What is it with CRESTY NECKS ?

Dr Jennifer Stewart BVSc BSc PhD Equine veterinarian, CEO Jenquine and Consultant Nutritionist Equine Clinical Nutrition

Obesity is defined by the World Health Organisation (WHO) as 'abnormal or excessive fat accumulation that may impair health’.

Horses are not immune one of the most important welfare issues of today. Surveys from certain equine populations, between 27 and 50% of horses are obese. In Australia and New Zealand 30-60% of leisure horses overweight – ie too fat! The gold standard to assess fat mass based on Archimedes’ principle that an object will displace its people holding their breath while completely submerged in water - impractical for use in horses!

Body condition scoring (BCS) is the most common method to principle of looking at and feeling the fat deposits. Although it found between higher BCS, problems with blood glucose levels of pasture-associated laminitis. Monitoring fatness in horses remains under-recognition of obesity by owners combined with the syndrome resistance’ and the specific patterns of fat accumulation and fatty adiposity’) around the prepuce (sheath), the udder, near the shoulders, crest.

There are several ways to assess how much fat a horse is carrying neck score’ is the easiest one to use – and a reliable sign that disease (Figure 2).

Figure 1. Measurement sites used in assessing fatness. The a relaxed upright position at approximately a 45° angle from the horizontal.

NC = neck circumference; NCH = neck crest height; NL = neck length; NC25% = neck circumference at 25% of neck length; NC50% = neck circumference at 50% of neck length; NC75% = neck circumference at 75% of neck length. HW = wither height; GC = girth circumference; WC = waist circumference; BL = body length;

Body condition scoring (BCS) is the most common method to assess fatness in horses - the basic principle of looking at and feeling the fat deposits. Although it has limitations, a link has been found between higher BCS, problems with blood glucose levels and previous or future episodes of pasture-associated laminitis. Monitoring fatness in horses remains challenging, perhaps due to under-recognition of obesity by owners combined with the syndrome in ponies of ‘weight-loss resistance’ and the specific patterns of fat accumulation and fatty thickening (known as ‘regional adiposity’) around the prepuce (sheath), the udder, near the shoulders, the tail head and the neck crest.

The cresty neck score (CNS) rates the accumulation of fat along the neck on a scale of 0 to 5 (Figure 2)

0 No visual appearance of crest (tissue apparent above the ligamentum nuchae). No palpable crest.

1 No visual appearance of crest, but slight filling felt with palpation

2 Noticeable appearance of crest, but fat deposited fairly evenly from poll to withers. Crest easily cupped in one hand and bent from side to side.

3 Crest enlarged and thickened, so fat is deposited more heavily in middle of the neck than toward poll and withers, giving a mounded appearance. Crest fills cupped hand and begins losing side to side flexibility.

4 Crest grossly enlarged and thickened, and can no longer be cupped in one hand or easily bent from side to side. Crest may have wrinkles/creases perpendicular to topline.

5 Crest is so large it permanently droops to one side.

Horses and ponies with a ‘cresty neck score’ of 3 or higher are at greater risk of developing laminitis.

In humans, abdominal/gut/belly fat, measured as waist circumference, is more closely linked to risk of diabetes and cardiovascular disease than fat elsewhere in the body. Similarly, in horses, fat deposited more heavily along the crest of the neck (‘cresty neck’), has been associated with altered metabolic states, including insulin resistance and an increased risk for laminitis. Insulin resistance = being unable to manage blood glucose levels. When blood glucose levels rise, insulin is released from the pancreas to ‘carry’ the glucose into the muscle and liver cells, where it is stored until it’s needed. Insulin ‘resistance’ occurs when the cells don’t respond to insulin. When this happens, glucose and insulin stay in the blood. High blood glucose and insulin can cause major health problems.

The metabolic syndrome of equids resembles the well-characterized syndrome in humans where excess body fat and insulin-resistance are linked (Table 1). Together they cause ‘metabolic syndrome’ (EMS) which is a derangement of several normal body processes. It has a genetic basis and in horses (and humans) that are genetically susceptible, the combination of an unhealthy diet + insufficient exercise is the path to metabolic syndrome.

In horses, EMS can be a consequence of giving starch/sugar-rich feed (Table 2.) or it may be seasonal and linked to the sugar/starch content of the pasture. Fatness is strongly linked to feeds with more than 15% NSC. Such feeds cause blood glucose to rise too high for too long.

