Rate of eating and collagen stiffness
Nutrition and rate of eating
Nutrition,rate of eating Collagen stiffening
The rate of absorption of dietary nutrients is important in ensuring that their post prandial blood concentration doesn’t overwhelm their metabolic processing. If this happens there is stress to the orderly metabolic system and alternative pathways used e. g. into storage tissues such as fat. The rate of digestion and absorption is dependent upon a series of events. 1. Chemical and and physical nature of the ingested food . 2. How much is eaten 3.Time taken to chew and swallow the food 4.Gastric emptying time 5. Rate of digestion and absorption of the bolus. The obvious examples of the clinical consequences of sustained nutrient overload are body weight, Type 2 diabetes ( carbohydrates) and coronary heart disease ( lipids). There are other examples. Isolated Systolic Hypertension, an important aetiological factor in developing strokes is characterised by a stiffening of the sorta wall and loss of compliance which results in increased systolic pressure. Increasing vascular stiffness causes a reduction in arterial compliance. (1) Colonic Diverticulosis is usually related to insufficient fibre in the diet resulting in increased intra-colonic pressure. But wall stiffening is a feature of the colonic wall with diverticulosis. In symptomatic diverticlular disease the passage of caecal contents for voiding as faeces requires increased colonic contractions by the rigid colonic tubular wall (2). In both conditions under the dynamic conditions of pulsatile flow, the forces exerted by the fluid on the vessel wall create stresses within the thickness of the vessel wall. This leads to higher shear stresses within the wall, thus putting higher loading on elastin and gradually leads to elastin fatigue. As elastin gradually fails, its load bearing function is taken over by collagen , the vessel wall becomes less elastic and more rigid . This is all part of the ageing process (3). The chemical changes in collagen and elastin are due to glycation, resulting in glycation end-products and altered cross-links (4). Glycation is a haphazard process that impairs the functioning of biomolecules. Glycation (sometimes called non-enzymatic glycosylation) is typically the result of covalent bonding of a protein or lipid molecule with a sugar molecule, such as fructose or glucose,a none enzymatic process. Endogenous glycations occur mainly in the bloodstream with a limited number of the absorbed simple sugars: glucose, fructose, and galactose. Fructose and galactose have approximately ten times the glycation activity of glucose. Glycation is the first step in the production of these molecules through a complex series of very slow Amadori reactions, Schiff base reactions, and Maillard reactions; which lead to advanced glycation endproducts (AGEs) (4).Some AGEs are benign, but others are more reactive than the sugars they are derived from, and the endothelium, fibrinogen, and collagen are damaged). Long-lived cells (such as nerves and different types of brain cell), long-lasting proteins (such as crystallins of the lens and cornea), and DNA may accumulate glycation products over time leading to substantial damage (5,6,7,8,9). Therefore the concentrations of glucose, fructose and galactose in the blood is relevant to the speed of the glycation process. Increases in blood concentrations post prandially are important A proven approach to control absorption is by eating foods with beneficial glycaemic index. (10). An alternative simple approach to avoid such processes could be dietary moderation . That is to eat less and to eat slowly . In this way there is no stressing of the metabolic capacity of the body. (11). This would modulate the metabolic impact of food eaten in a meal. This removes all the complications of what food to eat, provided the the major requirement of a sufficiency of dietary carbohydrates, fats, proteins, electrolytes, minerals and vitamins are met. In this way the glycation processes would be reduced. It has the merit of simplicity
References
1. Kocemba J, Kawecka-Jaszcz K, Gryglewska B, Grodzicki T. Isolated systolic hypertension: pathophysiology, consequences and therapeutic benefits. J Hum Hypertens 1998 ; 12 :621-6.
2. von Rahden BH, Germer CT.Pathogenesis of colonic diverticular disease. Langenbecks Arch Surg 2012 ;397:1025-33.
3. Muiznieks L D, Weiss A S and Keeley FW . Structural disorder and dynamics of elastin. Biochem Cell Biol 2010; 88 : 239–50.
4. Vlassara H . Advanced glycation in health and disease: role of the modern environment. Ann. N. Y. Acad 2005; 1043 : 452–60.
5. Goldin, A, Beckman J A, Schmidt AM, Creager MA . Advanced Glycation End Products, Sparking the Development of Diabetic Vascular Injury. Circulation 2006; 114: 597-605.
6. Soldatos, G, Cooper ME . Advanced glycation end products and vascular structure and function. Curr Hypertens Rep 2006 ; 8 : 472–478.
7. Koschinsky T, He CJ, Mitsuhashi T, Bucala R, Liu C, Buenting C, Heitmann K, Vlassara H (). Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Proceedings of the National Academy of Sciences 1997 ; 94 : 6474–9.
8. Malik NS, Moss SJ, Ahmed N, Furth AJ , Wall RS, Meek KM. Ageing of the human corneal stroma: structural and biochemical changes. Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease. 1992 ; 1138 : 222-228
9. Munch, G, Deuther-Conrad W, Gasic-Milenkovic J. Glycoxidative stress creates a vicious cycle of neurodegeneration in Alzheimer’s disease–a target for neuroprotective treatment strategies?. J Neural Transm . Suppl 2002 ; 62 : 303–307.
10. Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, Brand-Miller JC. Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies. Am J Clin Nutr 2008; 87:627-37.
