The Digest

Debunking the Myths Surrounding Dietary Carbohydrate: Role in the Onset of Type 2 Diabetes

The appearance of the article,‘Fat is not the major issue. Let’s bust the myth of its role in heart disease’, by cardiologist Aseem Malhotra, in October 2013, marked a turning point in the popular recognition of the underlying role of dietary sugar in the current epidemic of metabolic syndrome – the constellation of disorders characterised by excessive body fat, raised blood pressure and disturbances in the levels of fat, cholesterol and sugar in the blood, which culminate in an increased risk of heart disease, stroke and type 2 diabetes [1].

Dr Malhotra referred, in particular, to the sugar routinely added to processed foods to compensate for the perceived detrimental effect on taste brought about by the reduction in the amount of fat added to products by the food manufacturers. There is also, of course, widespread concern over the large quantities of sugar consumed in soft drinks, especially by children. For the reasons to be discussed below, these concerns are well justified: sucrose, the chemical name for common-and-garden table sugar, is indeed the dietary villain of our times. What is most unfortunate, however, is the way in which all carbohydrates (of which sucrose is but one type) seem by many to have been tarred with the same brush. The truth is that not all carbohydrates are harmful to health; and the danger is that by following ‘low carb’ diets – without reference to the type of carbohydrate – some people may be missing out on the health benefits to be derived from a diet rich in wholegrain, complex carbohydrates.

You often hear people refer to ‘good carbs’ and ‘bad carbs’; others talk of ‘processed’ and ‘refined carbs’, but the use of these terms is often confused in the sense that it bears no relation to the chemical forms in which carbohydrates occur (nor their effects on the human body). Indeed, it is the case – which I make below – that ‘unprocessed’ sugars, such as maple syrup and raw cane sugar, are no less detrimental to health than ordinary table sugar. Similarly, concerns expressed over the health effects of bread and pasta (both refined carbohydrates) are largely unfounded. There are even those who assert that wholegrain and wheat products are to be avoided, yet I would argue that – except for those with coeliac disease (about 1 in 100 of the population) or a genuine allergy to specific cereal proteins – these foods should form the basis of a healthy, balanced diet.

In the present article, I will explain the role played by dietary carbohydrate in health. The focus of attention will be the phenomenon known as ‘insulin resistance’, which underlies the alarming growth we are currently witnessing in the incidence of type 2 diabetes. Although there are genetic elements to the condition, type 2 diabetes is caused primarily by poor diet and lifestyle – to the extent that it is largely avoidable. However, the condition is avoidable only if well intentioned individuals are equipped with a sound understanding of the role played by diet in its development. Unfortunately, there is much misinformation being bandied about, especially where the important distinction between complex and simple carbohydrates fails to be appreciated.

Whereas Dr Malhotra’s article is concerned primarily with the role of sugar in heart disease, I will focus here on type 2 diabetes. There are two reasons for this. Firstly, the mechanisms underlying the two conditions have many common features – especially the central role of inflammation – and can, therefore, be seen as components of the wider condition we call metabolic syndrome. Secondly, I have described already (in considerable detail) the role of diet in the development of heart disease in my book Healthy Eating through Informed Choice [2]. In common with the approach used in my book, the current article assumes no prior scientific or medical knowledge on the part of the reader.

It is my aim to equip the reader with a good working knowledge and understanding of the role played by dietary carbohydrates in human health and disease using simple, everyday language and analogies. You will not be given a list of rules or ‘forbidden’ and ‘allowed’ foods, rather you will be guided through the underlying biological and biochemical principles – so as to be able to make your own, individual dietary choices. In other words, you will be in a position to make informed choices concerning the dietary and lifestyle changes you are prepared to make to avoid adding yourself to the grim, mounting statistic that is the incidence of type 2 diabetes.

When is a carbohydrate simple? When is it complex?

All carbohydrates consist of one or more individual sugar ‘building blocks’ (or ‘units’), often joined together to form very large structures – at least on the sub-microscopic, molecular scales encountered in chemistry! Glucose is one such individual unit; it is the main sugar in our blood. Fructose (fruit sugar) and galactose are also examples of single-unit sugars.

Glucose, fructose and galactose often occur joined together in pairs. Ordinary table sugar (sucrose), for example, consists of one glucose unit joined to one fructose unit. Similarly, lactose (the major sugar in milk) consists of one glucose unit joined to one galactose unit. Glucose, fructose, galactose, sucrose and lactose are all referred to as simple carbohydrates. They are sweet-tasting and are absorbed rapidly into the bloodstream from the digestive system: the single-unit sugars (glucose, fructose and galactose) are absorbed directly, whereas the double-unit sugars (sucrose and lactose) are first split into their respective, individual single-unit sugars.

In addition to joining with fructose or galactose to form sucrose and lactose, respectively, glucose units can join together to form chains of varying length. Maltose, consisting of two glucose units, is another example of a simple carbohydrate; it is produced from barley during the malting stage of beer production. Starch, however, which is of indeterminate size, consists of huge numbers of glucose units joined together. For this reason, it is referred to as a complex carbohydrate.

Starch is not sweet to the taste and, after ingestion, takes a relatively long time to release its glucose ‘building blocks’ into the bloodstream: in the digestive system, the long chains of linked glucose units are gradually disconnected from each other by a series of digestive enzymes. (Enzymes are specialised proteins which, rather like workers on a factory production line, have a specific ‘operation’ or ‘job’ to perform on a substance. In this case, their job is to bring about the dismantling – the digestion – of starch into individual glucose units.)

In just one gram of glucose, there are some 3,340,000,000,000,000,000,000 individual glucose units! If you eat a gram of glucose, this number of glucose units will pass directly into your bloodstream very quickly, causing a sudden rise in the level of the sugar in your blood. Eating the same number of glucose units in the form of starch – where they are linked together to form long chains – will also elevate your blood glucose level. However, the ‘peak’ concentration of glucose will be much lower: the response will be less acute. This is because starch must be digested before its glucose units can enter the bloodstream.

