enriched nutriceutical on the quality of fresh, cooled & frozen stallion semen. Theriogenology, 2005. 63(5): p. 1519-1527. 75. Hess, T.M., et al., Effects of Ω-3 (n-3) fatty acid supplementation on insulin sensitivity in horses. Journal of equine veterinary science, 2013. 33(6): p. 446-453. 76. Blanchard, T.L., et al., Management options for the aged breeding stallion with declining testicular function. Journal of Equine Veterinary Science, 2012. 32(8): p. 430-435. 77. Morris, D.D., et al., Effect of dietary alpha-linolenic acid on endotoxin-induced production of tumor necrosis factor by peritoneal macrophages in horses. American journal of veterinary research, 1991. 52(4): p. 528-532. 78. Morris, D.D., et al., Effect of dietary linolenic acid on endotoxin-induced thromboxane & prostacyclin production by equine peritoneal macrophages. Circulatory shock, 1989. 29(4): p. 311-318. 79. Schauermann, N.L., Effect of n-3 polyunsaturated fatty acid supplementation on circulating concentrations & mRNA expression of inflammatory cytokines in horses. 2010, Colorado State University. Libraries.

80. Vineyard, K.R., Dietary Omega-3 Fatty Acid Supplementation & Its Effect on Plasma & Cell Membrane Composition & Immune Function in Yearling Horses. 2008: University of Florida. 81. Hargreaves, B.J., Vitamin E status of thoroughbred horses & the antioxidant status of endurance horses. 2002, Virginia Tech. 82. Crandell, K. Observations & recommendations for feeding the endurance horses. in Proc Kentucky Eq Res Nutr Conf. Lexington, KY, USA. 2010. 83. Piccione, G., et al., Effect of dietary supplementation with omega 3 on clotting time, fibrinogen concentration & platelet aggregation in the athletic horse. Livestock Science, 2014. 161: p. 109-113. 84. Bondo, T. & S.K. Jensen, Administration of RRR‐α‐tocopherol to pregnant mares stimulates maternal IgG & IgM production in colostrum & enhances Vitamin E & IgM status in foals. Journal of animal physiology & animal nutrition, 2011. 95(2): p. 214-222. 85. Petersson, K., et al., The influence of Vitamin E on immune function & response to vaccination in older horses. Journal of animal science, 2010. 88(9): p. 2950-2958. 86. Muirhead, T., et al., The effect of age on serum antibody titers after rabies & influenza vaccination in healthy horses. Journal of veterinary internal medicine, 2008. 22(3): p. 654-661. 87. Ralston, S.L. & P.A. Harris, Nutritional considerations for aged horses. Equine Applied & Clinical Nutrition, 2013: p. 289-303. 88. Zeyner, A., Equine applied & clinical nutrition E-book: Health, welfare & performance. 2013: Elsevier Health Sciences. 89. Ralston, S.L., Evidence-based equine nutrition. Veterinary Clinics of North America: Equine Practice, 2007. 23(2): p. 365-384. 90. Pugh, D. Feeding the geriatric horse. Current concepts in equine nutrition. in Proceedings of the American Association of Equine Practitioners. 2002. 91. Vervuert, I. & M. Coenen. Nutritional management in horses: selected aspects to gastrointestinal disturbances & geriatric horses. in Proceedings of the 2nd European Equine Nutrition & Health Congress. 2004.

