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Phil Nuttridge continues his series of articles looking at the modern take on diet and nutrition. He explodes many of the dietary myths that have defined the latter decades of the twentieth century and left their legacy of chronic illnesses in the first decades of this century. In this month’s article he looks at insulin’s role in obesity, diabetes, heart disease and inflammation. More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram: CuttingCarbsUK
Maybe it is genes, may be it is lifestyle choices. Whichever it is, I am very fortunate: At 53 years old, I have a BMI of a little under 23 and I am no more than nine percent body fat. Not bad stats for an “old ‘un”! But this has not always been the case – there was a time in my life when I was quite the little porker. You could definitely pinch more than an inch anywhere and everywhere on my body. At the time though, everyone was rejoicing in that chubbiness and that’s because it was when I was born. I was a (very) big and bouncing baby!
It probably hasn’t escaped your notice that most of us are chubby at birth. In fact, new-born human babies can be upwards of fifteen per cent body fat. What is intriguing is that this is unique to Homo sapiens as we are the fattest babies in the animal kingdom and by quite a margin. The new-borns of our closest primate cousins do not make it into double-digit percentage body fats; even mammals we think of as fat, like seals, piglets and puppies, are rarely more than ten per cent fat at birth.
Carrying an extra-fat baby to term places huge energy demands on the pregnant mother. Taking the view that this is not just an ‘accident’ of Nature but rather a response to an evolutionary pressure, what survival advantage could this confer to human babies? Well, nutritional anthropology seems to have the answer and it all centres around the most energy demanding organ in our body – our brain.
Humans are big-brained and this is a trait that has helped us become the apex species on Earth. But at what stage in our development do we grow our large brains? If we grew our brains in the womb, this would require our mothers to develop wider hips to allow safe birthing. But wide-hipped bi-pedal humans are not good runners, bad news for a hunter-gatherer apex species. So, evolution has developed a clever solution to the problem: In the womb, the human brain develops to just a moderate size compared to the rest of the baby. Additionally the in-the-womb human baby is ‘packaged’ with the energy store and building material that enables it to crack-on growing a bigger brain after birth without having to wait for its eating habits to develop. Those energy and material stores are the rolls of chubbiness we are born with.
The clever thing for our nutritional journey is just how the baby becomes fat. It uses the same metabolic mechanism that (for example) bears use to pile-on the pounds just before Winter hibernation. That mechanism is reversible Insulin Resistance. Regrettably, as I shall show you, in the last fifty years this mechanism has back-fired on us humans and provides an eloquent explanation for the epidemics of obesity and Type II diabetes in the modern age. More of that later but firstly, I need to talk about insulin and what happens when we become resistant to it.
Insulin is the key hormone for lowering excess blood sugar levels in the body. When we have eaten a meal containing sugar or starch, the latter of which is broken down into sugar by our digestive enzymes, then sugar molecules (principally in the form of glucose) will be absorbed into our blood raising our blood sugar level. Short term this is fine, but our body does not like too much sugar in the blood for too long as these pesky glucose molecules just love attaching themselves to any and every protein molecule they can find. Proteins are fundamental to the chemistry, structure and function of our body cells – they form enzymes (the catalysts that facilitate chemical reactions), hormones, antibodies, transport molecules like haemoglobin, collagen and muscle fibres. But a glycolated protein, one that has been attacked by glucose, cannot do its designated job properly: Sugar with protein is bad news!
Glycolated proteins are bad news on another front too. Because they are ‘mongrel’ molecules not naturally found in the body, our immune system is likely to identify them as foreign invaders. Immune responses are triggered potentially leading to auto-immune disease and inflammation. Very bad news for our body.
To overcome this we have evolved clever chemistry to keep our blood sugar levels in check. The hypothalamus in our brain constantly monitors the concentration of sugar in the blood and if the level rises above a threshold value, signals are sent to the pancreas to release the hormone insulin. Insulin acts quickly and sets things in motion to get that extra sugar out of our blood.
Different parts of the body listen to insulin in different ways. In summary though, insulin mediates a metabolic switch: One setting of this switch, the way it is set in the absence of insulin, tells our body to give-up its fat reserves and use them for energy; the other side of the switch, triggered when insulin is circulating, tells our body to bolster its fat reserves and preferentially use sugar for energy.
How does insulin operate this switch? Well, it has a number of actions all of which combine to give this effect:
- Insulin controls entry of glucose into your muscle and fat cells. When insulin is present, important transport mechanisms in cell membranes open-up and allow glucose into the cells. This is key for insulin’s role in reducing blood sugar levels – open the cell doors and glucose will pass out of our blood and into those cells, thereby naturally reducing blood sugar. Significantly, the liver and brain cells which have high demands for energy do not need insulin for glucose to enter as they have transport mechanisms that are insulin independent.