Starch does not consist of just a single, long chain of linked glucose units. There are, in fact, two types of chain present in starch: amylose and amylopectin. Different starches (from different plant sources) contain different proportions of amylose and amylopectin, which is an important factor in determining how quickly a particular starch is digested and releases its glucose units into the bloodstream. Amylose consists of up to several thousand glucose units joined end-to-end, in single chains. Amylopectin also contains glucose units joined end-to-end, but it also has side-chains (every 24 to 30 glucose units), ‘branching off’ the main chain. Amylopectin can contain up to one million glucose units joined in this fashion.

Whereas amylopectin is digested relatively quickly, the digestion of the amylose component of starch is generally much slower. Starches are sometimes categorised into rapidly digested, slowly digested and resistant starch [3]. Generally speaking, the ease with which a particular starch undergoes digestion reflects its amylopectin content: the more amylopectin it contains (relative to amylose), the faster it will be digested [4]. However, other factors, relating to the physical structure of the starch – for example, its level of compactness, or whether or not it is encased by plant cell-wall materials, which restrict the accessibility of digestive enzymes – also play a role. The so-called resistant starch, which has a very high amylose content, can evade digestion in the small intestine and travel down to the large intestine, where it is acted on by bacteria. These bacteria convert the starch into particular fatty acids (the ‘building blocks’ of fats and oils), which are believed to be beneficial to the health of the gut: butyric acid, acetic acid and propionic acid suppress the growth of harmful bacteria, favouring, instead, the so-called probiotic, beneficial bacteria. Such fatty acids also have direct, beneficial effects on the cells lining the large intestine [4].

Resistant starch is in many respects similar to dietary fibre, which passes through the digestive system without being broken down. Like starch, fibre is a complex carbohydrate, consisting of linked glucose units, but in this case the glucose units are joined to each other by a different type of linkage – one which we humans do not have the necessary enzyme to break. Dietary fibre is nonetheless essential to good health: it speeds the passage of materials through the digestive system, thereby reducing the amount of time potentially harmful chemicals spend in the body. (Strictly speaking, a substance inside the digestive system is not actually in the body: the digestive tract is rather like the hole in a doughnut – it just happens to be a very long, convoluted hole!)

Maintaining a steady blood glucose level

A value of approximately 5 mmol/L is often given as the concentration of glucose in the blood of a healthy individual. The units (mmol/L), which may look unfamiliar to the non-scientist, give the number, rather than weight, of glucose units in each litre of blood: ‘5 mmol/L glucose’ is another way of saying 3,010,000,000,000,000,000, 000 individual units in each litre of blood. (It is rather like saying ‘five dozen eggs’ to mean 60 eggs.) Expressed in terms of its weight, this concentration of glucose corresponds to 0.9 grams per litre.

Glucose concentrations may be measured in whole blood, but more often than not they are obtained using blood plasma, which is the watery liquid remaining when the red blood cells and other such components have been removed. The concentration of glucose in whole blood is a little lower than that in plasma, but the small difference need not concern us here. Indeed, blood glucose levels do fluctuate: from about 4 mmol/L after an overnight fast to around 6 mmol/L after the consumption of a carbohydrate-containing meal.

It is important that blood glucose levels are maintained within a tight range. If the concentration is too low, then the blood will not be able supply the cells of the body with enough glucose to meet their energy requirements (for example, muscle cells, during exercise). To maintain blood glucose levels – between meals or during exercise, for example – the liver will release glucose into the blood from its ‘emergency stores’, which take the form of a complex carbohydrate called glycogen. Glycogen is similar in structure to the amylopectin component of starch, but it is more highly branched. Indeed, glycogen is often referred to as ‘animal starch’. Glycogen is made in the liver by linking together glucose units taken from the blood following a carbohydrate-containing meal. The liver can store approximately 75 grams of glycogen. A further 400 grams of glycogen is typically stored in the muscles, but this is used to provide glucose for the muscles themselves and is not released back into the blood. In total, these sources of glycogen represent some 1900 kilocalories (kcal) of stored energy – enough to meet the body’s glucose needs for about 16 hours.

Blood glucose can be ‘spared’ by the body switching to the use of fats, in place of carbohydrate, for energy. Highly-trained endurance athletes are able to switch to the use of fats more efficiently than non-trained individuals, which helps to eke out their glycogen stores. However, in addition to it being the preferred fuel of the brain, glucose is needed to extract the energy from fats, which are said to ‘burn in the flame of carbohydrates’. For these and other reasons, the body will go to considerable lengths to maintain blood glucose levels – even during prolonged fasting or severe exercise, when glycogen stores are depleted. Under these circumstances, the liver will generate glucose from non-carbohydrate substances (including proteins), which it releases into the blood. This de novo synthesis of glucose is called gluconeogenesis (the generation of ‘new’ glucose): it is what happens when a marathon runner ‘hits the wall’.

The consequences of too much glucose in the blood are of particular relevance to the development of chronic diseases, including type 2 diabetes and cardiovascular disease (heart disease and stroke). Obesity is also often referred to as being a disease, but to my mind it is not: it is a scenario, albeit an unhealthy one. Obesity can certainly lead to the development of disease, but in itself it is simply the body’s way of storing excess energy from the diet (often provided by excessive sugar). Even worse, we sometimes hear of people being ‘at risk’ of obesity (especially the poor), as though it were transmitted by a virus, but this is nonsense. There is no ‘risk’ involved; the equation is simple: if your energy intake is above the needs of your body, you store the excess energy as fat; if you expend more energy than you consume, then you lose weight. It is simply a matter of physics, not chance: you do not ‘catch’ obesity in the way you catch a cold or the flu.