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92. Stewart, A.J., Magnesium disorders in horses. Veterinary Clinics: Equine Practice, 2011. 27(1): p. 149-163. 93. Stewart, A.J., Magnesium Homeostasis & Derangement. Equine Fluid Therapy, 2015. 94. Coenen, M., Macro & trace elements in equine nutrition. Equine Applied & Clinical Nutrition: Health, Welfare & Performance, 2013: p. 190-228. 95. NRC Nutrient requirements of horses, 6th ed. 2007, National Academy Press: Washington, DC. 96. Frape, D., Equine Nutrition & Feeding p. 50. 2nd ed. 2000, Oxford: Blackwell Science. 97. Harrington, D., Influence of magnesium deficiency on horse foal tissue concentraion of Mg calcium & phosphorus. Br J Nutr 1975. 34: p. 45–57. 98. Vervuert, I., Major mineral & trace element requirements & functions in exercising horses. Nutrition of the exercising horse. EAAP publication, 2008. 125: p. 207-218. 99. Stephens, T.L., Mineral balance in juvenile horses in race training. 2002, Texas A&M University. 100. Nolan, M.e.a. Bone density in the juvenile racehorse fed differing levels of minerals in 17th Equine Nutr Physiol Soc Symp. 2001. 101. Davenport, C.e.a., Effects of enrofloxacin & magnesium deficiency on matrix metabolism in equine articular cartilage. Am J Vet Res 2001. 9: p. 33-38. 102. Counotte, G., G. Kampman, & V. Hinnen, Feeding magnesium supplement to foals reduces osteochondrosis prevalence. Journal of Equine Veterinary Science, 2014. 34(5): p. 668-674. 103. Toribio, R.E., et al., Effects of hypercalcemia on serum concentrations of magnesium, potassium, & phosphate & urinary excretion of electrolytes in horses. American journal of veterinary research, 2007. 68(5): p. 543-554. 104. Tam, M.e.a., Possible roles of magnesium on the immune system. . Eur J Clin Nutr 2003. 57: p. 1193–1197. 105.Bardgett M, e.a., Magnesium deficiency impairs fear conditioning in mice. . Brain Res 2002. 1038: p. 100–106. 106. Pearson, W. & J. MacNicol, Acute Effects of a

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Single-Dose Nutritional Product on Stress Response & Task Completion in Horses. Journal of equine veterinary science, 2017. 51: p. 86-91. 107. Dodd, J., et al., Magnesium aspartate supplementation & reaction speed response in horses. Journal of Equine Veterinary Science, 2015. 35(5): p. 401-402. 108. Frischmuth, C.e.a., Effects of a Magnesium Supplementation on heart rate & on the EEG of cross-bred horses passing the mare performance test at the Hessian Landgestüt at Dillenburg, in IVth European Congress on Magnesium. 1993. 109. Kempson, Nutritional management of horses with hoof diseases. Applied Equine Nutrition 2005, EUNCO: Wageningen Academic publishers 110. Blackman, M. & M. Moore-Colyer, Hay for horses: the effects of three different wetting treatments on dust & nutrient content. Animal Science, 1998. 66(3): p. 745-750. 111. Argo, C.M., A.H. Dugdale, & C.M. McGowan, Considerations for the use of restricted, soaked grass hay diets to promote weight loss in the management of equine metabolic syndrome & obesity. The Veterinary Journal, 2015. 206(2): p. 170-177. 112. Stewart, A.J., et al., Validation of diagnostic tests for determination of magnesium status in horses with reduced magnesium intake. American journal of veterinary research, 2004. 65(4): p. 422-430. 113. Heaton, F., Effect of magnesium deficiency on plasma alkaline phosphatase activity. Nature, 1965. 207(5003): p. 1292-1293. 114. Harris, P. & S. Dyson, Muscle disorders in the horse. Veterinary Practice (United Kingdom), 1996. 115. Hoffman, R., et al. Dietary Vitamin E supplemented in the periparturient period influences immunoglobulins in equine colostrums & passive transfer in foals. in Proceedings of the 16th Equine Nutrition & Physiology Symposium. 1999. 116. Harris, P., et al. Feeding & management advice for'tying up'/azoturia/Monday morning disease/equine rhabdomyolysis syndrome. in Proceedings of the1st BEVA & WALTHAM Nutrition symposia, Harrogate. 2005.


