By Dr. Francesco Casillo
The glycemic load is a parameter indicating the impact that a food, taken in certain quantities, has on blood sugar (blood sugar level). Knowing it and knowing how to calculate it is useful for different reasons, in essence, between those of well - being and beauty ; this is due to the implications and influences that the intake of carbohydrates (or sugars) - and the consequent release of insulin - generates on the body composition (lean mass and fat mass) and on the metabolism of the individual.
Notes on some metabolic and hormonal effects deriving from carbohydrate intake
The intake of carbohydrates (or sugars) generates a rise in blood sugar (blood glucose level). The consequent nutrient-specific metabolic-hormonal response prepared by the body results in the secretion of the hormone insulin.
For the central nervous system, insulin is the sign of the introduction of food as well as energy abundance; moreover, from this hormonal stimulus various metabolic and substratum effects follow, of which the most important are listed:
- Emphasis on glucose utilization
- Inhibition of lipolysis (ie: inhibition of the use of storage fats for energy purposes)
- Glycogen synthesis (storage of sugars in polymer chains in the form of glycogen in muscle tissue and in the liver).
- Lipogenesis: conversion of sugars into fatty acids, their esterification into triglycerides and storage in adipose tissue.
As mentioned above, the greater the glycemic impacts of a meal (ie high levels of glycemic load), the more marked are the effects induced by insulin. Among these effects there is also the increase in the deposition of triglycerides (fats) in adipose tissue, with an increase in body fat). This event - in addition to having repercussions on purely physical-aesthetic objectives (ie on being "in shape") - has, and above all, important repercussions on the health of the individual.
Glycemic load and physical-aesthetic condition (effects on physical form)
At this point it should be clear that - if through the disciplined conduction of a training program, the aim is to obtain a weight loss * - a NOT optimal management of the intake of carbohydrates (in its qualitative and quantitative components together) could not only not turn to the optimization of the result sought, but even to compromise the results, that is NOT to be suitable to the objectives of WEIGHT!
* intended as a prevalent reduction, relative (%) and absolute (kg), of FAT in favor of the lean one.
Adipose tissue and health
The need to promote a decrease in fat mass levels must not only be a reason for interest in improving the physical-aesthetic area, but also and above all a reason to best preserve one's state of health, protecting it from the physiopathological pitfalls that follow excesses of fatty deposits.
In order to better understand the implications and harmful effects of increasing adipose tissue on health, it is necessary to go through a brief introduction about the different anatomy of the different types of adipose tissue and their effects.
Notes on the anatomy of adipose tissue
Abdominal fat is divided into 2 macro classes:
- subcutaneous abdominal fat
- and intra-abdominal abdominal fat, which in turn is subclassified into:
- Visceral or intraperitoneal fat (mainly composed of omental and mesenteric fat)
- and retroperitoneal fat3.
Retroperitoneal fat represents a small part of intra-abdominal fat3.
Again, it has been seen that visceral fat, compared to retroperitoneal fat, has a higher correlation with systemic metabolic variables, including: plasma insulin levels, blood sugar level and systolic blood pressure3.
The excessive accumulation of body fat is responsible for a vicious circle of metabolic, substrate and hormonal alterations, favoring diabetes and future cardiovascular complications; in this sense, the negative effect on health is greater for visceral abdominal fat compared to that of peripheral gluteal-femoral adipose deposits1.
Visceral fat is an important connection between the different "faces" of the metabolic syndrome: glucose intolerance, hypertension, dyslipidemia and insulin resistance6.
However, it also emerged that subcutaneous fat - WHEN located in the trunk area (chest and abdomen) - contributes more to triggering phenomena of insulin resistance compared to the subcutaneous fat present in other regions of the body4; therefore, even subcutaneous fat - and not only visceral fat - as a component of central obesity, has a strong association with insulin resistance5.
Abdominal obesity (high percentages of visceral and subcutaneous abdominal fat) was also correlated to alterations in plasma lipoprotein levels, in particular the increase in plasma triglyceride levels and low levels of HDL2 (the latter more commonly known as : good cholesterol).
Two other noteworthy aspects are the following:
- abdominal-intra-abdominal-visceral fat has the highest lipolytic rate / response compared to other fat deposits1;
- due to its anatomy it is able to have effects on liver metabolism.
In fact, abdominal visceral adipocytes are more sensitive to the action of catecholamines than those that constitute abdominal subcutaneous fat2. The increased sensitivity to lipolytic processes due to catecholamines within the omental fat in non-obese subjects is associated with an increase in the number of beta 1 and beta 22 adrenergic receptors. All this is associated with an increased sensitivity of beta-adrenergic receptors 32.
