Chronic Meditation
Chronic inflammation has been shown to be a consistent pre-cursor to many metabolic diseases, such as obesity, fatty liver disease, atherosclerosis, insulin resistance, type II diabetes, degenerative disorders such as dementia, airway disease and some cancers.1 The relationship between diet, and more specifically refined carbohydrates, and chronic inflammation has been of high interest in the media in recent years. This interest could have a lot to do with the alarming rate that these metabolic diseases are growing. For example, The World Health Organization estimates that one billion adults worldwide are over weight, and 300 million of those are clinically obese, defined as having a body mass index equal to or greater than 30 kg m-3. (1)
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What is scarier still is the equally marked increase in obesity, and diagnosis of type II diabetes (formerly known as adult onset diabetes) among children.1 There has also been a heightened awareness for prevention measures of metabolic syndrome, a cluster of common pathologies including obesity, insulin resistance, dyslipidemia, and hypertension, usually resulting into diabetes type II or cardiovascular disease.2 Speculation of these rising numbers have to do with the food industry and its replacement of sucrose with fructose in an increasing amount of processed foods, particularly high fructose corn syrup (HFCS), because of the inexpensive cost of development. High fructose corn syrup can be found in everything from baked goods, condiments, and prepared desserts, but is mostly consumed in soft drinks and juice beverages. Intake of HFCS has increased from less than 0.5 grams daily per capita in 1970 to 53.9 grams daily per capita in 2003.3 Soft drink consumption has also increased 500% in the last 50 years, making it the leading source of added sugar in children’s diets.3 Obtaining an understanding of the metabolic differences in complex carbohydrates and refined carbohydrates is necessary when discussing the relationship of how over consumption of refined carbohydrates can cause chronic inflammation in the body, leaving it more vulnerable for a downward spiral effect towards other metabolic diseases. Goals of this paper are to define chronic inflammation and metabolic syndrome, discuss the metabolic pathway of refined carbohydrates and how that differs from complex carbohydrates, and discuss the relationship of how over consumption of refined carbohydrates can lead to chronic inflammation and metabolic syndrome. The body is an extraordinary system of complex and intricate checks and balances that work together to remain in constant homeostasis. One of those responses is inflammation. Short-term inflammation is beneficial and creates a small amount of stress on the body to be able to defend itself in case it is injured. This usually results in swelling, redness, pain and fever of the injured area(s), which was a crucial component of tissue repair.1 Low grade or chronic inflammation is not the same as described above. The long-term consequences of prolonged inflammation are often not beneficial.1 Although many of the same mediators are involved in obesity and diabetes, few short-term features of inflammation have actually been observed.1 The term meta-inflammation, a condition mainly triggered by nutrients and metabolic surplus, and engages a similar set of molecules and signaling pathways to those involved in short term inflammation, has been introduced to replace the terminology of “low grade” or “chronic” inflammation in order to easily differentiate the two terms.1 For the purpose of this paper I will simply use the word inflammation in the understanding that I am referring to “low grade”, “chronic,” or “meta-inflammation”. As discussed above, metabolic syndrome is a cluster of common pathologies including obesity, insulin resistance, dyslipidemia, and hypertension, usually resulting into diabetes type II or cardiovascular disease.2 Also mentioned above, due to its strong association with premature morbidity and mortality, there has been a heightened awareness of metabolic syndrome and an increase directed towards prevention2.