117. MĂŠlo, S., et al., Antioxidant & haematological biomarkers in different groups of horses supplemented with polyunsaturated oil & Vitamin E. Journal of animal physiology & animal nutrition, 2016. 100(5): p. 852-859. 118. Marlin, D.J., et al., Changes in circulatory antioxidant status in horses during prolonged exercise. The Journal of nutrition, 2002. 132(6): p. 1622S-1627S. 119. BAALSRUD, K.J. & G. Ă˜VERNES, Influence of Vitamin E & selenium supplement on antibody production in horses. Equine Veterinary Journal, 1986. 18(6): p. 472-474. 120. Siciliano, P.D. Vitamin E & IMMUNE FUNCTION IN HORSES. in CONFERENCE SPONSORS. 2004. 121. Saastamoinen, M.T. & W. Martin-Rosset, Nutrition of the exercising horse pp 1-48. Vol. 125. 2008: Wageningen Academic Pub. 122. Siciliano, P., A. Parker, & L. Lawrence, Effect of dietary Vitamin E supplementation on the integrity of skeletal muscle in exercised horses. Journal of animal science, 1997. 75(6): p. 1553-1560. 123. Williams, C., et al., Antioxidant supplementation & subsequent oxidative stress of horses during an 80-km endurance race. Journal of animal science, 2004. 82(2): p. 588-594. 124. Williams, C. & e. al, Comparison of oxidative stress & antioxidant status in endurance horses in three 80-km races. Equine & Comparative Exercise Physiology, 2005. 2(3): p. 153-157. 125. Kellon, E. Magnesium the Mighty Mineral. 2017; Available from: https://forageplustalk.co.uk/magnesium-mighty-mineral-dr-kellon/. 126. Davis, B.P., Evaluating the effectiveness of varying doses of supplemental tryptophan as a calmative in horses. 2016, Colorado State University. Libraries. 127. Davis, B.P., et al., Preliminary evaluation on the effectiveness of varying doses of supplemental tryptophan as a calmative in horses. Applied animal behaviour science, 2017. 188: p. 34-41. 128. Paradis, M., et al., Acute hemolytic anemia after oral administration of L-tryptophan in ponies. American journal of veterinary research, 1991. 52(5): p. 742-747. 129. Grimmett, A. & M. Sillence, Calmatives for the

excitable horse: a review of L-tryptophan. The Veterinary Journal, 2005. 170(1): p. 24-32. 130. Krook, L. & J.E. Lowe, Nutritional secondary hyperparathyroidism in the horse: with a description of the normal equine parathyroid gland. Pathologia veterinaria, 1964. 1(1_suppl): p. 1-98. 131. Krook, L., Dietary calcium-phosphorous & lameness in the horse. The Cornell veterinarian, 1968. 58: p. Suppl: 58. 132. Joyce, J., et al., Clinical study of nutritional secondary hyperparathyroidism in horses. Journal of the American Veterinary Medical Association, 1971. 158(12): p. 2033-2042. 133. Schryver, H., H. Hintz, & P. Craig, Calcium metabolism in ponies fed a high phosphorus diet. The Journal of nutrition, 1971. 101(2): p. 259-264. 134. Argenzio, R., et al., Calcium & phosphorus homeostasis in horses. The Journal of nutrition, 1974. 104(1): p. 18-27. 135. Walthall, J. & R. McKenzie, Osteodystrophia fibrosa in horses at pasture in Queensland: field & laboratory observations. Australian veterinary journal, 1976. 52(1): p. 11-16. 136. Capen, C., The calcium regulating hormones: Parathyroid hormone, calcitonin, & cholecalcitonin. Veterinary Endocrinology & Reproduction. Ed. LE McDonald, 4th Ed., Lea & Febiger, Philadelphia, London, 1989: p. 92-185. 137. Estepa, J., et al., An unusual case of generalized soft-tissue mineralization in a suckling foal. Veterinary pathology, 2006. 43(1): p. 64-67. 138. Mason, D., K. Watkins, & J. McNie, Diagnosis, treatment & prevention of nutritional secondary hyperparathyroidism in Thoroughbred race horses in Hong Kong. Equine practice., 1988. 10(3): p. 10-11. 139. Caple, I., J. Bourke, & P. Ellis, An examination of the calcium & phosphorus nutrition of thoroughbred racehorses. Australian veterinary journal, 1982. 58(4): p. 132-135. 140.Groenendyk, S. & A. Seawright, Osteodystrophia fibrosa in horses grazing Setaria sphacelata. Australian veterinary journal, 1974. 50(3): p. 131-132. 141.Hoskin, S. & E. Gee, Feeding value of pastures for horses. New Zeal& Veterinary Journal, 2004. 52(6): p. 332-341.