In obese subjects there is an increased lipolytic response to catecholamines in the abdominal area, rather than in the gluteal-femoral area and the aspect worthy of relevance is that the increased lipolysis of visceral fat is accompanied by a reduced sensitivity to the antilipolytic effect induced by 'insulina2.
This means that this framework can lead to an increased flow of free fatty acids into the portal venous system, with several possible effects on liver metabolism. These include: glucose production, VLDL secretion, interference with hepatic insulin clearance leading to a condition of dyslipoproteinemia, glucose intolerance and hyperinsulinemia2.
Furthermore, the abnormally high visceral fat deposition is known as visceral obesity. This phenotype of body composition is associated with the metabolic syndrome, cardiovascular pathologies and various neoplasms including breast, prostate and rectal colon cancer17.
And it is the visceral fat that contributes significantly to the level of free fatty acids in the blood stream compared to subcutaneous fat1.
Now we see, as schematically summarized in the graph, what happens when we are in the presence of high levels of visceral fat due to an incorrect lifestyle, characterized by hyperalimentation in synergy with a sedentary lifestyle.
1) Lipolysis phenomena on visceral fat and consequent increase in the level of fatty acids in the blood → 2) The fatty acids released into the bloodstream generate metabolic-hormonal repercussions on different levels: on the muscular area, on the liver and on the pancreas.
- 2a) At the level of skeletal musculature : there is a decrease in glucose transporters (GLUT-4) 8. So less glucose gets into the muscle cells! Furthermore, inhibition of the enzyme exocinase is also recorded, hence the inability to let glucose enter glycolysis9; this means poor ability to use glucose and reduced rates of muscle glycogen resynthesis10 (ready to use carbohydrate energy reserve). Also the increase of IRS-1 (insulin receptors) is inhibited 1.
Ultimately, changes in the muscles lead to hyperglycemia (increased presence of glucose in the blood)
- 2b) At the level of the pancreas . Although glucose represents the elective nutritional stimulus for insulin secretion, long chain fatty acids interact with a highly expressed receptor protein in the liver: GPR40. The interaction "fatty acid-GPR40" amplifies the stimulation of glucose on insulin secretion, thereby increasing blood levels7!
Ultimately, pancreatic alterations lead to hyperinsulinemia .
- 2c) At the level of the liver. A high flow of fatty acids in the liver induces a decrease in the extraction of insulin by the same liver, due to the inhibition of its receptor binding to the hormone, as well as of its degradation. All this inevitably leads to a condition of hyperinsulinemia, as well as the elimination of the suppression of hepatic glucose production2.
In addition, fatty acids also accelerate the gluconeogenesis2 processes (ie the production of glucose from other substrates: eg amino acids), further enhancing hyperglycemic states !
To make the picture even more nefarious, in response to the wide availability of fatty acids, the increased esterification of fatty acids, together with the reduced hepatic degradation of the "apolipoproteins B", leads to the synthesis and secretion of the atherogenic VLDL 2.
The summation of the effects exerted by fatty acids on different tissues leads to conditions of HYPERGLYCEMIA, therefore, to an altered metabolic-hormonal framework that predisposes to the metabolic syndrome!
In addition, the events evoked by fatty acids, deriving from the lipolytic process, on visceral fat lead to triggering and feeding a vicious circle that can be seen in a twofold key by way of example:
- The established hyperglycemic and hyperinsulinemic states favor further fat deposition.
- On the other hand, the evoked hyperinsulinemia is ANTITETIC due to the secretion of the hormone glucagon (hyperglycaemic hormone and also lipolytic ); in this way it also blocks lipolysis, that is the possibility of being able to use storage fats for energy purposes.
Here, then, that the addition of lipogenesis (fat formation) and antilipolysis (inhibition of fat catabolism) favors - in the subject that has high levels of visceral fat - further quantitative increases in the same, thus perpetuating the metabolic alterations of substrate of which he is responsible and invalidating the health of the individual!
In fact, due to the aforementioned reasons, in the overweight subjects the "De novo lipogenesis" is still evident even before the consumption of a meal! And this is positively correlated to the glycemic and insulinemic levels present in fasting13.
Adipose tissue and pathologies
Adipose tissue is the secretor of numerous adipokines (pro and anti-inflammatory molecules) which have profound effects on the metabolism.