The absorption of glucose into the bloodstream after a carbohydrate-containing meal causes the pancreas (an organ just below the stomach) to release insulin – a hormone – into the blood. Hormones are ‘communication agents’; they coordinate the actions in the body. Carried in the blood, insulin travels to all parts of the body, but only certain cells respond: those with the appropriate ‘receptor’ on their surface. The insulin receptor is rather like a lock, with insulin acting as the key. When insulin interacts with its receptor, various events are triggered inside the cell. Muscle cells and fat cells, for example, allow the entry of glucose from the blood. This involves the activation of special ‘glucose transporters’, of which we will learn more below. Although the uptake of glucose by the liver is not stimulated directly by insulin, the hormone prevents glucose release from the organ, so the effect of the liver is to bring about the net removal of glucose from the blood.

Glucose entering cells is ‘burned’ to release its energy. Surplus glucose from the blood is converted to glycogen in the liver and muscles for temporary storage. Once glycogen levels have been replenished – remember, the body can store around only 75 grams – any additional glucose will be converted to fat in specialised fat cells. As a walk through any town centre these days all too readily reminds us, the capacity of the body to store excess energy as fat is, by comparison, essentially unlimited. We also have other hormones, including glucagon, which stimulate the release of glucose from stored glycogen during fasting or exercise. As stated above, the liver will return glucose to the blood, whereas glucose released from glycogen stored in the muscles is used in situ. Glucagon also stimulates the breakdown of stored fat to release energy. Fat, however, cannot be converted back into glucose.

Diabetes: the failure to keep blood glucose levels in check

These days, we hear an awful lot about diabetes – the cardinal feature of which is the failure of the body to keep blood glucose levels in check. In type 1 diabetes, which presents most commonly in childhood, the pancreas is unable to produce insulin. By the careful management of their diet, and with appropriately-timed injections of insulin, individuals with this condition are able to maintain good control of their blood glucose levels and thereby minimise long-term health problems.

The vast majority of individuals with diabetes have the type 2 condition. Although there may be irregularities in insulin production in these patients, the key feature of their condition is insulin resistance, in which the problem lies at the level of the insulin receptor: insulin arrives at the cells, but they do not respond by allowing the entry of glucose from the blood. Type 2 diabetic patients may not require insulin injections; rather they are treated with drugs to increase the sensitivity of their cells to insulin. A healthy diet and exercise also play very important roles in the management of both types of diabetes. Indeed, lifestyle is a key factor in the development of type 2 diabetes. (Type 1 diabetes is believed to be an autoimmune condition, in which the body’s immune system destroys the insulin-producing cells in the pancreas; unlike the type 2 condition, it is not caused by an unhealthy lifestyle.)

There exists a continuum between the first signs of insulin resistance – a feature of metabolic syndrome – and full-blown type 2 diabetes. Initially, patients display normal blood glucose levels, but elevated levels of insulin. This state of affairs indicates that higher-than-normal amounts of insulin are needed to get the cells to respond and take up glucose from the blood. When elevated levels of the hormone are no longer sufficient to compensate for the insulin resistance, blood glucose levels rise slightly (this may be diagnosed on the basis of raised glucose levels following an overnight fast). Eventually, the condition progresses to overt type 2 diabetes, with the failure of the body to manage blood glucose levels.

What then, you ask, causes this insulin resistance and what are the steps that can be taken to prevent its onset? The good news is that there is much we can do through dietary and other lifestyle changes to avoid and – if we act early enough – reverse insulin resistance.

The pathway from elevated blood glucose to type 2 diabetes

Although research scientists have a very good understanding of some of the key features involved in the development of insulin resistance and type 2 diabetes, there are still questions to be answered concerning how these fit together to form a complete, coherent picture. Of these features, perhaps the most convincing and well understood involve the causal links between obesity and insulin resistance: being overweight is the most powerful ‘risk factor’ in the development of insulin resistance. I usually shudder at the mention of disease ‘risk factors’ – they often reflect a disproportionate level of trust placed in statistical analyses (number crunching). At best, risk factors give clues as to the possible causes of a disease; at worst, they lead scientists to confuse statistical rigour with mechanistic understanding. No matter how ‘powerful’ the statistics, if the underlying thinking is not there, the results will be flawed. A good example of this is provided by some of the studies which have sought to provide evidence of a link between the glycemic index and cardiovascular disease; I have discussed this matter elsewhere [5].

When it comes to the link between obesity and insulin resistance, however, a very convincing scenario has been described, explaining – in a step-by-step, mechanistic manner – how one event leads on to the next. Central to this process is chronic, low-level inflammation. There are well documented mechanisms explaining how adipose tissue (body fat) releases ‘chemical messengers’, whose effect is to provoke inflammation [6-9]. These messengers are similar to hormones, but they act more locally. They are generated naturally in the body for various reasons, including to help fight off infection. One of their jobs in adipose tissue is to help remodel its architecture during expansion (when a person lays down additional body fat). However, as the deposits of adipose tissue expand (during the development of obesity), various changes – involving an inadequate supply of oxygen to the deeper regions of the tissue, the death of individual fat cells and invasion of the tissue by cells of the immune system – culminate in the release of the aforementioned chemical messengers at enhanced levels. These ‘inflammatory mediators’ interfere with the ability of cells to respond to insulin, resulting in insulin resistance. To understand how this happens, it is necessary to look in closer detail at how insulin ‘instructs’ cells to take up glucose from the blood.