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142.McKenzie, R., Studies on calcium deficiency of horses induced by grazing tropical grasses containing oxalate. Proceedings 4th Bain Fallon Memorial Lectures, 1982: p. 75-83. 143.Menard, L., M. Marcoux, & G. Halle, A possible case of osteodystrophia fibrosa cystica in a horse. The Canadian Veterinary Journal, 1979. 20(9): p. 242. 144.Clarke, C., P. Roeder, & P. Dixon, Nasal obstruction caused by nutritional osteodystrophia fibrosa in a group of Ethiopian horses. Veterinary record, 1996. 138(23): p. 568-570. 145.Gusman, V., et al. Assessment of calcium, phosphorus, & oxalate intake & excretion by horses grazing Kikuyu grass pastures in Hawaii. in JOURNAL OF DAIRY SCIENCE. 2005. AMER DAIRY SCIENCE ASSOC 1111 N DUNLAP AVE, SAVOY, IL 61874 USA. 146.CHIBA, S., et al., Serum parathyroid hormone & calcitonin levels in racehorses with fracture. Journal of Veterinary Medical Science, 2000. 62(4): p. 361-365. 147.SASAKI, N., et al., Improvement of dietary total calcium to inorganic phosphorus ratio prevents progressive nutritional secondary hyperparathyroidism in ponies & donkeys. Journal of equine science, 2005. 16(3): p. 79-83. 148.Benders, N., K. Junker, & T. Wensing, Diagnosis of secondary hyperparathyroidism in. The Veterinary Record, 2001. 149: p. 185-187. 149. Williams, M.C., B.J. Smith, & L.V. Rafael, Effect of nitrogen, sodium, & potassium on nitrate & oxalate concentration in kikuyugrass. Weed technology, 1991. 5(3): p. 553-556. 150. Gonzalez, B. & V. VILLEGAS, “BIGHEAD� OF HORSES A HERITABLE DISEASE. 1928. 151. Ronen, N., J. Van Heerden, & S. Van Amstel, Clinical & biochemistry findings, & parathyroid hormone concentrations in three horses with secondary hyperparathyroidism. JS Afr Vet Assoc, 1992. 63(3): p. 134-136. 152. N, L., WSPA Project Lampang, in Lampang Pony Welfare Association. 2005. 153. David, J., N. Cohen, & R. Nachreiner, Equine nutritional secondary hyperparathyroidism. The Compendium on continuing education for the practicing veterinarian (USA), 1997.