There has been evidence showing a predisposition of people having symptoms of metabolic syndrome such as 1) abdominal obesity, 2) elevated TG levels 3) low HDL cholesterol levels, 4) increased blood pressure, and 5) impaired fasting glucose, to having a greater risk for developing cardiovascular disease or type II diabetes. These symptoms are not necessarily manifestations of age, but develop over a predisposed background of unhealthy eating, physical inactivity and chronic stressful situations at a young age2. More importantly, obesity has been linked because of the effect of being insulin resistant2. Although, diets high in fat were often to blame for weight gain, insulin resistance, and hyperlipidemia in humans and animals, recent research has shown the high intake of refined carbohydrates may also increase the risk of insulin resistance.2 Specifically those that are high in fructose have been shown to cause metabolic challenges resulting in weight gain, hypertension, and de nova lipogenesis.2, 3, …show more content…
4 Metabolism of complex carbohydrates differs from that of refined carbohydrates. Complex carbohydrates, often referred to as “starchy” foods, such as starchy vegetables, whole grains, or legumes break down in the body as glucose. Glucose is limited in the capacity to store glucose as glycogen and more importantly by the inhibition of glycolysis and further glucose uptake resulting in the effects of citrate and ATP to inhibit phosphofructokinase4. In contrast, refined carbohydrates, such as soda, candy, or processed foods, are broken down into fructose. Fructose is first delivered to the liver via the portal vein.4, 5 It is then phosphorylated in the liver by adenosine triphosphate, and the enzyme fructokinase catalyzes a reaction to form fructose 1 phosphate. Fructose 1 phosphate then splits into glyceraldehyde and dihydroxyacetone phosphate, both of which can be converted into glycerol
3 P.4, 5 Fructose is then metabolized into 2 triose phosphates and bypasses the main rate-controlling step in glycolysis, 6-phosphofructokinase.4, 5 This is where the main difference of complex versus refined carbohydrate metabolism happens.
Since fructose bypasses the last two regulatory steps (the reactions catalyzed by hexokinase and PFK-1), two key events can occur, 1) it is metabolized faster than glucose and 2) since fructose is independent of phosphofructose kinase (PFK) regulation, overconsumption of fructose (>40g in a 2000 calorie diet), results in increases of levels of visceral adipose tissue (VAT), and increased hepatic lipid levels from de nova lipogenesis. This reaction results in increased very low density lipoproteins (VLDL) synthesis and secreation.4 The over consumption of fructose might be explained by the insufficient signaling of appetite regulating hormones, insulin, leptin, and ghrelin to work at correct times, resulting in excess body weight and insulin resistance, both which are symptoms of metabolic syndrome.1,2,3,
5 Now that there is an understanding of the difference between complex and refined carbohydrate metabolism, we can discuss the relationship of how over consumption of refined carbohydrates can lead to chronic inflammation and metabolic syndrome. It was mentioned earlier how being insulin resistant was a precursor for obesity and thus metabolic syndrome. Insulin is a hormone, produced by the pancreas, which is central to regulating carbohydrate and fat metabolism in the body.5 Insulin stops the use of fat as an energy source by inhibiting the release of glucagon5. It removes excess glucose from the blood after meals, which otherwise could be toxic. When the body is functioning normally, and blood levels fall below a certain level, the body uses stored glycogen in the liver and muscles through a process called glycogenolysis.5 In contrast, insulin resistance is exactly what the name implies. Insulin becomes less effective at lowering blood glucose levels. When glucose fails to be cleared from the blood, it disrupts other functions in muscle and liver cells. Also, in fat cells, it reduces the metabolism of lipids, elevating the amount of free fatty acids and triglycerides in blood plasma. The combination of elevated blood fatty-acid concentrations (associated with diabetes type II), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood levels.5 Thus, high plasma levels of insulin and glucose are a major components of metabolic syndrome.5 When examining reviews 1,6 about inflammation and diet they discuss how macronutrients may produce oxidative stress and inflammatory responses in the post-prandial phase. The oxidative state involves increased superoxide dismutase generation, which in turn inactivates nitric oxide, a biological radical.6 However, in inflammation `when superoxide combines with nitric oxide it produces peroxnitrate, a potent and long live oxidant that is cytotoxic.6 Peroxynitrate induces other reactions, which result in increased levels of plasma nitrotyrosine (NT). An increase in plasma NT levels has been reported in association with post-prandial hyperglycemia and hypertriglyceridaemia, which is a risk factor for cardiovascular disease in non diabetic subjects, and may be a precursor of carotid intima media thickness in type II diabetes.6 ,7 Also, one study discovered a finding over a decade ago that tumour necrosis factor –a (TNF-a), is a pro-inflammatory cytokine that activates different signaling pathways, which induce a cascade effect to critical inhibitors of insulin action.1 TNF-a was overexpressed in the adipose tissue of obese mice provided the first clear link between obesity and chronic inflammation.1 Yet another