Carbohydrates, also known as carbohydrates or sugars, consist of a carbon chain to which the same elements that form water, namely hydrogen and oxygen, are bound. Carbohydrates are, for the most part, the architects of the establishment of a favourable hormonal framework for weight gain. In fact, taking in carbohydrates means encouraging the body to produce insulin, the anabolic hormone par excellence, the one that, more than any other, encourages the accumulation of new tissue. If, then, the carbohydrates consumed come from certain food sources, they can promote fat accumulation independently of hormonal influence. Regardless of one’s goals, however, whether they are for gaining or losing weight, it is never desirable to completely eliminate carbohydrates from the diet. One reason for this is that certain organs claim carbohydrates as their preferred source of nutrition (e.g. the brain). Such organs can only feed on other ‘fuels’ (ketone bodies) in emergency situations. In order to meet the needs of these organs, therefore, one must always introduce at least a small amount of carbohydrates in the diet. Another reason for including an appropriate amount of carbohydrates in the diet lies in their effect on the immune system. It is well known, in fact, that strenuous physical activity, such as the training of busy athletes, often leads to a decrease in immune defences. Well, Bishop (2001) showed how the intake of carbohydrates in athletes can reduce the immune system imbalances due to the application of the training load. More specifically, carbohydrate intake implies a reduction in pro-inflammatory activity due to particular molecules called cytokines. Finally, carbohydrates also have positive effects on body composition.

Insulin: the anabolic hormone par excellence

  As we have already discovered, whenever food containing carbohydrates is consumed, it is broken down during digestion into the chemically simplest sugar of all: glucose, the only one that can circulate in the blood stream. But the amount of glucose in the blood, called glycaemia, can never exceed a certain limit, otherwise there would be very seriousrepercussions on health, even coma (remember the talk about homeostasis). This is why the human organism has set up natural defences to prevent this eventuality: whenever sugar is consumed, and blood sugar rises, two molecules called incretins are activated, namely GPL-1 and GIP. These incretins cause the activation of a gland called the endocrine pancreas (also known as the islets of Langerhans). The endocrine pancreas then produces the hormone insulin and releases it into the bloodstream along with glucose. Insulin, as a hormone, acts as a real messenger: it signals to all the cells in the body with which it comes into contact that there is an overabundance of glucose in the blood and that there is a risk of hyperglycaemia (that condition of excess blood sugar that the body fears so much). The cells that have ‘received the message’ then, under physiological conditions, take up as much glucose as possible from the blood, keeping it for themselves. In doing so, the blood is cleared of excess sugar and blood sugar levels return to normal. However, insulin is mostly an enemy of people who wish to lose weight. In fact, when the insulin communicates its message to the cells, the latter do not only take in glucose from the blood, but take in everything they can get their hands on, including fat, which is consequently accumulated. Moreover, while, as we have seen, insulin encourages the accumulation of new fat, it also prevents the disposal of already accumulated fat. This hormone, in fact, has the ability to hinder the process of excess fat disposal operated by particular chemical structures called hormone-sensitive lipases, i.e. special enzymes. Enzymes are chemical catalysts, i.e. their task is to facilitate and speed up certain reactions. There are many enzymes, all different, within the human body, and each class specialises in catalysing a specific chemical reaction. The enzymes with whose activity insulin interferes are the hormone-sensitive lipases HSL and MAGL. These enzymes catalyse a chemical reaction that takes place within adipocytes. The reaction catalysed by HSL and MAGL is that of emptying the adipose cells of the fat they contain. When this reaction is blocked by the action of insulin, the goal of losing weight becomes very difficult to achieve. Another mechanism by which insulin prevents excess fat from being disposed of is by interfering with other hormones that can make people lose weight. I am referring, in particular, to adrenalin and noradrenalin, which have the ability to enhance the activity of hormone-sensitive lipases. Once insulin has blocked these hormones as well, losing weight becomes even more difficult. Finally, the last mechanism by which insulin prevents the disposal of fat is vasoconstriction. Blood vessels, in fact, are made of muscle tissue, and muscle tissue is elastic. As they are elastic, they can vary the width of their lumen. When they narrow, blood circulates poorly and badly; conversely, when they widen (within certain limits), blood circulates well and abundantly. Well, insulin causes the blood vessels to constrict to the point of impeding blood circulation. Now, excess fat, in order to be finally disposed of, must first leave the place where it has been accumulated, and then reach, via the blood, the place where it will be burned. If the circulation of the blood is defective, the fat will not be able to reach that site, so it will not be ‘burnt’. So, since insulin causes vasoconstriction, and since this condition is not compatible with good blood circulation, this hormone prevents excess fat from being disposed of. The obvious consequence of everything discussed in this paragraph is that when there is a lot of insulin in the blood circulation (blood) (when, that is, insulinemia is high), the body is very prone to gaining weight. It is quite clear, therefore, that since eating carbohydrates causes insulinemia to rise, these nutrients favour the establishment of a hormonal framework unfavourable to weight loss. It is not just a question of calories. Conversely, those seeking weight gain may be facilitated by an increase in blood insulin levels. Similarly, high insulin levels are essential for good recovery and, more generally, for good cell trophism. In fact, it is thanks to insulin that cells can take up the nutrients consumed during exertion, as well as the plastic substances necessary for the reconstruction of structures damaged by physical load.