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154. Franceschi, V.R. & H.T. Horner, Calcium oxalate crystals in plants. The Botanical Review, 1980. 46(4): p. 361-427. 155. Blaney, B., R. Gartner, & R. McKenzie, The inability of horses to absorb calcium from calcium oxalate. The Journal of Agricultural Science, 1981. 97(3): p. 639-641. 156. Gartner, R.e.a., Availability of calcium in oxalate-containing tropical grasses to horses & cattle. Recent Adv Animal Nutr in Australia, 1981. 157. McKenzie, R. Poisoning of horses by oxalate in grasses. in Plant Toxicology, Proceedings of the Australian-USA Poisonous Plant Symposium, Brisbane, Australia, quoted by Nutr. Abstr. 1985. 158. McKenzie, R., Purple pigeon grass (Setaria incrassata): a potential cause of nutritional secondary hyperpharathyroidism of grazing horses. Australian veterinary journal, 1988. 65(10): p. 329-330. 159. Hintz, H. & H. Schryver, Availability to ponies of calcium & phosphorus from various supplements. Journal of Animal Science, 1972. 34(6): p. 979-980. 160. Cheeke, P.R., Endogenous toxins & mycotoxins in forage grasses & their effects on livestock. Journal of Animal Science, 1995. 73(3): p. 909-918. 161. Marais, J., Factors affecting the nutritive value of kikuyu grass (Pennisetum clandestinum)-a review. Tropical grasslands, 2001. 35(2): p. 65-84. 162. Swartzman, J., H. Hintz, & H. Schryver, Inhibition of calcium absorption in ponies fed diets containing oxalic acid. American journal of veterinary research, 1978. 39(10): p. 1621-1623. 163. Aguilera-Tejero, E., et al., Effects of exercise & EDTA administration on blood ionized calcium & parathyroid hormone in horses. American journal of veterinary research, 1998. 59(12): p. 1605-1607. 164. Toribio, R.E., et al., Comparison of serum parathyroid hormone & ionized calcium & magnesium concentrations & fractional urinary clearance of calcium & phosphorus in healthy horses & horses with enterocolitis. American journal of veterinary research, 2001. 62(6): p. 938-947.


165. Toribio, R.E., et al., Hysteresis & calcium set-point for the calcium parathyroid hormone relationship in healthy horses. General & comparative endocrinology, 2003. 130(3): p. 279-288. 166. Whalen, J.P. & L. Krook, Periodontal disease as the early manifestation of osteoporosis. Nutrition, 1996. 1(12): p. 53-54. 167. Jowsey, J., E. Reiss, & J.M. Canterbury, Long-term effects of high phosphate intake on parathyroid hormone levels & bone metabolism. Acta Orthopaedica Scandinavica, 1974. 45(6): p. 801-808. 168. Gries, C.L., Mechanisms of bone resorption in nutritional secondary hyperparathyroidism. Dissertation Abstracts: B, 1966. 27. 169. Kintner, J.H. & R.L. Holt, Equine osteomalacia. Philippine Journal of Science, 1932. 49: p. 1-90. 170. Freestone, J.F. & T.L. Seahorn, Miscellaneous conditions of the equine head. Veterinary Clinics of North America: Equine Practice, 1993. 9(1): p. 235-242. 171. Stewart, J., O. Liyou, & G. Wilson, Bighead in horses–not an ancient disease. Aust Equine Vet, 2010. 29: p. 55-62. 172. Gartner, R., B. Blaney, & R. McKenzie, Supplements to correct oxalate-induced negative calcium & phosphorus balances in horses fed tropical grass hays. The Journal of Agricultural Science, 1981. 97(3): p. 581-589. 173. McKenzie, R., et al., Control of nutritional secondary hyperparathyroidism in grazing horses with calcium plus phosphorus supplementation. Australian veterinary journal, 1981. 57(12): p. 554-557. 174. Blaney, B., R. Gartner, & R. McKenzie, The effects of oxalate in some tropical grasses on the availability to horses of calcium, phosphorus & magnesium. The Journal of Agricultural Science, 1981. 97(3): p. 507-514. 175. McKenzie, R., B. Blaney, & R. Gartner, The effect of dietary oxalate on calcium, phosphorus & magnesium balances in horses. The Journal of Agricultural Science, 1981. 97(1): p. 69-74. 176. Naude, F.R.a.T., Veterinary Toxicology, ed. R. Gupta. 2012: Elsevier. 177. Khadijah, m.R.R.A.W.W., A review of oxalate poisoning in domestic animals: tolerance & performance aspects. Animal Physiology & Animal Nutrition, 2013. 97(4): p. 605-614.