As adipose tissue increases the secretion of pro-inflammatory adipokines increases and that of anti-inflammatory adipokines decreases19.
Obesity (especially from visceral fat, since the latter produces more cytokines than the subcutaneous one) represents a state / condition of chronic systemic inflammation, given that visceral fat is positively correlated to the Protein C Reactive (inflammatory marker) 19, 21
Chronic systemic inflammation is recognized to be the cause of multiple forms of cancer as well as other pathological states: type 2 diabetes, metabolic syndrome, atherosclerosis, dementia, cardiovascular problems18, 20.
Furthermore, inflammation causes alterations in the sensitivity of receptors to insulin, thus promoting insulin resistance.
Insulin resistance promotes the development of tumors through different mechanisms. Neoplastic cells use glucose to proliferate, therefore hyperglycemia favors carcinogenesis due to the establishment of an environment favorable to tumor growth18.
There is a positive association between elevated circulating levels of insulin and glucose and an increased risk for colorectal and pancreatic cancer18.
Insulin receptors and insulin-sensitive glucose transporters seen at the level of the average temporal region of the brain that presides over memory formation suggest the importance of insulin for the maintenance of physiological and appropriate cognitive function. The direct relationship between the impaired insulin and IGF signaling and the increased AΒ peptide deposition in amyloid plaques responsible for neurodegeneration was discussed.
Poor insulin levels or insulin resistance in the brain would be responsible for neuronal death due to the lack of the presence of tropic deficits in energy metabolism, thus also favoring the potegenesis of one of the most common forms of dementia: the disease of Alzheimer21.
And as mentioned, insulin resistance is mediated by inflammatory processes that occur within the growth of adipose tissue.
One of the possible solutions aimed at inducing an improvement in the state of health consists in favoring a decrease in the deposits of adipose tissue, especially that of the abdominal area.
This can be done through the combined action of
- a balanced eating style on a daily basis
- the conduct of a regimen of regular exercise adapted to one's psycho-emotional-physical-motor readiness
- an improvement in one's lifestyle by modulating stressors.
Although a dietary introduction that is higher than its actual metabolic and energy needs is never a choice to be taken into consideration, it is as difficult as it is rare for the definition of "hyper" to be of predominantly protein and / or lipid derivation without significantly involving the glucidic sphere.
This is due to purely cultural aspects and practical needs.
- "Culturali": since it is in the Italian culture to have meals in the main meals (breakfast, lunch and dinner) with cereals, farinaceous and their derivatives (bread, pasta, pizza, breadsticks, crackers etc.), while it is not common to eat compound meals from EXCLISIVELY PROTEIN and LIPID foods (only meat and / or fish for example).
- Of "practical need" since in the breaks of work or study or in any case in the time windows that interrupt the main meals (ie: mid-morning and mid-evening) it is not customary to dine with totally protein foods (meat, eggs, fish), but with purely or partially glucidic foods: sandwiches, sandwiches, yogurt with fruit, crackers, fruit fast food meals etc).
In fact, overweight, obese subjects reporting pathologies related to such weight status are certainly not those who report in their dietary style a protein and lipid hyperintroduction WITH CONTEMPORARY low or absent carbohydrate (carbohydrate) introduction; it is instead true the opposite, that is that their weight status (if it does not derive from genetic diseases and / or uncompensated hormonal dysfunctions) - from a point of view of eating habits - is correlated to a prevalent carbohydrate-dietary consumption in terms of% and / or absolute.
Given that carbohydrate food sources are an important part of a balanced nutritional regime (and this is especially true for those food sources that have a chemical-physical spectrum of important nutritional value from different points of view: type of carbohydrates, fiber content, content vitamin-mineral, water content, and alkalinizing capacity, etc.), it is not a question of excluding them but of knowing how to manage them qualitatively and quantitatively for the optimum of one's psycho-physical performance and to maintain one's health or maintain one's health.
In fact, food sources with high glucidic content, typical of western nutritional regimes, generate a high glycemic response favoring the postprandial oxidation of carbohydrates, thus depressing that of fats; therefore, they are prone to favoring the accumulation of fat12.
On the other hand, approaches that generate a low glycemic response can improve body weight control as they promote satiety, minimize postprandial insulin secretion and support the preservation of insulin sensitivity12.
This is supported by the fact that many studies have reported higher body weight loss values when nutritional regimens within a low calorie context predicted low glycemic index food sources compared to those with high glycemic index12.