Table 2. Nonstructural carbohydrate NSC (NSC = starch + sugar) levels in common feedstuffs

Feeds >12% are not recommended for horses and ponies with insulin resistance

Throughout their 55 million-year evolution, horses have developed ‘thrifty genes’ which allowed them to survive times of feed scarcity. Genetically susceptible horses quickly become fat when food is abundant and excessively rich (with no intervening periods of famine or ice ages!!) and exercise is limited. Exercise in domestic horses compares poorly to wild and free-range horses. Free-range and feral horses exercise for around 16km/day; horses in a 40 acre paddock about 7km/day and stabled horses for 1km.

In addition, fat is no longer dismissed as a benign deposit of stored energy. Fat cells produce a range of hormones that affect insulin, blood vessels, the immune system, body mass and body composition. The fat cells in horses’ necks (and humans’ bellies) produce more hormones than fat cells elsewhere in the body and these hormones increase the risk of metabolic

syndrome. The other thing that happens to fat cells is that when they are packed too full with fat they swell and squash off their blood vessels, reducing blood and oxygen supply and becoming ‘sick’ and toxic. Another source of toxicity in horses with cresty necks, is ‘glucotoxicity’ which is caused by high sugar in the blood and inside the cells. High blood sugar damages blood vessels and the hoof. In the hoof, glucotoxicity causes the blood vessels to constrict, reducing blood flow to the foot and laminae.

The most common causes of laminitis presented to vets are endocrine (ie hormonal - especially insulin) and metabolic disorders – both related to insulin and blood sugar. Early recognition of horses with insulin resistance means preventive measures can be taken earlier – before the disease progresses to laminitis. Excellent research from the University of Queensland confirmed that the amount of neck fat is a reliable sign of insulin dysregulation and a stronger identifier of impending laminitis, than BCS. Eliminating feeds that are over 12% starch and sugar (NSC) and replacement of sugar and starch-based feeds with low NSC feeds (Table 2.) underpins dietary management. The term ‘pasture-associated laminitis’ describes cases of laminitis that occur in seemingly healthy horses and ponies grazing pasture – between 45 and 60% of cases occur under these circumstances, and in addition to elimination of sugar/starch/ NSC-rich feeds, preventing grazing may be necessary to prevent laminitis in EMS-prone horses and ponies.

Identification of healthy horses and ponies that are genetically predisposed to EMS before they become affected is the aim. But until genetic testing is readily available, owners should work with their veterinarians to monitor their horses’ laminitis risk. Knowledge of what’s going on with cresty necks and monitoring blood insulin and glucose levels are the cornerstone. The WHO recognizes that obesity is more than just a threshold amount of fat tissue. It is a sign of metabolic diseases and dysfunctional fat depots that are potentially harmful to health. Some owners don’t recognise that their horse is ‘fat’– making picking up on early signs of insulin resistance really important. Insulin resistance and metabolic disease can also lead to abnormal hoof growth rings, separation of the hoof wall from the white line and seedy toe as the laminae weaken. Small areas of haemorrhage

(caused by damage to the lamina blood vessels) in the seedy toe area might also be seen. So keep an eye on those necks and hooves as they are likely to be the first sign of disease, and have your veterinarian check your horse’s insulin levels.

How good are you at assessing how fat your horse is?

https://www.mdpi.com/2306-7381/9/10/544

How to score your horse’s neck using studies from Queensland University of Technology, Laminitis Survey: https://cms.qut.edu.au/__data/assets/pdf_file/0009/329616/how-to-assigna-cresty-neck-score.pdf

© Dr J H Stewart December 2022

All content provided in this editorial is for general use and information only and does not constitute advice or a veterinary opinion. It is not intended as specific medical advice or opinion and should not be relied on in place of consultation with your equine veterinarian.

ABOUT THE AUTHOR –

Dr Jennifer Stewart

CEO BVSc BSc PhD Dip BEP Equine Veterinarian and Consultant Nutritionist

Dr Jen Stewart has been an equine veterinarian for more than 40 years and an equine nutritionist for more than 10 years. Jen has been developing premium formulas for studs, trainers and feed companies in Australia and around the world and regularly consults to leading international studs and trainers in various countries.

Jen has spent a fair bit of time researching and being involved in nutritional management of developmental orthopaedic diseases, colic, tying-up, laminitis, performance problems, post-surgery and other conditions. And is currently the only practicing equine veterinarian and clinical nutritionist in Australia. Jen’s promise is to continue to BRING SCIENCE TO YOUR FEED BIN.

www.jenquine.com