review reported a mixed meal from a fast food chain has also been shown to activate necrosis factor kB associated with reactive oxygen species (ROS) by mononuclear cells.6 Generation of ROS and raised circulating levels of inflammatory cytokines, such as TNF-a, interleukin 6 (IL-6), and interleukin 18 (IL-18) increases the inflammation response and putting those with already compromised systems in further jeopardy of additional damage.6. In summery, the alarming rate of refined carbohydrate consumption may be an important contributor to the epidemic of obesity and type II diabetes in both children and adult populations. Historically, small amounts of fructose from naturally occurring fruits and other complex foods were easily metabolized by the liver. The increasing amounts of high fructose/low glucose from high glucose/low fructose diets has strained the liver, resulting in disturbances in glucose metabolism and glucose uptake pathways, and has significantly enhanced the rate of de novo lipogenesis and TG production. The response of inflammation can be used as a biomarker for the over production of pro inflammatory cytokines. Chronic inflammation sets up the foundation for insulin resistance, which normally if gone untreated will result into other metabolic and cardiovascular diseases, however if caught in time does have positive outcomes of reversal with lifestyle and dietary changes are made. There needs to an awareness of the how the overconsumption of refined carbohydrates is affecting our health as a nation. Education in the understanding of metabolic pathways of refined carbohydrates might make people more conscience of dietary choices for the future for not only their own, but their families health as well.
Figure 1 Dietary patterns high in refined starches, sugar, and lipids and poor in natural antioxidants and fibre may produce an inflammatory milieu characterized by raised ROS generation and unbalance between inflammatory and anti-inflammatory cytokines. Visceral obesity may also be favoured by ‘Western’ dietary patterns and contributes to inflammation. The risk of metabolic syndrome, type 2 diabetes, and atherosclerosis is ultimately increased by the separate or com- bined effects of inflammation, insulin resistance, and visceral obesity.
What is scarier still is the equally marked increase in obesity, and diagnosis of type II diabetes (formerly known as adult onset diabetes) among children.1 There has also been a heightened awareness for prevention measures of metabolic syndrome, a cluster of common pathologies including obesity, insulin resistance, dyslipidemia, and hypertension, usually resulting into diabetes type II or cardiovascular disease.2 Speculation of these rising numbers have to do with the food industry and its replacement of sucrose with fructose in an increasing amount of processed foods, particularly high fructose corn syrup (HFCS), because of the inexpensive cost of development. High fructose corn syrup can be found in everything from baked goods, condiments, and prepared desserts, but is mostly consumed in soft drinks and juice beverages. Intake of HFCS has increased from less than 0.5 grams daily per capita in 1970 to 53.9 grams daily per capita in 2003.3 Soft drink consumption has also increased 500% in the last 50 years, making it the leading source of added sugar in children’s diets.3 Obtaining an understanding of the metabolic differences in complex carbohydrates and refined carbohydrates is necessary when discussing the relationship of how over consumption of refined carbohydrates can cause chronic inflammation in the body, leaving it more vulnerable for a downward spiral effect towards other metabolic diseases. Goals of this paper are to define chronic inflammation and metabolic syndrome, discuss the metabolic pathway of refined carbohydrates and how that differs from complex carbohydrates, and discuss the relationship of how over consumption of refined carbohydrates can lead to chronic inflammation and metabolic syndrome. The body is an extraordinary system of complex and intricate checks and balances that work together to remain in constant homeostasis. One of those responses is inflammation. Short-term inflammation is beneficial and creates a small amount of stress on the body to be able to defend itself in case it is injured. This usually results in swelling, redness, pain and fever of the injured area(s), which was a crucial component of tissue repair.1 Low grade or chronic inflammation is not the same as described above. The long-term consequences of prolonged inflammation are often not beneficial.1 Although many of the same mediators are involved in obesity and diabetes, few short-term features of inflammation have actually been observed.1 The term meta-inflammation, a condition mainly triggered by nutrients and metabolic surplus, and engages a similar set of molecules and signaling pathways to those involved in short term inflammation, has been introduced to replace the terminology of “low grade” or “chronic” inflammation in order to easily differentiate the two terms.1 For the purpose of this paper I will simply use the word inflammation in the understanding that I am referring to “low grade”, “chronic,” or “meta-inflammation”. As discussed above, metabolic syndrome is a cluster of common pathologies including obesity, insulin resistance, dyslipidemia, and hypertension, usually resulting into diabetes type II or cardiovascular disease.2 Also mentioned above, due to its strong association with premature morbidity and mortality, there has been a heightened awareness of metabolic syndrome and an increase directed towards prevention2.