- Insulin tells the liver to stop producing glucose and start producing glycogen. Our liver is very good at making glucose from fats and proteins. In fact, because of this gluco-neogenesis, all the glucose needs of our body can be met from fat and protein and consequently there is no minimum daily requirement for eating carbohydrate. The same is not true for fat and protein. Although the liver can make a lot of protein and fat building blocks, not all can be made and so our diet must contain these ‘essential’ fat and protein components. Our health will quickly fail if we stop eating protein and fat yet we will survive, even thrive, if we cut our carbohydrate intake. Our liver naturally pumps away producing glucose but this process stops as soon as insulin is detected. Instead, the liver switches to converting blood glucose into glycogen, a storage form of glucose, that takes glucose out of harms way and stores it as a ‘banked’ fuel for later.
- Insulin tells the liver to make triglycerides. The body can only bank so much glycogen. After this limit is reached any further glucose is then converted to fatty acids and triglycerides destined for storage in the skin. And these are the real bad guys. Although I will save my demolition of the ‘cholesterol is bad’ fallacy to a later article, let me say at this stage that the blood measure that IS correlated to worsened cardiovascular outcomes, is blood triglyceride level. The higher blood triglyceride, the more the chance of developing cardiovascular disease. And those triglycerides come from insulin-mediated processing of excess sugar.
- Insulin inhibits the breakdown and metabolic use of adipose fat. The adipose fat is the fat that lines the skin. It is the fat that makes us look fat. When there is too much sugar around, insulin tells the body to stop burning fat for energy and use sugar instead. Under the control of insulin, the pathways that mobilise fat and use it for energy cease and instead the body goes full-on into the mode of deriving energy from sugar and converting any excess sugar to storage fat.
Insulin therefore tells our cells to cling on to our fat reserves and add to them if there are excess carbs around. You can see that if you want to lose weight and be healthy, then ideally you need to eat minimal amounts of the food that trigger insulin: You need to eat fewer carbs. That clipperty-clop sound you can hear right now is my hobby-horse trotting off into the sunset!
One other point to make here is that insulin also has an anabolic effect on the body in that it mediates tissue growth and replacement. Insulin telling the fat cells in our skin to take-up glucose in order to make bigger adipose reserves is one example of this anabolic function. Other anabolic pathways controlled by insulin include the production and uptake of structural proteins, the expression of genes and the replication of DNA all essential for tissue regeneration and growth. Of course we need this and so some insulin is essential. However, too much insulin too often will over-stimulate these anabolic functions and excessive cellular regeneration, unchecked, leads to uncontrolled cell proliferation, the bedrock of cancer. Even non-malignant proliferation can be problematical if those tissues are for example, our fat cells or the cells lining your blood vessels. The perfect storm of inflammation and cell proliferation – both caused by excess insulin – can lead to atherosclerosis, the thickening of blood vessel walls and a precursor to heart disease. They used to think that eating too much fat thickened our artery walls but now we know that it is from excess carb-triggered insulin.
The recurring message here is that for good health outcomes we need to control our insulin levels – we need to avoid producing too much too often.
Compounding this problem, the insulin mechanism is itself under attack if we follow a diet perpetually consuming large amounts of starch and sugar. The persistent triggering of insulin to deal with the daily spikes in blood sugar levels begins to takes it toll. The insulin receptors on the cell membranes of the target cells start needing higher concentrations of insulin in order to be triggered. We could say they start becoming partially deaf to the insulin message. This is the start of Insulin Resistance. Insulin Resistance then sets up a vicious and escalating cycle: If the insulin receptors become a little ‘hard-of-hearing’, the pancreas will respond by releasing a bit more insulin into the blood to get its message across. But these higher levels of insulin sustained over a period of time will make the receptors even more deaf. So the pancreas has to release yet more insulin to get its message ‘out there’. In this ever escalating sequence, eventually the pancreas will no longer be able to release enough insulin to get its message across to all the target organs – the receptors have become just a little too deaf. This is Type II Diabetes. Once this condition has developed the body is no longer able to control the spikes in blood sugar brought about by the sugars and starches in the diet. Those glycolated proteins we met early can now go on the rampage!