The flip side of the coin: reactive hypoglycaemia

  It has been seen that the consumption of carbohydrates causes insulin production to increase and that, as a result of insulin’s action, blood sugar levels fall. But the mechanism by which insulin reduces blood sugar levels does not always work perfectly. When sugars are digested and poured into the blood too quickly, the endocrine pancreas enters a kind of emergency state whereby it produces more insulin than is needed to bring blood sugar back to normal. This then causes the opposite problem: blood sugar levels that are too low (however compatible with a physiological situation). Lower blood sugar levels result, on the one hand, in an intense craving for sugary foods and, on the other hand, if the situation occurs during physical exertion, in the reduction of glucose stores available to the muscles to produce metabolic energy, with obvious negative effects on performance. If the craving for sugar is satisfied, the cycle begins again: blood sugar rises, the endocrine pancreas produces too much insulin, we go into reactive hypoglycaemia and cravings for sugary foods arise again. And so on, in a perennial vicious circle that contributes to abundant glycaemic spikes. Moreover, when one finds oneself in a situation of reactive hypoglycaemia, if one is in the habit of consuming a lot of carbohydrate-rich foods, the metabolic situation is such that it causes a loss of muscle mass, which is rarely desired by athletes (and not only). More specifically, the body, not being able to store glucose in an unlimited way, as it can do with fat, and having, on the other hand, the need to receive it continuously, since it cannot take it from the blood, is forced to produce it itself. Here a particular chemical process is triggered in the liver, called gluconeogenesis (which we have already encountered). This process involves the formation of new glucose from precursors. Well, these precursors, for the most part, are proteins that the body takes from the muscles. The consequence is, as I anticipated, a decrease in muscle mass and, therefore, in the abilities associated with it.