There has been evidence showing a predisposition of people having symptoms of metabolic syndrome such as 1) abdominal obesity, 2) elevated TG levels 3) low HDL cholesterol levels, 4) increased blood pressure, and 5) impaired fasting glucose, to having a greater risk for developing cardiovascular disease or type II diabetes. These symptoms are not necessarily manifestations of age, but develop over a predisposed background of unhealthy eating, physical inactivity and chronic stressful situations at a young age2. More importantly, obesity has been linked because of the effect of being insulin resistant2. Although, diets high in fat were often to blame for weight gain, insulin resistance, and hyperlipidemia in humans and animals, recent research has shown the high intake of refined carbohydrates may also increase the risk of insulin resistance.2 Specifically those that are high in fructose have been shown to cause metabolic challenges resulting in weight gain, hypertension, and de nova lipogenesis.2, 3, …show more content…
4 Metabolism of complex carbohydrates differs from that of refined carbohydrates. Complex carbohydrates, often referred to as “starchy” foods, such as starchy vegetables, whole grains, or legumes break down in the body as glucose. Glucose is limited in the capacity to store glucose as glycogen and more importantly by the inhibition of glycolysis and further glucose uptake resulting in the effects of citrate and ATP to inhibit phosphofructokinase4. In contrast, refined carbohydrates, such as soda, candy, or processed foods, are broken down into fructose. Fructose is first delivered to the liver via the portal vein.4, 5 It is then phosphorylated in the liver by adenosine triphosphate, and the enzyme fructokinase catalyzes a reaction to form fructose 1 phosphate. Fructose 1 phosphate then splits into glyceraldehyde and dihydroxyacetone phosphate, both of which can be converted into glycerol
3 P.4, 5 Fructose is then metabolized into 2 triose phosphates and bypasses the main rate-controlling step in glycolysis, 6-phosphofructokinase.4, 5 This is where the main difference of complex versus refined carbohydrate metabolism happens.