We recall that insulin, released into the bloodstream in response to elevated levels of glucose, stimulates certain types of cell (notably muscle cells and fat cells) to take up glucose by binding to a receptor on the cell surface; only cells bearing the insulin receptor are able to respond to the hormone. In response to its engagement with insulin, the receptor ‘transmits’ or ‘conveys’ information to the inside of the cell. This involves the activation or ‘switching on’ of enzymes and other proteins inside the cell. One such protein is the ‘glucose transporter’ we encountered earlier; its job is to transfer glucose from the blood into the cell. However, this transporter is not activated directly, in a single step; rather, there is a series of proteins between the receptor and the transporter (‘middlemen’, as it were), which link the two. We can imagine this series of steps proceeding as follows: insulin binds to its receptor ⇨ the receptor activates Protein A ⇨ Protein A activates Protein B ⇨ Protein B activates Protein C ⇨ Protein C activates the glucose transporter.

This signalling cascade not only provides lots of sites (steps) at which the process can be regulated, it results in amplification of the message: because one insulin receptor can activate several units of Protein A, each of which can activate several units of Protein B and so on, the occupation of a single insulin receptor can trigger the recruitment of several glucose transporters. Furthermore, branches off this main Protein A ⇨ Protein B ⇨ Protein C pathway allow additional proteins to be switched on. Therefore, as well as activating the glucose transporter, enzymes involved in the ‘burning’ of glucose inside cells (to release its energy) can also be activated. Similarly, enzymes involved in the conversion of glucose to glycogen (or fat) might also be activated; the exact response will depend on the particular tissue type (e.g. muscle or fat) and the circumstances (e.g. whether or not energy is needed to meet the needs of exercise or is being stored following an overindulgent supper).

One particularly important branch off this Protein A ⇨ Protein B ⇨ Protein C sequence involves the activation of a series of proteins whose job it is to stimulate growth: as well as its role in the regulation of glucose uptake, insulin is an important growth factor. As their name suggests, growth factors are necessary for the growth and survival of cells (another example is the so-called ‘insulin-like growth factor 1’, IGF1, which I have discussed elsewhere [2]).

It appears there is a degree of antagonism between the routes from the insulin receptor to the glucose transporter and those that lead to the stimulation of cell growth. In individuals with persistently high levels of insulin in their blood (a condition referred to as ‘hyperinsulinaemia’), which, as we have seen, occurs during the development of insulin resistance and type 2 diabetes, the ‘growth-response route’ from the insulin receptor appears to be in a state of persistent activation, whereas the pathway leading to activation of the glucose transporter is deactivated. This antagonism involves the direct inactivation of the proteins linking the receptor to the transporter (Proteins A, B and C) by proteins involved in the growth response. Put simply, proteins involved in the growth response ‘flip the off-switch’ on Proteins A, B and C. Thus, whilst excessive insulin in the bloodstream can – on the one hand – be seen as the body’s attempt to compensate for the failure of its cells to respond to the hormone, we can – on the other hand – see that too much insulin in the blood can be the cause of this resistance.

It is likely that insulin resistance can occur as a temporary, physiological (i.e. normal) response to changes in nutrient supply: it is one of the many mechanisms by which the body responds to short-term changes in the diet. However, under conditions of chronic insulin resistance, leading to type 2 diabetes, it is clear that these physiological responses have gone awry and progressed to a pathological state.

Through mechanisms similar to those employed by proteins involved in the growth response to insulin, the inflammatory mediators released from adipose tissue – at excessive levels in obesity – are believed to act by ‘flipping’ the very same off-switches on the proteins linking the insulin receptor to the glucose transporter. Thus, we have a direct, causal link between obesity and – by way of inflammation – insulin resistance.

Before we consider in detail the links between dietary carbohydrate and insulin resistance (which might by now appear to be self-evident), we must first consider some additional links involving obesity. In obese individuals, there is a much higher turnover of the intermediates involved in what, for want of a better term, can be called ‘fat handling’ – namely, the movement of fats (and their chemical components) in and out of adipose tissue, whether for storage or breakdown. These intermediates, which can be thought of as ‘partially-dismantled fats’, can activate proteins involved in mediating the growth response to insulin [6,10]. As we have seen above, these proteins can, in turn, ‘switch off’ the proteins responsible for conveying the message from the insulin receptor to the glucose transporter (Proteins A, B and C in the scenario used above). One ‘fly in the ointment’ of this model has been a dilemma known as the ‘athlete’s paradox’: endurance-trained athletes can have higher levels of fat in their muscles than obese individuals and those with type 2 diabetes, yet they are noted for their high insulin-sensitivity. Indeed, and as mentioned above, the muscles of endurance-trained athletes have an enhanced ability to use fats as a fuel, thereby sparing the body’s glycogen reserves. This increased fat usage is associated with increased fat turnover and, consequently, elevated levels of those partially-dismantled fats, believed to cause insulin resistance in the obese. The solution to this paradox would seem to lie in the fact that, in contrast to endurance athletes, obese individuals have a reduced ability to ‘burn’ these fat intermediates, allowing them to ‘hang around’, as it were, and activate the proteins involved in the growth response.

The story concerning the role of adipose tissue and obesity in the development of insulin resistance and type 2 diabetes is far from complete (and not without its contradictions), but what we can say with certainty is that the progression to these maladies does not follow a single route. It is more of a tangled web of interrelating processes, which converge and climax to create the aforementioned pathological conditions. Into this maelstrom we can throw carbohydrates, but we must be very careful to distinguish between the effects of simple carbohydrates, such as ordinary table sugar (sucrose), which cause sudden, short-term but highly elevated ‘spikes’ in blood glucose levels, and complex carbohydrates (i.e. starch), which cause slower, more moderate elevations in glucose over prolonged time periods.