Glycaemic Index and blood glucose management

  Not all carbohydrates have the same influence on insulin: some are digested and absorbed very quickly, so that they cause a rapid rise in blood glucose. Others, on the other hand, pass through the blood more slowly, causing blood sugar to rise moderately, but remain moderately high for a relatively long time. Let us try to illustrate this concept with an example: let us assume that an individual consumes 100 g of rapidly absorbed carbohydrates. These are all immediately digested and released into the bloodstream. The endocrine pancreas finds itself going from a situation where blood sugar is relatively stable to a condition of severe hyperglycaemia, so it starts secreting insulin. And it secretes more than it needs, so reactive hypoglycaemia occurs, which leads to gaining weight and losing muscle mass. If the same individual, on the other hand, consumes 100g of slow-absorbing carbohydrates, of these only 10g are digested and absorbed immediately (the numbers are approximate), while the rest remain in the digestive system. Blood glucose, therefore, rises very little, and the endocrine pancreas is perfectly able to regulate blood glucose effectively. The amount of insulin secreted is small. Following the action of this hormone, the 10g of carbohydrates that have entered the bloodstream are absorbed by the cells and blood glucose drops again. Here, then, of the 100g of carbohydrates consumed, the second 10g group arrives in the blood. And the cycle begins again: the endocrine pancreas secretes insulin in adequate quantities, blood sugar drops, and then rises again as soon as the third 10g group arrives. And so on. Now, let us be clear that carbohydrates are not absorbed ‘in groups’. It is rather a more or less rapid flow from the digestive system to the blood. All that is being done here is to simplify the process to make it more understandable. The information that really matters is that fast-absorbing carbohydrates give rise to reactive hypoglycaemia, whereas slow-absorbing ones (if consumed in moderation) do not. Now, in this paragraph we have roughly classified carbohydrates into two distinct categories: fast-absorbing and slow-absorbing. Even this, however, is a mere simplification adopted for didactic purposes. In reality, there are many intermediates between these two extremes. More specifically, it is possible to quantify how quickly carbohydrates are poured into the bloodstream by means of a numerical index: the glycaemic index (GI). The higher the glycaemic index, the faster the carbohydrates are absorbed. Glycaemic indices refer to foods. Thus, every food has its own glycaemic index. You can find an exhaustive list of glycemic indexes of foods on glycemic-index.net. As can also be seen on that website, if we want to classify foods by glycaemic index, we can divide them into three groups:

1. foods with a high glycaemic index: the GI is above 50;
2. medium glycaemic index foods: the GI is between 36 and 50;
3. low glycaemic index foods: the GI is below 36.

According to Siu (2004), the latter should be preferred during training.

Aspects influencing the glycaemic index

  In this section, the factors influencing the glycaemic index of foods will be discussed in detail. A practical list is provided below:

• amount of carbohydrates contained per 100g of food. As a matter of course, the more carbohydrates consumed in the context of a single meal, the more blood sugar will rise. Therefore, consuming 100g of a food containing 20g of carbohydrates will not have the same effect on blood sugar as consuming 100g of a food containing 90g of carbohydrates. The higher the carbohydrate density of the food, the higher its glycaemic index will be;
• simplicity of the chemical structure of the carbohydrates contained in food. As we have already seen, the only sugar that can circulate in the blood is glucose. Well, the more complex the chemical structure of the carbohydrates contained in food, the longer the time taken by the digestive system to reduce it to glucose. Hence, complex carbohydrates have, barring other GI-raising characteristics, a relatively low glycaemic index. Based on the complexity of their chemical structure, carbohydrates are commonly classified into monosaccharides (also known as osides), and osides. The former, united by the suffix -ose or -oso in the spelling, consist of carbon, hydrogen and oxygen in such a proportion that the carbon atoms are equal in quantity to the oxygen atoms, while the hydrogen atoms are equal to the sum of the carbon and oxygen atoms (in the language of chemistry: C H O_n2nn ). These are the so-called simple sugars which (with exceptions) have a rather high GI. As for the osides, however, these can be classified into holosides and heterosides. The former consist of covalently (i.e. strongly) bonded monosaccharides and differ in the number of monosaccharides from which they are composed. More specifically, disaccharides are composed of two monosaccharides, oligosaccharides of between three and ten monosaccharides, and polysaccharides of more than ten monosaccharides. Heterosides, on the other hand, are monosaccharides, disaccharides or oligosaccharides linked to a particular non-sugar molecule called an aglycone. As can easily be guessed, the chemical structure of osides is more complex than that of oxyosides;
• presence of protein, fat or fibre within the food. Protein, fat and fibre-rich foods are notoriously slow to digest. Therefore, the greater the presence of these within the food, the lower the glycaemic index;
• physical state of foods. Liquid foods, such as broths and soups, generally have a higher GI than solid foods;
• average acidity of the meal. Consuming relatively acidic foods helps to lower the GI of all the foods eaten in the context of the same meal. This is especially true for bread: if it is made with sourdough, which is more acidic than brewer’s yeast, commonly used by bakers, the GI will be lower;
• artificial sweeteners. Artificial sweeteners are alternatives to the more classic sugar that possess an enormously higher sweetening power than the latter. In fact, a very small amount, often almost entirely free of calories, is sufficient to achieve the same result in terms of sweetness infused into the food as is normally achieved with several grams of sugar. It is therefore understandable why many people who wish to limit their calorie consumption prefer this solution to sugar for sweetening food. Now, while indeed artificial sweeteners have the advantage of reducing the calorie content that the food would have had if sugar had been added, these products possess a ‘dark side’ of which it is good to be aware: the moment they are taken, the perception of a sweet taste predisposes the body to digest, absorb and handle carbohydrates. And even if, then, those carbohydrates do not arrive, the consumption of a minimal amount of sugars in the food (e.g. those in cappuccino milk, with an artificial sweetener added instead of sugar), will be such as to cause a far more significant insulin spike than if the artificial sweetener had not been taken.

