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Sasa
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Carbohydrates
kcal./gram: 4
Carbohydrates may be classified as monosaccharides, disaccharides, or polysaccharides by the number of sugar units they contain. Monosaccharides contain 1 sugar unit, disaccharides contain 2, and polysaccharides contain 3 or more. Polysaccharides are often referred to as complex carbohydrates because they are long chains of sugar units, whereas monosaccharides and disaccharides are simple carbohydrates. The difference is important to nutritionists because complex carbohydrates take longer to metabolize since their sugar units are processed one-by-one off the ends of the chains. Simple carbohydrates are metabolized quickly and thus raise blood sugar levels more quickly resulting in rapid increases in blood insulin levels.
Several lines of evidence indicate lifestyle-induced hyperinsulinemia and reduced insulin function (i.e. insulin resistance) as a decisive factor in many disease states. For example, hyperinsulinemia and insulin resistance are strongly linked to chronic inflammation, which in turn is strongly linked to a variety of adverse developments such as arterial microinjuries and clot formation (i.e. heart disease) and exaggerated cell division (i.e. cancer). Hyperinsulinemia and insulin resistance (the so-called metabolic syndrome) are characterized by a combination of abdominal obesity, elevated blood sugar, elevated blood pressure, elevated blood triglycerides, and reduced HDL cholesterol. The negative impact of hyperinsulinemia on prostaglandin PGE1/PGE2 balance may be significant.
The state of obesity clearly contributes to insulin resistance, which in turn can cause type 2 diabetes. Virtually all obese and most type 2 diabetic individuals have marked insulin resistance. Although the association between overfatness and insulin resistance is clear, the exact (likely multifarious) causes of insulin resistance remain less clear. Importantly, it has been demonstrated that appropriate exercise, more regular food intake and reducing glycemic load (see below) all can reverse insulin resistance in overweight individuals (and thereby lower blood sugar levels in those who have type 2 diabetes).
Obesity can unfavourably alter hormonal and metabolic status via resistance to the hormone leptin, and a vicious cycle may occur in which insulin/leptin resistance and obesity aggravate one another. The vicious cycle is putatively fuelled by continuously high insulin/leptin stimulation and fat storage, as a result of high intake of strongly insulin/leptin stimulating foods and energy. Both insulin and leptin normally function as satiety signals to the hypothalamus in the brain; however, insulin/leptin resistance may reduce this signal and therefore allow continued overfeeding despite large body fat stores. In addition, reduced leptin signalling to the brain may reduce leptin's normal effect to maintain an appropriately high metabolic rate.
There is debate about how and to what extent different dietary factors -- e.g. intake of processed carbohydrates, total protein, fat, and carbohydrate intake, intake of saturated and trans fatty acids, and low intake of vitamins/minerals -- contribute to the development of insulin- and leptin resistance. In any case, analogous to the way modern man-made pollution may potentially overwhelm the environment's ability to maintain 'homeostasis', the recent explosive introduction of high Glycemic Index- and processed foods into the human diet may potentially overwhelm the body's ability to maintain homeostasis and health (as evidenced by the metabolic syndrome epidemic).
kcal./gram: 4
Carbohydrates may be classified as monosaccharides, disaccharides, or polysaccharides by the number of sugar units they contain. Monosaccharides contain 1 sugar unit, disaccharides contain 2, and polysaccharides contain 3 or more. Polysaccharides are often referred to as complex carbohydrates because they are long chains of sugar units, whereas monosaccharides and disaccharides are simple carbohydrates. The difference is important to nutritionists because complex carbohydrates take longer to metabolize since their sugar units are processed one-by-one off the ends of the chains. Simple carbohydrates are metabolized quickly and thus raise blood sugar levels more quickly resulting in rapid increases in blood insulin levels.
Several lines of evidence indicate lifestyle-induced hyperinsulinemia and reduced insulin function (i.e. insulin resistance) as a decisive factor in many disease states. For example, hyperinsulinemia and insulin resistance are strongly linked to chronic inflammation, which in turn is strongly linked to a variety of adverse developments such as arterial microinjuries and clot formation (i.e. heart disease) and exaggerated cell division (i.e. cancer). Hyperinsulinemia and insulin resistance (the so-called metabolic syndrome) are characterized by a combination of abdominal obesity, elevated blood sugar, elevated blood pressure, elevated blood triglycerides, and reduced HDL cholesterol. The negative impact of hyperinsulinemia on prostaglandin PGE1/PGE2 balance may be significant.
The state of obesity clearly contributes to insulin resistance, which in turn can cause type 2 diabetes. Virtually all obese and most type 2 diabetic individuals have marked insulin resistance. Although the association between overfatness and insulin resistance is clear, the exact (likely multifarious) causes of insulin resistance remain less clear. Importantly, it has been demonstrated that appropriate exercise, more regular food intake and reducing glycemic load (see below) all can reverse insulin resistance in overweight individuals (and thereby lower blood sugar levels in those who have type 2 diabetes).
Obesity can unfavourably alter hormonal and metabolic status via resistance to the hormone leptin, and a vicious cycle may occur in which insulin/leptin resistance and obesity aggravate one another. The vicious cycle is putatively fuelled by continuously high insulin/leptin stimulation and fat storage, as a result of high intake of strongly insulin/leptin stimulating foods and energy. Both insulin and leptin normally function as satiety signals to the hypothalamus in the brain; however, insulin/leptin resistance may reduce this signal and therefore allow continued overfeeding despite large body fat stores. In addition, reduced leptin signalling to the brain may reduce leptin's normal effect to maintain an appropriately high metabolic rate.
There is debate about how and to what extent different dietary factors -- e.g. intake of processed carbohydrates, total protein, fat, and carbohydrate intake, intake of saturated and trans fatty acids, and low intake of vitamins/minerals -- contribute to the development of insulin- and leptin resistance. In any case, analogous to the way modern man-made pollution may potentially overwhelm the environment's ability to maintain 'homeostasis', the recent explosive introduction of high Glycemic Index- and processed foods into the human diet may potentially overwhelm the body's ability to maintain homeostasis and health (as evidenced by the metabolic syndrome epidemic).