Insulin abuse: the role of carbohydrates in the development of type 2 diabetes

I use the term ‘insulin abuse’ to describe the ingestion of carbohydrates in amounts so excessive that they overtax the ability of insulin to bring blood glucose levels back under control. Consider, for example, the ingestion of a 330 mL can of Coca-Cola®. According to the nutritional information available for the product sold in the UK, a single can of this beverage contains some 35 grams of ‘sugars’ (10.6 grams per 100 mL). ‘Sugars’ is a generic term for all simple carbohydrates; since the ingredients panel lists ‘sugar’ as the only such ingredient, we can assume this is sucrose (i.e. ordinary table sugar). We recall that sucrose is a disaccharide, each unit of which consists of one glucose unit joined to one fructose unit. Once it reaches the small intestine, sucrose is broken down (digested) very rapidly into separate glucose and fructose units. These two monosaccharides are then absorbed into the bloodstream. The 35 grams of sucrose in a single can of Coca-Cola® would release approximately 18 grams of glucose and the same amount of fructose (the slight increase in total mass reflects the water added to sucrose during its cleavage).

First of all, we will consider the fate of the glucose ‘half’ of sucrose. Assuming that the total volume of blood in an adult male, weighing around 70 kg, is about 5 litres (reported values do vary and are lower for females), and assuming a blood glucose concentration (between meals) of 5.0 mmol/L, we can calculate that a 70 kg man has, in total, approximately 5 grams of glucose in his bloodstream. If the 18 grams of glucose released upon the digestion of the sucrose from a single can of Coca-Cola® were added to the bloodstream of this male, without any intervention by insulin, the total amount of glucose in his blood would reach 23 grams; this would translate into a blood glucose concentration of some 25 mmol/L! The fact that the blood glucose concentration in healthy individuals rarely exceeds about 8 mmol/L (a total of approximately 7 grams in 5 L of blood), bears testimony to the remarkable ability of insulin to promote the removal of glucose from the blood.

In front of the 330 mL can of Coca-Cola® shown in the photograph is 35 grams of sugar – the approximate amount in the can. The smaller pile to the left shows, for comparison, 5 grams of glucose – the total amount of glucose the body attempts to maintain in its entire blood system.

To my mind, the regular ingestion of sugar in the quantities typical of modern, westernised diets amounts to an abuse of this regulatory system. As if a 330 mL can of soft drink were not enough, I shudder to think of the ‘strain’ put on the body by the massive quantities of sugar in some of the larger servings of these drinks sold by the fast-food outlets. An information sheet produced by McDonald’s USA, for example, shows that a ‘Large’ serving of its Coca-Cola®Classic contains a staggering 76 grams of sugar! Even the ‘Medium’ and ‘Child’ servings contain 55 and 28 grams, respectively [11]. With this level of abuse, little wonder those poor, old insulin receptors finally throw in the towel: they are being absolutely bombarded with insulin as the body attempts to prevent the blood turning to syrup!

The very high levels of insulin produced in response to the sudden, acute rises in blood glucose levels that follow such massive influxes of the sugar from the small intestine are believed to lead to insulin resistance. It seems that, at such high levels of stimulation by the hormone, there is a change in how the insulin receptor responds: the balance between the pathways leading to recruitment of the glucose transporter and those leading to cell growth is shifted to favour the latter. When the insulin receptor is in this ‘mode’, proteins involved in the growth response begin to deactivate those involved in recruitment of the transporter: it is as though the receptor is ‘toning down’ its sensitivity to the hormone – it is acting to prevent the influx of a huge, overwhelming amount of glucose into the cell.

This response bears many of the hallmarks of the mechanisms through which insulin resistance develops in obesity: in particular, it is associated with inflammation. Sudden, large peaks in blood glucose levels cause cells to produce a group of potentially harmful chemical species – referred to as ‘free radicals’ – from oxygen. Free radicals have been referred to as ‘cellular vandals’ – they are normally very short-lived, but are highly reactive and so can cause a huge amount of damage during their fleeting existence. (Much of the damage caused to cells by harmful forms of radiation – including X-rays and gamma-rays – is mediated by free radicals.) In fact, oxygen-derived free radicals are generated ‘accidentally’ at very low levels in all cells, largely as a natural consequence of our use of oxygen to extract the energy from food (i.e. when we ‘burn’ food). It is only when free radicals are generated in inappropriate amounts – at the wrong time or place – that problems arise. Although free radicals usually get a bad press, they do have a positive side to their character. Indeed, they play key roles in many regulatory processes; nitric oxide (nitrogen monoxide), for example, is a radical involved in the lowering of blood pressure. (Enhanced levels of nitric oxide generation are believed to be responsible, in part, for the beneficial effects of dark chocolate on the cardiovascular system!)

The key oxygen-derived free radical generated during the ‘burning’ of food in our cells is the superoxide radical. This species is also produced by certain cells of the immune system, where one of its effects is to stimulate the production of inflammatory mediators – the same mediators that are produced at excessive levels by the fat deposits (adipose tissue) of obese individuals and cause insulin resistance. There are well established biochemical mechanisms through which glucose, when present in excess, is known to stimulate cells to produce high levels of the superoxide radical [12-15]. Cells which are exposed to excessive levels of oxygen-derived free radicals are often described as being under ‘oxidative stress’. This reflects the nature of the damage inflicted upon cell components – such as proteins, fats and DNA – by free radicals (chemists classify the underlying chemical processes as oxidation reactions).

What is highly pertinent to the present discussion is the finding that it is the sudden, sharp elevations in blood glucose concentration – typically following the ingestion of sugars (glucose and sucrose) – that result in oxidative stress and the consequent production of inflammatory mediators. The longer-term, but milder, elevations in glucose levels seen following the ingestion of complex carbohydrates (i.e. starch) are not associated with oxidative stress [13]. Thus we have a direct, mechanistic link between the ingestion of large servings of sugar, the sudden high ‘peaks’ in blood glucose levels, oxidative stress, inflammation and insulin resistance.