These factors are valid for all foods, but for those containing starch (a particular carbohydrate), it is necessary to point out others. These foods, in fact, are not only influenced by the above-mentioned factors, but also by the following:

• amylose/amylopectin ratio: starch is made up of two different types of polymers (components), namely amylose and amylopectin. The former has a linear chemical structure, while the latter has a branched one. Now, the digestion of food is mediated by particular enzymes (which, remember, are chemical catalysts), which ‘attach’ themselves to the food and ‘take it apart’. The enzymes that digest starch are able to attach themselves more easily to amylopectin than to amylose, slipping in between the branches. As a consequence of this, the speed of digestion of amylopectin is faster than that of amylose. This is why starchy foods containing more amylose than amylopectin have a lower glycaemic index than those containing more amylopectin;
• cooking. When a starch is subjected to high temperatures, a chemical process known as gelatinisation takes place. This process implies an increase in the GI. As a rule, therefore, raw foods have a lower glycaemic index than cooked foods;
• technological manipulation of the food. Whenever a food is subjected to special technological procedures to increase its tastiness or preservability, the glycaemic index increases. This type of manipulation includes genetic modification (genetically modified starches are already infamous to discerning consumers), dextrinisation, and all those processes, such as cereal abburrification and refining (discussed in the food appendix), which aim to deplete food of some of its components (e.g. fibre);
• pasta making. This is the process whereby the dough is extruded through the die under strong pressure (another process that will be discussed in more detail in the appendix). This process promotes the production of heat, which in turn causes the production of a film on the proteins contained in the food. This film slows down the process of starch gelatinisation that takes place during cooking, thus reducing the glycaemic index. However, pasta-making, despite what the name might suggest, is not carried out for the production of all types of pasta. For instance, lasagne and ravioli do not undergo pastification. These, therefore, have a higher GI than other types of pasta;
• retrogradation of starches. This is, in a nutshell, the reverse process of gelatinisation. When a food is cooked, we have seen, the starch it contains is gelatinised. When it is then left to cool after cooking, the process of starch retrogradation takes place. This is why foods that are cooked and then stored in the refrigerator for a few days, or frozen, generally have a lower glycaemic index than those that are consumed as soon as cooking is finished. It is remarkable that after starch is retrograded, it acquires a kind of resistance to gelatinisation again. Therefore, if you cook the pasta, freeze it, then thaw it and reheat it, during the reheating process, gelatinisation, if it takes place at all, will be less than during the first cooking. The glycaemic index will still remain relatively low;
• degree of ripeness of fruit and vegetables, as well as storage time for tubers. Fruits and vegetables that contain starches (e.g. apples, bananas, potatoes, etc.) increase their glycaemic index as their degree of ripeness increases. For example, green bananas have a lower glycaemic index (40) than fully ripe bananas (65), just as potatoes stored for a long time have a higher glycaemic index than early potatoes;
• size of flour grains. During the process of crushing starchy products to produce flour, the smaller the resulting grains, the higher the glycaemic index of the food. In fact, the smaller the particles, the more digestible they become.