178. James, L.F., Oxalate toxicosis. Clinical Toxicology, 1972. 5(2): p. 231-243. 179. Senthilkumar, S., et al., PRECISENESS OF CHELATED MINERALS ON THE PERFORMANCE OF ANIMALS.

Jenquine provides quality ethical products which have been tested with extensive clinical field trials by veterinarians & horses owners. Jenquine products are formulated & produced in Australia using APVMA licensed & ISO accredited facilities. Jenquine’s promise is to continue to BRING SCIENCE TO YOUR FEED BIN.

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WINTER FEEDING By Dr Jennifer Stewart Cooler weather makes winter a favourite time for horses – no flies & midges or itchy sweating just running free & soaking up the winter sun! Cool temperatures mean less stress - & more time in the ‘thermoneutral zone’ (TNZ), the temperature range in which horses do not need to sweat or shiver. The TNZ varies with age, gender, breed, weather, exercise & feed. Notwithstanding that with a skin temperature of around 30°C, horses lose heat to the air around them whenever the air temperature is below 30°C. The colder the air, the greater the heat loss will be. But, because of the heat generated by digestion & movement, horses do not need to shiver until the temperature is less than zero for a weanling & less than –15°C for an adult horse. We can help horses stay warm in winter by providing plenty of roughage – hay or pasture is best, & oats too have a role in certain situations. High fibre feeds produce body heat when they are fermented by hindgut bacteria breaking down the fibre – the by-products of which are heat & nutrients for the horse. High starch feeds, such as corn, molasses & sweet feeds do not generate this fermentative heat - they can increase their energy & excitability, but they dont generate significant core body heat. As a rule of thumb, the most efficient way to keep horses warm during winter, is to feed more highly-digestible hay, at 2–2.5% of body weight & in a ratio of 50-60% lucerne & 40-50% grassy/ oaten hay /beet pulp. When the weather is wet & windy energy needs increase a further 40-50% & some oats may be useful – but not more than 1-2kg per meal – always start with a small

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amount & increase slowly to allow the gut bacteria time to adapt to the increased starch. An occasional bran mash is not harmful, & it can be a great way to give horses a treat on cold nights. Bran should be restricted to less than 10% of the diet as it contains 9 times as much phosphorus than calcium. A separate calcium supplement may be necessary. High phosphorus & low calcium & minerals in grain can unbalance the diet, especially for young, pregnant or working horses — a well-balanced concentrate, based on vegetable protein meals, vitamins & minerals will correct the imbalances. Increasing the oil in the diet is another safe & effective way of increasing energy – especially for working & performance horses. Impaction colics are more common in winter, partly because mature hay & pasture have a lower water content than young pastures, but also because horses drink less if the water is <2°C. If your winter brings ice & snow, make sure clean fresh water is available - horses have to consume ten times their water requirement in snow conditions to meet their needs, & they need to use energy to raise the temperature of the snow to body temperature. This is a huge energy drain &, when hay is poorly digestible, can lead to gut impaction colic. Enjoy the cooler weather – & remember every horse is different so keep a watchful eye on body condition & growth.


DROUGHT FEEDING By Dr Jennifer Stewart Feeding a horse is usually the largest cost of ownership – & never more so than in times of drought. With a little planning & knowledge of how to construct a diet with alternative feedstuffs, it is possible to provide a pretty well-balanced diet. In drought years, good quality forage may be too expensive or unavailable. So let’s look at the safety & efficacy of options for feeds. Forage/fibre is the mandatory cornerstone for gut & horse health. Even in drought times a minimum of 1% of bodyweight in fibre must be provided. Table 1 shows the minimum amount of roughage that must always be fed – even in times of drought, & the minimum total daily feed intake which can be 90% roughage or a mixture of roughage + concentrate. Table 1. Minimum total daily intakes Daily Min amount of fibre (1% of bodyweight) Bodyweight kg fibre 300kg 3kg 400kg 4kg 500kg 5kg 600kg 6kg

