Hardly a day goes by without some mention in the press and health magazines about this disease in us as though it’s a new disease.
Yet it’s been known about for thousands of years; the Egyptians, Asian-Indians, Greeks, and Romans all recognised human diabetes as a definitive disease, where the sufferer was prone to produce copious amounts of ‘honey urine’, so said due to it being honey coloured and, maybe surprisingly, attractive to ants. Until the discovery of insulin and its use in the 1920s the sufferer would go into steady decline and die prematurely.
Remarkably 1,500 year ago, Asian-Indians identified the two types of diabetes: the juvenile form (Type 1) and the obesity-linked form (Type 2). Although we refer to the two types by numbers, it is more accurate to name them insulin-dependent diabetes mellitus (IDDM) for the first and the non-insulin-dependent form (NIDDM) or insulin-resistant DM for the second.
In animals it is more correct to use the terms insulin-dependent and non-insulin-dependent, where the former is commoner in dogs than cats and the latter more common in cats than dogs. Only about 2 cats in a thousand are diabetic; dogs are more prone at about one in a hundred. The theory behind the lower incidence in cats is their lifestyle and nutrition being linked to a preference for a high protein diet – live animals with minimal scavenging. They cannot digest carbohydrates well as a result of dietary refinement over the millennia for the nutrient appearing rarely on the cat’s menu. And like human NIDDM, they develop it late in life: 70-90% having the problem is more than seven years of age.
So, the cat points us to the potential cause for diabetes in all of us. I say ‘all of us’ since the species now seen with the disease get more numerous by the year. We suffer from it and now so do our nearest companion animals: dogs and cats, now extended to guinea-pigs, rabbits, ponies and horses. Carbohydrate seems to be the villain of the piece; the more refined it is the faster it is converted to sugars that put excess strain on insulin production and function. Conversely the slower it is converted as in starches (called complex carbohydrates) found for example in potato and whole grains the easier insulin, and more correctly the pancreatic gland that produces it, can cope with the demand.
But that’s not the whole story. Horses have been eating the same diet for ages through to the current day and yet they increasingly are seen becoming diabetic-obese as a sequel to a malfunctioning metabolism. They suffer the full range of causes: IDDM, NIDDM, hormonal primary, e.g. adrenal gland malfunction, pregnancy, and impaired glucose tolerance. It is literally an extremely complex syndrome. Yet there may still be a missing causal element common to all species, but substantially illustrated by this animal - and that’s called stress.
Stress, more correctly termed strain with stress as the sequel, is a very complex event with sequelae that may be short term and of little significance or more prolonged and hugely damaging. Stress can invoke, according to its intensity and prolongation, a response from the adrenal gland (among other endocrine glands also called upon to respond) to produce a hormone (cortisol) that stretches to the limit the islet cells in the pancreas that secrete insulin. Not only that the type of insulin or the receptors for the insulin within the tissues become blunted or not recognised once its secretion becomes excessive and prolonged, i.e. insulin resistant. While this theory does not present the complete picture it does add a potentially large piece in the jigsaw of an alarmingly common problem.
So, what do we do about it? The management of the diabetic case, with or without insulin injections – oral drugs are not effective in dogs and cats – is similar to diabetes’ prevention. REACT stands for Routine, Exercise, Awareness, Constancy, and Testing.
Routine is to feed small meals and often, which produces a lower insulin output. That may be against the received wisdom of once-a-day feeding, but for the dog or cat in the problem age range or the diabetic of whatever type it is the sensible way forward.
Exercise is a component of the calories out matching the calories in. Not all calories eaten can be used up by exercise (yes, especially if you are a cat), but the regular walk or game does alter the metabolic rate so calories are quicker and more completely burnt off.
Awareness in managing the diabetic case encompasses all the above plus being watchful for factors of weight gain or loss, lethargy, fluid intake and output, indigestion and the general factors of clear, bright eyes, clean and shiny coat and happiness.
Constancy means sticking to the same diet from day to day; that may be boring to us but not to them. Keeping the proportions of carbohydrates (as said they are less critical to the cat’s nutrition), proteins and fats the same, while ensuring optimal essential fatty acids, ensures the pet’s metabolism is predictably keyed into what is presented in the bowl. Fixed formulations are best; they exist as specifically designed proprietary feeds and are highly suited to managing the diabetic. Home menus do not work; there are too many chances for imbalance in formulation and unknown outcomes.
Testing completes the set. Balancing a diabetic case is doing more than observational monitoring. Daily or weekly blood and urine testing are essential for the pet’s well-being. In most cases other tests are appropriate on an intermittent basis to check kidney and liver function, red and white cell counts and of course sight. By the time diabetes is recognised in dogs and cats the excessive blood sugar leads to the deposition of sorbitol in the lens of the eye. This attracts water from the eye fluids into what is meant to be a relatively dry tissue; wet equals cataract and cataract equals dwindling sight.
If you suspect your pet might be overweight or even obese check out the body condition score charts provided on the Pet Food Manufacturers’ Association web site: http://www.pfma.org.uk/pet-size-o-meter/