Since fructose bypasses the last two regulatory steps (the reactions catalyzed by hexokinase and PFK-1), two key events can occur, 1) it is metabolized faster than glucose and 2) since fructose is independent of phosphofructose kinase (PFK) regulation, overconsumption of fructose (>40g in a 2000 calorie diet), results in increases of levels of visceral adipose tissue (VAT), and increased hepatic lipid levels from de nova lipogenesis. This reaction results in increased very low density lipoproteins (VLDL) synthesis and secreation.4 The over consumption of fructose might be explained by the insufficient signaling of appetite regulating hormones, insulin, leptin, and ghrelin to work at correct times, resulting in excess body weight and insulin resistance, both which are symptoms of metabolic syndrome.1,2,3,
5 Now that there is an understanding of the difference between complex and refined carbohydrate metabolism, we can discuss the relationship of how over consumption of refined carbohydrates can lead to chronic inflammation and metabolic syndrome. It was mentioned earlier how being insulin resistant was a precursor for obesity and thus metabolic syndrome. Insulin is a hormone, produced by the pancreas, which is central to regulating carbohydrate and fat metabolism in the body.5 Insulin stops the use of fat as an energy source by inhibiting the release of glucagon5. It removes excess glucose from the blood after meals, which otherwise could be toxic. When the body is functioning normally, and blood levels fall below a certain level, the body uses stored glycogen in the liver and muscles through a process called glycogenolysis.5 In contrast, insulin resistance is exactly what the name implies. Insulin becomes less effective at lowering blood glucose levels. When glucose fails to be cleared from the blood, it disrupts other functions in muscle and liver cells. Also, in fat cells, it reduces the metabolism of lipids, elevating the amount of free fatty acids and triglycerides in blood plasma. The combination of elevated blood fatty-acid concentrations (associated with diabetes type II), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood levels.5 Thus, high plasma levels of insulin and glucose are a major components of metabolic syndrome.5 When examining reviews 1,6 about inflammation and diet they discuss how macronutrients may produce oxidative stress and inflammatory responses in the post-prandial phase. The oxidative state involves increased superoxide dismutase generation, which in turn inactivates nitric oxide, a biological radical.6 However, in inflammation `when superoxide combines with nitric oxide it produces peroxnitrate, a potent and long live oxidant that is cytotoxic.6 Peroxynitrate induces other reactions, which result in increased levels of plasma nitrotyrosine (NT). An increase in plasma NT levels has been reported in association with post-prandial hyperglycemia and hypertriglyceridaemia, which is a risk factor for cardiovascular disease in non diabetic subjects, and may be a precursor of carotid intima media thickness in type II diabetes.6 ,7 Also, one study discovered a finding over a decade ago that tumour necrosis factor –a (TNF-a), is a pro-inflammatory cytokine that activates different signaling pathways, which induce a cascade effect to critical inhibitors of insulin action.1 TNF-a was overexpressed in the adipose tissue of obese mice provided the first clear link between obesity and chronic inflammation.1 Yet another review reported a mixed meal from a fast food chain has also been shown to activate necrosis factor kB associated with reactive oxygen species (ROS) by mononuclear cells.6 Generation of ROS and raised circulating levels of inflammatory cytokines, such as TNF-a, interleukin 6 (IL-6), and interleukin 18 (IL-18) increases the inflammation response and putting those with already compromised systems in further jeopardy of additional damage.6. In summery, the alarming rate of refined carbohydrate consumption may be an important contributor to the epidemic of obesity and type II diabetes in both children and adult populations. Historically, small amounts of fructose from naturally occurring fruits and other complex foods were easily metabolized by the liver. The increasing amounts of high fructose/low glucose from high glucose/low fructose diets has strained the liver, resulting in disturbances in glucose metabolism and glucose uptake pathways, and has significantly enhanced the rate of de novo lipogenesis and TG production. The response of inflammation can be used as a biomarker for the over production of pro inflammatory cytokines. Chronic inflammation sets up the foundation for insulin resistance, which normally if gone untreated will result into other metabolic and cardiovascular diseases, however if caught in time does have positive outcomes of reversal with lifestyle and dietary changes are made. There needs to an awareness of the how the overconsumption of refined carbohydrates is affecting our health as a nation. Education in the understanding of metabolic pathways of refined carbohydrates might make people more conscience of dietary choices for the future for not only their own, but their families health as well.
Figure 1 Dietary patterns high in refined starches, sugar, and lipids and poor in natural antioxidants and fibre may produce an inflammatory milieu characterized by raised ROS generation and unbalance between inflammatory and anti-inflammatory cytokines. Visceral obesity may also be favoured by ‘Western’ dietary patterns and contributes to inflammation. The risk of metabolic syndrome, type 2 diabetes, and atherosclerosis is ultimately increased by the separate or com- bined effects of inflammation, insulin resistance, and visceral obesity.