Malonil-CoA: another problem

  We have seen what happens when a carbohydrate meal threatens to disrupt the delicate balance (called, in physiology, homeostasis) of blood sugar. But, with regard to accumulated sugars, the amount of those in the blood is not the only thing that matters in keeping the body healthy. In fact, there can also be too much glucose inside the cells. The problem actually does not arise within certain limits, since glucose, as a carbohydrate, is a source of calories. In other words, once, following the message sent by the endocrine pancreas by means of insulin, cells have taken up glucose from the bloodstream, they can use it to derive the energy they need to survive. Sometimes, however, the glucose in the bloodstream is so much that it exceeds the energy requirements of the peripheral cells. Under these circumstances, the body builds up stocks: the excess glucose is converted into glycogen, a molecule that we have already encountered and which consists of a form of glucose more suitable for storage. Glycogen, we repeat, is stored in the liver and muscles. The latter will use it for themselves should there be a glucose shortage in the body in the future. The liver, on the other hand, will make it available to all those cells that need it (to be reached by blood). Glycogen, however, as repeatedly explained, can only be stored to a very small extent (unlike fat which, as one can easily imagine, can be stored almost indefinitely). So what happens to glucose that exceeds both the most immediate needs of peripheral cells and the storage capacity of liver and muscles? We have seen that cells can derive the energy they need to survive through aerobic metabolism in the context of that complex sequence of chemical reactions known as the Krebs or citric acid cycle. Well, when glucose is excessive, the Krebs cycle becomes overloaded. This leads to the formation of a molecule known as malonyl-CoA. This molecule is often converted to a large extent into some particular type of fat known as medium-chain fatty acids, and there you get fat. To be precise, the much-feared cholesterol belongs to this class of fats. Furthermore, irrespective of malonyl-CoA’s ability to turn into fat, it has the potential to hinder the fat ‘burning’ process: β-oxidation. This process is in fact mediated by a set of different chemical structures, known as carnitine-dependent complexes, whose activity is hindered by malonyl-CoA.

Insulin resistance and chronic hyperglycaemia

  Taking in more carbohydrates than the cells need immediately and are able to store in the form of glycogen also exposes us to another problem, far more serious than the formation of malonyl-CoA. I am talking about that situation which is the antechamber to senile diabetes: insulin resistance. When carbohydrate consumption is really high, the cells, in response to the ‘call’ of insulin and in an attempt to cleanse the blood of excess glucose, find themselves literally drowning in glucose. Thus, no matter how many insulin molecules reach the peripheral cells, the latter cease to take up glucose from the blood. Wanting to give a few more chemistry clues, there are special proteins called GLUT-4 on the cell membranes whose job is to pick up the insulin message and communicate it to the cell so that the latter starts to take up glucose from the blood. When the cell is overloaded with glucose, the GLUT-4 molecules present on the membrane are removed, so the cell remains insensitive to the insulin’s prompt. The consequence is that the amount of sugar in the blood remains constantly high. The endocrine pancreas copes with this situation by producing even more insulin in an attempt to get the peripheral cells to cooperate. The result of this operation is a constantly high insulin level which, as seen before, is a major impediment to the slimming process.

The effect of insulin on adipocytes

  We have seen that when the amount of glucose in the blood exceeds both the immediate needs of the peripheral cells and the storage capacity in the form of glycogen, a hormonal framework is set up which, on the one hand, leads to the accumulation of fat mass and, on the other, is the prelude to diabetes. The fate of glucose that is not consumed by cells and cannot be stored in the form of glycogen remains to be defined. Now, of all the cells in the body with which insulin can communicate, there are also adipocytes. Nevertheless, adipose cells behave very differently from other cells in the presence of insulin resistance induced by excess glucose. Whereas, in fact, in other cells the amount of GLUT-4 on cell membranes is reduced, in adipocytes it increases. This means that adipocytes, unlike other cells, become very prone to absorb glucose from the blood in the event of insulin resistance. But this does not mean that they become able to store it as such or in the form of glycogen. Adipocytes, in fact, are cells dedicated solely to storing fat. The only way to store excess glucose, therefore, is to turn it into storage fat. Which actually happens, once again, because of insulin. This hormone, in fact, is able to activate the lipoprotein lipases present in adipocytes. These structures, in fact, transform glucose into fat.