Min total Feed intake fibre+/- concentrate 4.5kg 6kg 7.5kg 9kg

In addition to hay & pasture, there are many other high fibre feeds that can be used to totally replace or partially replace the roughage portion of your horse’s diet. Table 2. lists some alternative roughage sources & if they can replace hay. Roughage Lucerne hay/chaff Grass hay Haylage Straw Beet Pulp Hulls Whole corn plants

Fed instead of hay Yes Yes Yes Yes No No No

Feeds with moderate levels of fibre (11%-15% crude fibre) can also serve as an alternative during drought. These lower fibre feeds can’t totally replace the roughage your horse needs, but they can reduce the amount of hay you have to feed. Start by ensuring your horse receives at least 1% of its body weight per day in roughage (Table 1). Then use moderate fibre feeds to complete the remaining portion of the diet. The feedstuffs in Table 2 can be fed to ‘stretch’ the hay supply – & in some cases replace it. So when chaff & hay are not available or too expensive, the following feedstuffs can be used: cereal grain straw, ground corn cobs, hulls, whole corn plants can be pelleted & fed to horses for an energy source but, to provide a balanced diet, a protein, vitamin & mineral supplement must also be fed. By taking the time to carefully select top quality roughage (ie low in dust, mould, contaminants & weeds) & continually monitor consumption patterns, you can make sure you’re providing the best possible diets in times of scarcity. If grains increase in price, look at alternatives such as bran (usually wheat or rice), but as they are low in calcium & very high in phosphorus, it’s absolutely necessary to provide calcium. Beet pulp is safe & higher in calcium than phosphorus – but low in protein, Vitamins A, B & D. To correct deficiencies in the feedstuffs, include a small amount of a correctly-formulated concentrate. Depending on age, weight, work & reproductive status only 300-700g should be required to balance most diets. Pregnant, lactating & especially growing horses benefit from lucerne – so if it is in limited supply, reserve it for these horses. Go to our website to read more... www.jenquine.com/news/drought-feeding

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SPRING FEEDING & PASTURES By Dr Jennifer Stewart Most plants increase their growth in spring — photosynthesis ramps up when sunshine increases. Plants are sugar factories photosynthesis produces carbohydrates (CHO) which promotes growth. Horses become sleek & the need to feed is reduced – at last feeding costs go down! This is great expect for horses & ponies at risk of insulin resistance & prone to laminitis! Although we recognise many, many breeds of pony – there are really only 2 groups: those that have foundered & those that are going to founder! Because the CHO or ‘carbs’ (starch, sugar & fructans) concentration of forages are highly variable, & because they have a role in laminitis/founder, equine polysaccharide storage myopathy (EPSM), & equine metabolic syndrome (ie insulin resistance or peripheral Cushing’s) pasture must be considered when deciding which horse should graze, when they should graze & for how long. At night, photosynthesis stops (due to lack of sunlight) & the plants burn stored sugar to stay alive. What this means to horses & us as owners, is that carb levels are lowest from 3am to 10am, peak in the afternoon (doubling every 3 hours on warm, sunny days) & decline after as darkness descends, continuing to fall throughout the night – making early morning the safest time for at-risk horses to graze. Also, don’t allow at-risk horses access to seed heads – which are very high in carbs. Weeds like chicory, dandelion & thistles can also be dangerously high in carbs. Other strategies include keeping grass short (6-8cm) & leafy; adequate moisture & fertiliser to encourage growth & utilisation of carb. There is a belief that pasture grown without fertiliser is more