Before we consider the role of the fructose ‘half’ of sucrose in this scenario, it is important to remind ourselves that the development of insulin resistance and type 2 diabetes does not proceed via a single, step-by-step sequence of events: it is more of a tangled web, in which several pathological factors and processes converge to produce the disease state. As well as its direct stimulation of superoxide generation in cells, glucose slowly modifies proteins by attaching itself to them [16-18]. This phenomenon forms the basis of the ‘HbA1c test’ used to assess the long-term control of blood glucose levels in diabetic patients: haemoglobin, the protein responsible for carrying oxygen in the blood, is slowly modified by the addition of glucose. High levels of this modified form of haemoglobin, called HbA1c – perhaps measured by a clinician every few weeks – indicate the poor long-term management of blood glucose levels by the patient (e.g. through dietary means or insulin injections).

Proteins modified by the addition of glucose (so-called ‘glycated proteins’) can lead to inflammation: not only are they recognised as being ‘foreign’ by the immune system, which reacts by activating cells involved in inflammatory responses, they can stimulate the production of inflammatory mediators through their engagement with special receptors on cells (in much the same way as insulin engages with its receptor). Before glycated proteins can interact with these receptors, they must undergo further modification by processes involving free radicals, resulting in the formation of ‘advanced-glycation end products’ (AGE for short). Several types of cell have special receptors on their surface for these products; the receptors are known as RAGE (‘receptors for AGE’). The engagement of RAGE stimulates cells to produce yet more superoxide radicals and inflammatory mediators. This merely serves to worsen an already dangerous situation: under these conditions, proteins involved in cell growth are activated, including the proteins whose actions lead to insulin resistance (see above).

Whilst all proteins are potential targets for modification by glucose addition, the glycation of proteins involved specifically in the control of blood glucose levels may be of particular significance. For example, in much the same way as the modification of a key may mean it no longer fits its lock, the direct glycation of insulin – itself a protein – may prevent its recognition and engagement with the insulin receptor [19]. Similarly, glycation of the insulin receptor may compromise its ability to associate with its hormone. There is also the possibility that the modification of proteins in the pancreas (the organ in which blood glucose levels are ‘sensed’) may lead to the impaired production and release of insulin.

Although we have seen, then, that the glucose ‘half’ of sucrose, when ingested in excessive amounts, is harmful to us in its own right, there is also the fructose component to consider. We recall from earlier that the sugar in a 330 mL can of Coca-Cola® releases around 18 grams of glucose and 18 grams of fructose upon digestion. Although I will not repeat here the detailed description I have given elsewhere of the mechanisms through which fructose is believed to contribute to the development of disease [2], I will pick out a few salient points which relate to the present discussion on insulin resistance and type 2 diabetes.

In addition to being able to add on to proteins in a manner similar to that described for glucose, fructose causes particular problems in the liver. Whereas the liver is able to maintain good control of the amount of glucose it converts to fat, this is not the case for fructose. By ‘bypassing’ the regulatory steps in place for glucose, fructose is converted to fat in the liver very readily indeed: the more fructose the organ is presented with, the more fat it produces. This phenomenon is responsible for the so-called ‘non-alcoholic fatty liver disease’ associated with excessive fructose consumption, especially from foods sweetened with high-fructose corn syrup. Needless to say, the well-established biochemical mechanisms described above, in the context of obesity, serve to link high levels of fat turnover with insulin resistance.

Due to the ease with which fructose is converted to fat by the liver, it can be argued that the fructose component of ordinary sugar carries an even greater burden of responsibility than the glucose component for the current obesity crisis. Let’s not, however, go down the path of the fad diets advocating the free use of glucose but the ‘banning’ of fructose. Regardless of whether they are in the form of table sugar, high-fructose corn syrup, dextrose (another name for glucose), maltose, cane sugar, molasses, honey or maple syrup, excessive dietary sugars will be turned into fat if the energy requirements of the body are exceeded: it’s all a matter of energy balance and is quite a separate issue from the problems associated with those sudden, large rises in blood glucose levels caused by the ingestion of sugars (which, though accentuated in obesity, are harmful to all of us). Moreover, do not be conned by those who speak of ‘natural’ sugars, nor be misled by the claims made concerning some of the so-called ‘healthy’ fruit juices targeted at children. Many of these contain sugar at levels similar to those in the conventional sugary drinks, such as Coca-Cola®, which at least do not pretend to carry health-promoting properties! Some of the fruit juices marketed at children – or their well-meaning parents – contain added sugar, but even those which contain only ‘natural’ fruit sugars are excessively sweet. The alarmingly high sugar content of some of these drinks was the subject of recent coverage in The Telegraph [20,21].

We are all aware of how important it is to eat lots of fruit (as a source of vitamins), so you might think that it makes no difference how fruit is consumed – whether in the form of a smoothie, a concentrated juice or as the whole fruit itself. Of course, fruit does contain natural sugars: fructose – the monosaccharide we encountered earlier, in connection with fatty liver disease – being the main one. The point is that when you eat a whole fruit, it takes time to release its sugars in the digestive system. Fruit consists of tiny cells (‘compartments of life’); these have tough outer walls, which must be ruptured (e.g. by chewing) before the sugar within can be released. When you ingest a mechanically-processed fruit juice, this has all been done for you, so the sugars enter your bloodstream more rapidly than if had you eaten the unprocessed fruit. The problem is only exacerbated when the fruit juice has been concentrated or – Heaven help us – sweetened with added sugars. If you must drink fruit juices, stick to small servings, taken with meals. This way, at least, other food components may slow down absorption of the sugars.

