When things go wrong: the disease processes of diabetes

When things go wrong: the disease processes of diabetes

Dale Pinnock
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Published by
Quadrille Publishing
978 184949 541 7

A big part of my whole ethos is that we should be educated and empowered when it comes to our health, so we can do our best to be sitting in the driver’s seat. Having a bit of an overview of what is happening in terms of your own health puts you in a better position to understand how to take the right action. I believe that we should be as informed as possible about our own health. So, here is a bit of a guide to how things go wrong in type-2 diabetes, before we move on to discuss what can be done to address the issue.

Insulin resistance

Insulin resistance is essentially the first stage in the many processes that are creating and exacerbating the metabolic chaos that is afflicting the modern Western world.

In the last couple of decades we have seen massive increases in many chronic degenerative diseases and modern medicine is really struggling to manage them successfully. Many of these diseases are centred around key metabolic processes: cardiovascular disease, diabetes and so on.

These are on the increase on a drastic scale. I’d go as far as to say that they are now running at epidemic proportions in the Western world. Just look at the numbers. This truly isn’t an exaggeration.

One element that has been seen as a major link between these metabolic issues is insulin resistance: the series of events that cause our cells to stop listening to the insulin that we produce. So, what causes this? Well, before we get on to the biggest and main cause, there certainly can be a genetic factor at play here. While in almost 90 per cent of cases it is due to lifestyle, genetic tendencies do exist. Some people do show a greater genetic susceptibility towards insulin resistance, regardless of any other influences, such as diet and lifestyle. However, this is only in a very small number of cases. On the whole, insulin resistance arises almost totally because of lifestyle factors, the biggest of those being – as we are beginning to see – the food that we eat!

What causes insulin resistance?

When we eat, the food is broken down by digestion into its constituent parts: macronutrients (proteins, fats and carbohydrates) and micronutrients (vitamins, minerals, trace elements and so on), which then go on to enter the bloodstream following absorption and are shipped around to different places to do different jobs.

When sugars from our diet enter the bloodstream, our body releases the hormone insulin in response. It is the job of insulin to bind to specialised insulin receptors built into our cells. When insulin binds to these receptors, it causes a response that opens up ‘doorways’ in the cell that allow glucose to enter, so it can be utilised as energy.

When we consume foods that are whole and complex and don’t contain large amounts of simple sugars, this series of events takes place consistently, evenly and painlessly. However, when we consume foods that release their sugars very quickly, or that are a concentrated source of simple sugars, we basically start to carpet-bomb the bloodstream with sugar. This causes our bodies to respond by pumping out higher levels of insulin. Every now and again, this is not a problem, such as having a piece of chocolate once in a while. But when it goes on for weeks, months, years, decades, things can begin to go seriously wrong.

Consistently excessive levels of insulin soon start to raise the suspicions of the cells it is communicating with. It’s almost like the boy that cried wolf. When insulin is consistently being kicked out of the beta cells in the pancreas in response to the floods of blood sugar, the cells will eventually begin to think that something is up. They will start to question what is going on with insulin and whether it really knows what on earth it is doing.

When this occurs, the cell receptor basically starts to think that insulin is getting a little too carried away with itself and feels it is best ignored. So, the receptor ignores insulin, it basically becomes less receptive to the signal that insulin is sending out.

Now, being something of a persistent character, insulin doesn’t take ‘no’ for an answer. With reduced cellular response to insulin, there is a reflex increase in production of insulin from the beta cells of the pancreas. As far as they are concerned, there isn’t enough insulin out there to get its message heard. This increased production can work for a while but, before long, the insulin receptors really do dig their heels in and become even more resistant to insulin. Strangely enough, this state is called insulin resistance! It is a situation which some would say is pre-diabetic. I certainly agree that, unchecked, it sets the stage for type-2 diabetes. At this point, blood glucose levels start to rise notably as cells become less receptive and we begin to see medical signs of a state called hyperglycaemia: consistently elevated blood glucose.

Insulin resistance and obesity

However, diabetes is only one outcome of insulin resistance; the worst-case scenario that arises after prolonged, untreated insulin resistance. There is an epidemic of metabolic chaos sweeping the Western world.