Research also shows that not all of the insulin receptors and not all of the pathways from each receptor become equally deaf to insulin. If we have fatty liver disease for example, then it is likely that the liver becomes deaf to the insulin message rather quickly. This is very bad news. Remember how through the process of gluco-neogenesis the liver pumps out glucose when it thinks the body needs it? Normally the insulin message will tell the liver to stop doing this but if the liver has become deaf to insulin, it will continue to pump out glucose even though there is already raised glucose in the blood (the event that triggered the insulin in the first place). Blood sugar therefore goes up and not down. But, and it does seem to depend on your genetic disposition, many of us have fat skin cells that only very slowly become deaf to the insulin message. You will recall that insulin tells these fat cells to mop-up blood glucose and convert it to fat for storage and avoid burning it for energy. If the skin cells remain sensitive to every drop of insulin in circulation, then they will go into overdrive adding to their fat reserves because of the excess insulin triggered by a resistant liver. This is the metabolic pathway to obesity.
Just stepping aside of the argument here, this fits very nicely into my hobby horse that calorie counting is not enough to manage weight loss. Our insulin model and particularly the model of how with partial insulin resistance our skin fat cells are listening to an overloaded message of insulin to store fat, shows that weight gain is very much under hormonal control. And because insulin is the hormone in control, how much weight you gain is dependent on the sugar and starch in your diet.
Continuing with our insulin resistance story, you may remember that some of the functions of insulin are anabolic – they stimulate cell growth and proliferation. Good in small measure but not so good in excess. This anabolic pathway in the insulin receptors is less likely to become insulin resistant than the glucose absorbing pathway. So, in a body experiencing rising surges of insulin, those anabolic pathways, just like the skin fat cells, are listening to every drop of insulin. Cell proliferation, atherosclerosis and inflammation, all triggered by the anabolic functions of insulin, become rife.
You can now see that excess insulin is not a good thing. Obesity, type II diabetes, inflammation, cancer, atherosclerosis are all the long term consequences. Notice how this list is the rogue’s gallery of non-communicable chronic diseases prevalent in the 21st century, all mediated by insulin resistance in turn triggered by regular excess sugars and starches in your diet. It doesn’t stop there as insulin is an antagonist to leptin, the hormone we met in my last article that tells us when we are full. An Insulin resistant metabolism that throws large amounts of insulin into your blood will therefore depress levels of leptin and thereby suppress one of the key signals that you are full. A high carb diet = High insulin = Low leptin = Always hungry. Insulin Resistance seems to be our enemy.
But here’s the thing. Becoming insulin resistant has been an advantage to us in our evolutionary past. This takes me back to our fat babies.
It seems that during the third trimester of the pregnancy, the human baby flicks the insulin resistance switch and becomes temporarily insulin resistant. It starts to pile-on the pounds of fat and by the time the baby is born we have the perfect fat baby. But, and this is key, the insulin resistance switch is reversible; once the baby is born, it flicks the switch back and normal metabolism is restored. So, having a metabolism that can become insulin resistant has served Homo sapiens well in the past. It has also probably helped us through the odd ice age too. As times have become tough for humans when ice ages approach, we have probably had to rely more on starch reserves in underground vegetables for energy. If consuming these in quantity makes us pile on the pounds of fat (through insulin resistance) those pounds of fat have almost certainly made our survival of the cold more likely. Evolution will therefore have placed a selective advantage on those with the insulin resistance genes.
To a limited extent this continued to be a survival advantage up until our very recent history. Each Winter there would be a survival advantage to those carrying a few extra pounds of subcutaneous fat – an extra layer of protective warmth. How clever would it be if we could trigger piling on a few pounds in the Autumn in readiness for the approaching Winter.
Until the era of supermarkets and the removal of seasonality of foods, humans would only have had access to significant amounts of sugar and starch in the Autumn in the form of fruits, berries and starchy root vegetables. Consuming these in the Autumn glut would temporarily overload our insulin mechanisms triggering mild insulin resistance in turn promoting our skin cells to store more fat. We therefore get those few extra pounds of insulating body fat in readiness for the upcoming Winter. The key thing though for our evolution is that we then stop eating those sugars and starches at the end of Autumn because they are no longer available. Our insulin mechanisms restore to normal function, insulin levels fall allowing us to mobilise and metabolise those fat reserves and enabling us to live off them during the Winter. But modern 21st century Man lives in a perpetual Autumn as starch and sugar are available year-round causing perpetual insulin resistance to obesity. What once gave us a survival advantage has now turned against us.
Next month, in my article entitled How to “Phil” Your Plate, I shall take a side-step from the modern science of nutrition and talk a little about the practicalities of feeding ourselves in a way that manages insulin and leptin. Click here to read this article
Thanks again Phil. You have a way of making technical issues understandable