Conclusions: debunking the myths

I hope I have managed to convince readers that it is a gross oversimplification to say all ‘carbs’ are unhealthy and contribute to metabolic syndrome, including insulin resistance and type 2 diabetes. Every time I read or hear an ‘expert’ discussing the role of carbohydrates in health and disease, without making the crucial distinction between complex carbohydrates and simple sugars, my heart sinks in utter exasperation. I think of the harm being done to the well-intentioned individuals, keen to eat a healthy diet, who are being misled into believing that this nutrient group should be avoided altogether. The fact is, complex carbohydrates – ideally from minimally-processed sources, including whole grains, brown rice, root vegetables and wholemeal flour – should, along with fruits and vegetables, form the mainstay of any healthy eating programme. Complex carbohydrates should provide the majority of one’s energy (calorie) intake, followed by fats and oils. Although proteins have the same calorific content as carbohydrates, their main role in the diet is to provide amino acids – the building blocks of proteins – for growth and repair.

My primary motivation in writing this article has been to dispel the widespread myth that complex carbohydrates, namely starch, are harmful because they increase blood glucose levels. Whilst this is the case for simple sugars, which cause sharp ‘peaks’ in blood glucose concentration, the milder, slower elevations in blood glucose following the ingestion of starch are not associated with biochemical changes that lead to insulin resistance.

This position is supported, for example, by a study carried out by Luis Monnier and colleagues at the University of Montpellier [13]. Using a special sensor placed under the skin, these researchers monitored glucose levels in a group of patients with type 2 diabetes over a period of three days; they also measured the levels of damage induced by free radicals (i.e. levels of ‘oxidative stress’). A very strong relationship – a positive correlation – was found between the level of free-radical damage and glucose. Crucially, this damage was not correlated with the absolute concentration of glucose, but rather with the size of the swings in the concentration of the sugar (calculated as the average difference between the peaks and nadirs in glucose concentration). The researchers found no correlation between free-radical damage and HbA1c, which, as we saw earlier, is a measure of long-term, sustained glucose levels. I reiterate: only the acute glucose fluctuations were associated with oxidative stress.

The study reported by Monnier and colleagues was carried out on individuals with existing type 2 diabetes. However, as we saw above, studies using a wide range of cell types have established that high levels of glucose stimulate production of the superoxide free radical [14,22,23]. Indeed, the biochemical mechanisms responsible for this phenomenon have been known for decades [24]. Increases in the production of oxygen-derived radicals, when stimulated by excessive glucose, are associated with the production of inflammatory mediators, which we have already seen play a causative role in insulin resistance. Given the fact that it is the sudden, sharp rises in blood glucose levels that are associated with oxidative stress and the production of inflammatory mediators, it is appropriate to revisit our earlier consideration of the differential effects of simple sugars and complex carbohydrates on blood glucose profiles.

We have seen how starches, depending on their amylopectin content, can be categorised into rapidly digesting, slowly digesting and resistant forms. However, the fact is that no form of starch causes the sudden ‘peaks’ in blood glucose concentrations seen with sucrose (table sugar) or glucose. This is a very important point because many people seem to make the naïve assumption that the ingestion of foods with a high glycemic index (GI) necessarily results in high levels of blood glucose. I have discussed elsewhere, at considerable length, why this is not the case [5]. Some starch-rich foods (e.g. rice and bread) can have a high GI, but this is because blood glucose levels are being averaged over a two-hour period. These starch-rich foods never bring about the excessively high blood glucose ‘peaks’ seen with foods containing simple sugars, even though the latter may have lower GI values; this is because the acute, severe increases in blood glucose they bring about are relatively short-lived and are, therefore, averaged out to produce deceptively low GI values over the two-hour measurement period [2].

There are scientific papers which show, very clearly, this difference in the response of blood glucose levels to the ingestion of sugars and starches. For example, Mark Daly and colleagues have shown how a high-sucrose diet causes blood glucose ‘peaks’ that are not matched by a diet high in starch [25]. Similarly, Talya Lavi and co-workers have demonstrated that the ingestion of 50 grams of carbohydrate in the form of glucose causes a much higher elevation in blood glucose levels than the same amount of carbohydrate in the form of a high-fibre cereal. Even cornflakes, which it can be argued constitute a highly-processed, starch-rich breakfast cereal, failed to increase blood glucose peaks to the same extent as glucose [26]. These researchers also monitored the functioning of cells lining the blood vessels: they found that high glucose blood levels, induced by glucose (but not by the high-fibre cereal, containing an equivalent amount of carbohydrate), were associated with the impaired functioning of these cells. This finding provides a mechanistic link between the ingestion of simple sugars and cardiovascular disease.

Support for the notion that, in addition to not resulting in sharp ‘peaks’ in blood glucose levels, starch-rich foods do not stimulate the release of excessive amounts of insulin – which, as we have seen, is associated with inactivation of the insulin receptor and, thereby, insulin resistance – is provided by the work of Renate Wachters-Hagedoorn and colleagues [27]. These researchers showed that, whereas the ingestion of 55 grams of glucose caused blood levels of the sugar to reach almost 9 mmol/L, a similar amount of carbohydrate in the form of either corn starch or corn pasta resulted in levels rising barely above 6 mmol/L. Similarly, whereas glucose caused insulin levels in the blood to increase approximately 5-fold, the equivalent amount of corn starch or corn pasta caused the level of the hormone to increase by just over 2-fold.

It might be expected that, the more quickly a starch is digested and releases its glucose units in the small intestine, the greater its impact on blood glucose levels. However, this does not appear to be the case. The categorisation of starch into the rapidly digesting, slowly digesting and resistant forms is based largely on measurements carried out in test tubes: starch samples are incubated with a cocktail of digestive enzymes and the rate of glucose release is measured using a simple test for the sugar [3,4,28]. However, the level of glucose in the blood at any particular moment is determined not only by how quickly the sugar is absorbed from the small intestine, but also how quickly it is removed from the blood by cells, particularly those in muscle and fat tissue. The situation can be likened to trying to fill a bucket with water when there is a hole in it. The level of water in the bucket at any particular moment depends not only on how quickly water is being added, from the tap, but also on how quickly it is leaving through the hole. In this analogy, the role of insulin is to control the size of the hole: the larger the ‘hole’, the more quickly glucose leaves the blood (i.e. is taken up by cells).