This is manifesting in what is termed ‘metabolic syndrome’. It is a cluster of several symptoms, but essentially all are linked to insulin resistance. When insulin levels are raised for long enough, one of the first clinical manifestations we would be aware of is abdominal obesity. This is the incredibly hard-to-shift fat that collects around the middle. You know the stuff. It is the fat that no amount of hours on the treadmill will shift and no diet – so far – has even touched.

There are two main reasons for this occurring when we have insulin resistance issues. Firstly, if insulin is higher, that generally means blood sugar is higher, and blood sugar that is too high must be dealt with. In normal circumstances, this excess of sugar would be taken up by cells and put to use in the manufacture of energy. However, when cells are resistant to insulin, their capacity to take in glucose is restricted. This leads to an excess of glucose that needs to be shifted! So, what happens next is a reaction called lipogenesis where, in short, the sugar gets converted into fats.

These fats, known as triglycerides, are much easier to be got rid of, as they are able to be carried away and stored in our adipose tissue (body fat). Insulin opens the gates within adipocytes (fat cells) to let these fatty acids in. What happens in normal situations is that these fatty acids will go into fat cells for storage but, when insulin levels fall, they can freely flow back out again and be used by the body as energy.

Unfortunately, when insulin is high it becomes like a one-way flow of traffic, with fatty acids collecting in the adipocytes (fat cells) and insulin keeping them from coming back out again. Before long, this becomes a pattern of weight gain and no amount of exercise will get rid of it. Get insulin under control, on the other hand, and you will see this stubborn fat disappearing for the first time.

Insulin resistance, increased cholesterol and high blood pressure

The next clinical manifestation that may be seen during insulin resistance / metabolic syndrome is an increase in cholesterol and blood fats. In light of what has just been said, this should be quite a logical thing. When sugar turns into triglycerides, it is carried to the adipose tissue through the general circulation, so blood fats go up. This causes an increase in the production of the body’s fat transport system: the lipoproteins. These are specialised carriers that ferry fats and cholesterol around the body. When triglycerides go up, the first thing that happens is the body produces more of something called VLDL or Very Low Density Lipoprotein. This gets degraded by various enzymes and becomes LDL.

Both VLDL and LDL are considered atherogenic, which means they are thought to play a role in the instigation of heart disease. They are believed to be susceptible to oxidation, causing localised inflammation which can damage the vessel walls. They are also believed to be more capable, under the right circumstances, of penetrating the walls of the blood vessels, where they instigate the beginnings of a plaque (a build-up of fatty material). Another major complication of insulin resistance is high blood pressure. This may be due to altered kidney function, or it could be due to influences on the endothelium, affecting vascular dynamics. The exact link isn’t clear, but we know it is there.

So in essence, you may know someone, or you yourself, may have the triad of issues that are considered metabolic syndrome: type-2 diabetes / pre-diabetes, high LDL cholesterol and high blood pressure. These are all caused – or at least exacerbated – by a breakdown of our body’s ability to handle simple sugars and the chain of events that unfold as a result of this.

Beta cell dysfunction

The next step in the progression from insulin resistance to full-blown type-2 diabetes, when this occurs, is a dysfunction of the beta cells in the pancreas. As we have seen earlier on, beta cells are the specialised cells found in an area of the pancreas called the islets of Langerhans. Their job is to store and release insulin. After prolonged states of insulin resistance and hyperglycaemia, in most cases, the next step is an impairment in the function of the beta cells. There is a progressive reduction in the amount of insulin they secrete. There is still much discussion and research around why this may be the case. The most likely scenarios at present are glucotoxicity and elevation of free fatty acids.

When blood glucose levels are consistently high and insulin is failing to induce a cellular response (insulin resistance), the level of glucose can become toxic. This is a state called glucotoxicity and can cause untold damage. In the beta cells it is believed that glucotoxicity can cause mitochondrial dysfunction, increase oxidative stress and ultimately lead to apoptosis: cell death! As we have also seen, elevated blood glucose can lead to an increase in fatty acids in the blood. This increase in free fatty acids is also believed to instigate changes in the cell that lead to apoptosis. At this stage of beta cell dysfunction, individuals may be advised by their doctor that they need to inject themselves with insulin. They are essentially at the same place as a type-1 diabetic.

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