The pro-insulin-independent effect of carbohydrates

  We have seen that the anabolic action of carbohydrates is mostly due to their ability to stimulate insulin secretion. In some cases, however, carbohydrates can cause an increase in fat mass independently of the action of insulin. In order to best illustrate how this happens, a brief premise on carbohydrate sources is necessary here: some carbohydrate-rich foods, more particularly those based on cereals, are often subjected by the manufacturer to a process, known as refining, whereby the fibrous covering of the cereal (the bran) is removed. The aim is to obtain a more palatable food. The most typical example contrasting refined foods with whole foods (i.e. including bran) is bread. Refined bread is light brown in the crust and white on the inside. Wholemeal bread, on the other hand, has a darker appearance. Well, refined foods, sources of carbohydrates, can cause phlogistic phenomena (i.e. tissue inflammation). The reader will probably already be familiar with inflammation: it involves redness, a burning sensation, discomfort and pain. Not all inflammations, however, present these symptoms. Some inflammations, in fact, are silent (without symptoms). Now, when a cell in the body is subject to inflammation, whether silent or symptomatic, its metabolic activity tends to be reduced, with the consequence that this cell will burn fewer calories than a non-inflamed cell would normally burn. This effect may have only a marginal influence on body composition (indeed, there are aspects that should be paid more attention to when setting up a dietary protocol than the selection of unrefined foods), but it is nevertheless worth bearing in mind this deleterious effect of carbohydrates from refined foods.

Carbohydrates and oxaloacetate

  As mentioned above, these nutrients do not only have anabolic effects. One of the catabolic effects of carbohydrates is due to their ability to stimulate the production of a molecule known as oxaloacetate. More specifically, within the Krebs cycle, a chemical reaction, among others, takes place that leads to the formation of oxaloacetate, which, in muscle, promotes β-oxidation. Well, the more glucose muscle cells can rely on for the Krebs cycle, the more oxaloacetate is produced and, consequently, the more fat is disposed of.

Carbohydrates and the hormone leptin

  We have previously learned that leptin, or satiety hormone, is produced by adipocytes when they fill up with fat. Adipocytes, however, are not the only gland that produces leptin within the human body. The pituitary gland can also do this. Now, one very important thing to keep in mind is that the human body also produces leptin in response to insulin secretion. In other words, the more insulin you produce, the higher levels of leptin will also be produced. This is why low carb diets (i.e. those diets with low carbohydrate intake) only work for a limited period of time (in my experience, maximum 16 weeks). After a while, due to chronically low insulinemia, leptin levels drop so much that cellular metabolic activity is reduced. Hence, you gain weight.

Insulin and muscle cell lipoprotein lipase

  We have seen that chronically high insulinemia is extremely dangerous, both for body composition and, more generally, for health. Insulin, however, has the power to hinder the establishment of the state of insulin resistance. Amongst all its actions, in fact, insulin reduces the activity of lipo-protein-lipases in muscle cells. We have already encountered lipo-protein-lipases and seen that their function is to promote the storage of new fat. However, lipo-protein-lipases do not exist solely in adipocytes. There are, instead, also in myocytes, i.e. in muscle cells. And the fact that they are less active in the latter, resulting in less fat being stored inside them, has an interesting positive implication: GLUT-4 are encouraged to move across the cell membrane. This implies prevention of insulin resistance. Let it be clear, however, that when glucose levels are very high, this defence mechanism, put in place by insulin itself, is by no means sufficient, so the phenomenon of insulin resistance still takes place.