Whilst we have seen that insulin does a sterling job in keeping blood glucose levels under control, it does not work alone in this capacity. In response to the appearance of glucose in the small intestine, specialised cells lining the intestine release a hormone known as ‘GIP’ (glucose-dependent insulinotropic polypeptide). The main job of GIP is to stimulate the pancreas to release insulin into the blood. Thus, although much of the insulin released into the blood by the pancreas occurs in direct response to the organ’s detection of glucose in its own blood supply, GIP speeds up the release of insulin by acting as an ‘early-warning system’. This is why, after a meal, the level of insulin in the blood increases before the level of glucose increases: GIP ‘goes ahead’ and ‘warns’ the pancreas that glucose is about to enter the bloodstream from the small intestine.

Although this elaborate mechanism is unable to prevent ‘peaks’ in blood glucose following the ingestion of large quantities of simple sugars (found, for example, in soft drinks), in which the system is simply overwhelmed with glucose, it does seem to cope well with starches. In a very interesting paper published in 2012, Coby Eelderick and colleagues describe a series of experiments which show that foods containing slowly- and rapidly-digestible starches bring about a similar response in blood glucose levels [29]. Specifically, they found that, although the starch present in bread is digested more rapidly than that in pasta, resulting in a more rapid rate of uptake of glucose into the blood, both foods elicit similar changes in blood glucose levels. In the case of bread, it seemed that the rapid appearance of glucose units in the small intestine resulted in the production of more GIP, which stimulated the production of more insulin. (In other words, GIP ‘went ahead’ and told the pancreas to make a bigger hole in the bucket!) Some nine years earlier, Simon Schenk and colleagues had reported similar observations (in studies involving breakfast cereals), but these workers did not appear to consider the role of GIP or similar ‘messengers’ in the phenomenon [30].

It is worth commenting that, although the findings of Eelderick and colleagues suggest that there is little difference between the effects of rapidly- and slowly-digesting starches on blood glucose levels, they do bring about different insulin responses [29]. We have seen how both insulin and glucose can contribute to the development of insulin resistance (the former by overstimulation of the insulin receptor and the latter through protein glycation), so it remains to be established how significant is the distinction between the rapidly- and slowly-digesting forms of starch. Whatever the significance of any difference in relation to the development of insulin resistance, starch is simply not on the same planet when it comes to the harm done by the excessive intake of simple sugars!

Dietary advice

My advice is to stick to minimally-processed foods for your starches – e.g. wholemeal bread, brown rice, wholegrain grains and cereals – and you will have nothing to worry about. Those leading the anti-wheat movement express concerns that the more moderate, but sustained, elevations in blood glucose brought about by the consumption of starch can lead to greater levels of protein glycation and formation of AGE. However, I think these people are overlooking the fact that there can never be zero levels of protein glycation: as long as there is glucose in the blood, there will be protein glycation. In health, blood glucose levels are maintained at close to 5 mmol/L. Moderate increases above this value, even when prolonged, are not likely to cause problems.

Avoiding starch in an attempt to prevent protein glycation and AGE formation altogether is as futile and ridiculous as trying to avoid breathing air in order to prevent the formation of oxygen-derived free radicals: the formation of these products is the price we humans, and all other respiring creatures, have to pay for extracting the energy stored in carbohydrates – and for using oxygen to facilitate this process. Low-levels of damage involving free radicals and protein glycation are an integral part of the natural (healthy) ageing process: we have evolved elaborate defence systems to enable us to slow down this inevitable process, so let’s do it with good grace! It is futile (and, indeed, counterproductive) to try to prevent this.

Research is certainly needed to investigate the relationship between the rates of protein glycation and blood glucose concentrations. Speaking as a chemist, the kinetics are unlikely to display simple second-order behaviour. What I suspect is that, at very high glucose concentrations (at the ‘peaks’), new targets for protein glycation may come into play. Whereas the low-level, background protein glycation reactions may be of little consequence (e.g. involving blood proteins that are frequently replaced), the sugar may react with more critical proteins when present at particularly high concentration. These critical targets might include regulatory regions of the ‘messenger’ proteins we encountered earlier, including the insulin receptor itself.

It is very reassuring that other foods can have a beneficial impact on the response to starch ingestion [31]. Almonds, for example, appear to be highly effective in suppressing blood glucose levels in response to the ingestion of bread. Vinegar – a key ingredient in those healthy, Mediterranean salad dressings (not to mention the olive oil and salad itself) – has a similar effect. Light exercise is also hugely beneficial in this regard, so keep up with the gardening and don’t miss out on those long walks between the Christmas indulgences!


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Mark Burkitt

Westcott Research and Consulting

Article published 28 November 2014

If you would like to learn more about the role of diet in health and disease (including heart disease and cancer), it is recommended you read Dr Burkitt’s book, Healthy Eating through informed Choice (Troubador Publishing, 2014, ISBN: 9781783064793).

Whilst the book is written in non-technical language and is intended primarily for readers with absolutely no background in science, it is hoped that trained scientists and health professionals will also find the material to be of interest. The book is extensive in its scope and challenges some of the conventional views on the role of diet in human disease, questioning – in particular – the wisdom of the mainstream advice to consume a diet high in polyunsaturated vegetable oils. It is explained how the high susceptibility of polyunsaturates to damage by free radicals means they, rather than saturated fats, are likely to be a major cause of human disease (along with sugar, of course!).

Dr Burkitt's book is available for purchase from [Troubador Publishing], [Amazon], [WHSmith], [Blackwell's] and all other good book shops.

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