11. Cohn C, Joseph D. Role of rate of ingestion of diet on regulation of intermediary metabolism ” meal eating” vs. “nibbling . Metabolism 1960 ; 9 : 492-500
The rate of absorption of dietary nutrients is important in ensuring that their post prandial blood concentration doesn’t overwhelm their metabolic processing. If this happens there is stress to the orderly metabolic system and alternative pathways used e. g. into storage tissues such as fat. The rate of digestion and absorption is dependent upon a series of events. 1. Chemical and and physical nature of the ingested food . 2. How much is eaten 3.Time taken to chew and swallow the food 4.Gastric emptying time 5. Rate of digestion and absorption of the bolus. The obvious examples of the clinical consequences of sustained nutrient overload are body weight, Type 2 diabetes ( carbohydrates) and coronary heart disease ( lipids). There are other examples. Isolated Systolic Hypertension, an important aetiological factor in developing strokes is characterised by a stiffening of the sorta wall and loss of compliance which results in increased systolic pressure. Increasing vascular stiffness causes a reduction in arterial compliance. (1) Colonic Diverticulosis is usually related to insufficient fibre in the diet resulting in increased intra-colonic pressure. But wall stiffening is a feature of the colonic wall with diverticulosis. In symptomatic diverticlular disease the passage of caecal contents for voiding as faeces requires increased colonic contractions by the rigid colonic tubular wall (2). In both conditions under the dynamic conditions of pulsatile flow, the forces exerted by the fluid on the vessel wall create stresses within the thickness of the vessel wall. This leads to higher shear stresses within the wall, thus putting higher loading on elastin and gradually leads to elastin fatigue. As elastin gradually fails, its load bearing function is taken over by collagen , the vessel wall becomes less elastic and more rigid . This is all part of the ageing process (3). The chemical changes in collagen and elastin are due to glycation, resulting in glycation end-products and altered cross-links (4). Glycation is a haphazard process that impairs the functioning of biomolecules. Glycation (sometimes called non-enzymatic glycosylation) is typically the result of covalent bonding of a protein or lipid molecule with a sugar molecule, such as fructose or glucose,a none enzymatic process. Endogenous glycations occur mainly in the bloodstream with a limited number of the absorbed simple sugars: glucose, fructose, and galactose. Fructose and galactose have approximately ten times the glycation activity of glucose. Glycation is the first step in the production of these molecules through a complex series of very slow Amadori reactions, Schiff base reactions, and Maillard reactions; which lead to advanced glycation endproducts (AGEs) (4).Some AGEs are benign, but others are more reactive than the sugars they are derived from, and the endothelium, fibrinogen, and collagen are damaged). Long-lived cells (such as nerves and different types of brain cell), long-lasting proteins (such as crystallins of the lens and cornea), and DNA may accumulate glycation products over time leading to substantial damage (5,6,7,8,9). Therefore the concentrations of glucose, fructose and galactose in the blood is relevant to the speed of the glycation process. Increases in blood concentrations post prandially are important A proven approach to control absorption is by eating foods with beneficial glycaemic index. (10). An alternative simple approach to avoid such processes could be dietary moderation . That is to eat less and to eat slowly . In this way there is no stressing of the metabolic capacity of the body. (11). This would modulate the metabolic impact of food eaten in a meal. This removes all the complications of what food to eat, provided the the major requirement of a sufficiency of dietary carbohydrates, fats, proteins, electrolytes, minerals and vitamins are met. In this way the glycation processes would be reduced. It has the merit of simplicity
References
1. Kocemba J, Kawecka-Jaszcz K, Gryglewska B, Grodzicki T. Isolated systolic hypertension: pathophysiology, consequences and therapeutic benefits. J Hum Hypertens 1998 ; 12 :621-6.
2. von Rahden BH, Germer CT.Pathogenesis of colonic diverticular disease. Langenbecks Arch Surg 2012 ;397:1025-33.
3. Muiznieks L D, Weiss A S and Keeley FW . Structural disorder and dynamics of elastin. Biochem Cell Biol 2010; 88 : 239–50.
4. Vlassara H . Advanced glycation in health and disease: role of the modern environment. Ann. N. Y. Acad 2005; 1043 : 452–60.
5. Goldin, A, Beckman J A, Schmidt AM, Creager MA . Advanced Glycation End Products, Sparking the Development of Diabetic Vascular Injury. Circulation 2006; 114: 597-605.
6. Soldatos, G, Cooper ME . Advanced glycation end products and vascular structure and function. Curr Hypertens Rep 2006 ; 8 : 472–478.
7. Koschinsky T, He CJ, Mitsuhashi T, Bucala R, Liu C, Buenting C, Heitmann K, Vlassara H (). Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Proceedings of the National Academy of Sciences 1997 ; 94 : 6474–9.
8. Malik NS, Moss SJ, Ahmed N, Furth AJ , Wall RS, Meek KM. Ageing of the human corneal stroma: structural and biochemical changes. Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease. 1992 ; 1138 : 222-228
9. Munch, G, Deuther-Conrad W, Gasic-Milenkovic J. Glycoxidative stress creates a vicious cycle of neurodegeneration in Alzheimer’s disease–a target for neuroprotective treatment strategies?. J Neural Transm . Suppl 2002 ; 62 : 303–307.
10. Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, Brand-Miller JC. Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies. Am J Clin Nutr 2008; 87:627-37.
11. Cohn C, Joseph D. Role of rate of ingestion of diet on regulation of intermediary metabolism ” meal eating” vs. “nibbling . Metabolism 1960 ; 9 : 492-500