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“natural” & healthier. In fact, grasses grown under nitrogen or phosphorus deficiency are higher in NSC than those grown with optimum amounts of fertiliser. Preventing horses from grazing on sunny, cool spring days (when growth slows & carbs accumulate), & avoiding stubble (high in sugars), & grazing muzzles also have a role. Muzzles reduce bite mass & only allow access to the tops of leaves where carb concentrations are lowest. If grazing is restricted, hay must be supplied. But like the plants from which it is made, hay can have wildly varying carb levels, so check NSC (the sum of starch, sugar & fructan) levels when you buy hay – & only get hay that is <12%, preferably 10% NSC. Oat hay is often thought to be ‘less rich’ than lucerne hay, but although protein levels are higher, the carb levels are usually ½ that of oat hay – the best lucerne hay for horses is stemmy with lots of purple flowers. B Horses whether on & off pasture almost always require mineral & vitamin supplementation – but feeds (that include grain by-products such as mill-run, pollard, bran, millmix or hominy meal) are not recommended due to their carb content – stick with fibre-oil rich feeds, or pasture lick blocks that have been balanced for the vitamins & minerals deficient in all pasture & hay. Magnesium deficiency often occurs on spring pasture, which is low in magnesium – so consider supplementing magnesium. Colic also increases in horses on spring pasture due to gas production & low fibre intake – feeding some beet-pulp or hay will increase fibre & the weight of the gut – helping prevent sections from floating off in to the wrong location – which predisposes to displacements, torsions & twists.


LAMINITIS EMERGENCY FIRST AID By Dr Jennifer Stewart Early intervention & protective effects of ice water can prevent the development & progression of laminitis. Digital hypothermia (immersing the legs in an ice slurry) during the developmental phase can ameliorate laminitis & is increasingly being recognized as being protective also for the prevention & treatment of laminitis. The major results of ice therapy are profound antiinflammatory effects, pain relief (analgesia) & slowing of tissue metabolism – which reduces oxygen consumption by the damaged tissues & protects them from trauma & lack of oxygen. Laminitis changes are generally seen as irreversible, so prevention in horses at risk & halting the progression of acute laminitis are key areas to focus on. Most cases of laminitis occur due to metabolic disturbances secondary to high carbohydrate feed, hay or pasture. At risk horses & ponies should be watched carefully for a while every day, because the laminitis is often insidiously progressive and episodic, making identification of the developmental period difficult – & it is in this period that the greatest benefits of icing can be used. There are four stages in the onset and progression of laminitis: 1. developmental 2. acute 3. subacute 4. chronic - persistent mild to severe lameness, further mechanical collapse of the foot, recurrent abscesses, hoof wall deformation However you can make the ice slurry is good. A 5 litre bag secured with duct tape around the lower limbs & hooves is enough to cool the legs - refill ice every 2 hours as needed. Commercially available wader-style boot modified to include the hoof will do the trick, as will a rubber ice boot to just below the carpus (knee) & hock. Cold gel-wraps (4º C) for 30 minutes reduces surface

temperature over the cannon bone for 3 hours – but the profound & sustained reduction in deep tissue temperature with iced-water immersion is better than the cold-packs & wraps. Commercially available ice packs & cold-gel applications don’t usually drop hoof temperature below 20º C. Based on current information, hoof wall temperatures should be less than 10º C. To achieve this, the hoof must be cooled as well as the limb – which cools the blood entering the hoof. Immersion of the limb from just below the knees & hocks in ice + ice water achieves this – although it’s labour-intensive, the benefits are worth it. Emergency diet Diet is also critically important in the early stages. Feeding laminitic horses can be a challenge. This emergency diet provides short-term guidelines for horses that have suddenly developed signs of laminitis. - Grass hay : 1.5 – 2% of current body weight (soaked to remove sugars) - Beet pulp (unmolassed) : 0.5 – 1kg (rinsed) - Iodised salt : 30 – 60g - Magnesium oxide : 10 – 15g - Vitamin E : 1000mg (iu) - Linseed :100g The total daily amount should be divided into at least 3 feeds per day. Dietary management including a decision on whether or not affected animals should be allowed to return to pasture is another important consideration. Obese, insulin resistant animals should be held off pasture for 2–3 months, allowing time for implementation of dietary restriction and increased physical activity that result in weight loss and improved insulin sensitivity. A good outcome requires a dedicated team of vets, farriers & owners – & upon who’s constant care, a good outcome is possible.

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