Although glycemic control plays a crucial role in modulating the insulin response, this aspect assumes a greater relevance especially in overweight subjects. In fact, it was found that, following a hyperglucidic meal, overweight subjects reported hyperinsulinemia as well as higher concentrations of fatty acids and triglycerides compared to lean subjects13.
The inappropriate modulation of the glycemic load is also responsible for affecting the lean mass levels.
In fact, it has been observed that HIGH glycemic loads determine a negative nitrogen balance due to the stimulation of proteolytic hormones12 (ie hormones that act on protein destruction).
Furthermore, aberrant glycemic load values, besides triggering the metabolic alterations described, are also conditioning subsequent eating behaviors, in terms of selecting the quality and quantity of food sources for meals to follow. This is due to various metabolic and hormonal factors. In fact, HIGH glycemic loads determine a greater decline in leptin levels and also a rapid decrease in glycemic levels with the consequence of less temporal stimulation of gastrointestinal receptors for CCK, GLP-1 and GIP and, therefore, also in their lower stimulation direct and / or indirect temporalization of the centers of satiety of the brain12, 14.
In addition, high levels of glycemic load have been positively associated with the risk of colorectal cancer16.
For various reasons, including those so far exposed, it is absolutely desirable to lead a healthy lifestyle that emphasizes attention to a balanced and balanced nutritional style, within the frequency of daily meals, qualitative choice and quantity of the foods that make up the individual meals and the optimal ratio of nutrients within individual meals, as well as towards the constant practice of physical activity (better if guided by a valid trainer or personal trainer ), which must promote the optimization of the systems metabolic-hormonal to promote the health of the individual.
GLICEMIK is the valid calculator that allows you to become aware of the glycemic impact and its consequences (including the stimulation of the processes that favor the increase of fat mass) induced by the combination of qualitative and quantitative meanings of the nutritional style.
On the network (internet) there are several sources that allow you to calculate the glycemic load, whereas, instead, the convenience at hand for those who have a smart phone resides in applications aimed at this purpose.
Practical examples of the two types of calculations that can be performed with Glicemik
"I would like to know the glycemic load value induced by 250g of pizza or 250g of banana or 100g of dates or other foods to become aware of the propensity that these values have in impacting blood sugar and / or favoring phenomena of accumulation of body fat".
OR
“I would like to know how many grams of banana or apple or pizza or other foods correspond to a low glycemic load value, for example 10, so as not to stimulate the processes of accumulation of body fat.
Glicemik is available
- for android
- for Iphone
Page facebook //www.facebook.com/Glicemik
Bibliography
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2) Bernard Léo Wajchenberg Subcutaneous and Visceral Adipose Tissue: Their Relation to the Metabolic Syndrome Endocrine Reviews December 1, 2000 vol. 21 no. 6 697-738
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7) Nature. 2003 Mar 13; 422 (6928): 173-6. Epub 2003 Feb 23.
Free fatty acids regulate insulin secretion from pancreatic beta cells through GPR40.
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8) Vettor R, Fabris R, Serra R, Lombardi AM, Tonello C, Granzotto M, Marzolo MO, Carruba MO, Ricquier D, Federspil G, and Nisoli E. Changes in FAT / CD36, UCP2, UCP3 and GLUT4 gene expression during lipid infusion in skeletal and heart muscle rat. Int J Obes Relat Metab Disord 26: 838-847, 2002.
9) Thompson AL and Cooney GJ. Acyl-CoA inhibition of hexokinase in rat and human skeletal muscle is a potential mechanism of lipid-induced insulin resistance. Diabetes 49: 1761–1765, 2000
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11) Dresner A, Laurent D, Marcucci M, Griffin ME, Dufour S, Cline GW, Slezak LA, Andersen DK, Hundal RS, Rothman DL, Petersen KF, and Shulman GI. Effects of free fatty acids on glucose transport and IRS-1-associated phosphatidylinositol 3-kinase activity. J Clin Invest 103: 253-259, 1999
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13) Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men. Iva Marques-Lopes, Diana Ansorena, Iciar Astiasaran, Luis Forga, and J Alfredo Martínez. Am J Clin Nutr February 2001 vol. 73 no. 2 253-261
14) Interaction of insulin, glucagon-like peptide 1, gastric inhibitory polypeptide, and appetite in response to intraduodenal carbohydrate. JH Lavin, GA Wittert, J Andrews, B Yeap, J MWishart, HA Morris, JE Morley, M. Horowitz, and NW Read..Am J Clin Nutr September 1998 vol. 68 no. 3 591-598
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Volume 2012 (2012), Article ID 986823, 13 pages
