Antoaneta Sawyer, Ph.D.
Syndrome X is frequently associated with a state of low-grade systemic, chronic inflammation, induced by abdominal obesity that can secondarily exacerbate the syndrome and induce insulin resistance (Reaven & Laws, 1999). Other study shows results that adults with metabolic syndrome show evidence of a low-grade, despite persistent inflammation (Challem, 2003). First who speaks on the role of insulin resistance in humans and its connection with disease appearance is Reaven (1988). The main pro-inflammatory component in metabolic syndrome pathophysiology represents a combination of vascular dysfunction (endothelial dysfunction and microalbuminuria), a proinflammatory state (elevated CRP, elevated cytokines TNF-a, IL-6), decreased adiponektin levels, and a prothrombotic state (increased fibrinogen, and antifibrinolytic factors) with insulin resistance and visceral adiposity (Bechmann, Libby & Creager, 2005). The circulating levels of inflammatory cytokines- tumor necrosis factor (TNF) and interleukin-6 and their receptors are evaluated in a multicenter clinical trial in 1,200 patients with advanced heart failure (Deswal et al., 2001). Their conclusion is that cytokines and cytokine receptors are independent predictors of mortality in patients with advanced heart failure.
Another study has shown that even children and adolescents with metabolic syndrome are more likely to show evidence of low-grade inflammation than those without metabolic syndrome. The researchers claim that percentage of children and adolescents with elevated concentration of CRP (>3.0 mg/ l) is almost four times higher among those with the metabolic syndrome compared to those who did not have the syndrome. An association between obesity and elevated concentrations of CRP in children and adolescents has been clearly established (Earl et al, 2002; Ford et al., 2004). Several other authors speculate on the cascade of disorders or abnormalities in which excess fat promotes increased insulin resistance that in turn promotes even more fat formation (Wood, 2006). The author explains that “adipose tissue is not a passive but an active endocrine organ, and sends us signals while secreting fatty acids and peptide hormones (cytokines), called collectively – adipocytokines (p.10). Adipocytokines act locally or peripherally to influence glucose and fatty acid metabolism, insulin sensitivity, adipocyte differentiation, chronic inflammation, and the immune response. In extremely obese individuals, adipose tissue produces excessive amount of cytokines, and the output of adiponectin is diminished. Chronic inflammation based on the excess of inflammatory cytokines reportedly induces higher insulin resistance in adipose tissue and muscles. All of the above creates a vicious circle which appears to heighten the connection between obesity and inflammation (Armstrong, 2006).
Multiple markers of chronic systemic inflammation, including C-reactive protein (CRP), are often increased as fibrinogen, interleukin 6 (IL–6), and tumor necrosis factor-alpha (TNFα). Many authors have pointed out to oxidative stress as a common link in metabolic syndrome pathogenesis as a consequence of increased uric acid levels caused by dietary fructose (Temelkova-Kurktschiev et al., 2002). The cellular mechanisms behind insulin resistance appearance as potential link to inflammation are studied by (Perseghin, Petersen & Shulman, 2003). Researchers are linking levels of the C-reactive protein that indicates tissue inflammation in the body to future risk of heart attack, stroke, cancer and chronic lung disease. The molecule, known as C-reactive protein (CRP), is produced by the liver and indicates that tissues are inflamed because of injury. Some research has suggested that CRP levels might be as important a cause of heart attacks as cholesterol in the blood. In a new study published Dec. 22 in The Lancet (2009), researchers led by John Danesh of the University of Cambridge looked over findings from 54 research projects that analyzed more than 160,000 people in 18 countries. But the association may be the result of other risk factors related to heart disease, such as smoking, rather than the protein itself, researchers said. The researchers report that other factors -- such as smoking, obesity and cholesterol levels better explain links between CRP and heart disease. More research is needed, they write, partly "to assess whether evidence of low-grade inflammation mainly indicates external triggers (e.g., socioeconomic position or infection), insulin resistance, hereditary predisposition, or some combination of such factors." Matsusawa (2007), writes,” Recently, adipocytes have been shown to be recognized as endocrine cells that secrete a variety of bioactive substances known as adipocytokines, among which, adiponectin, a newly found adipose tissue-specific collagen-like protein has been noted as an important antiatherogenic and antidiabetic protein and then proceeds, “Visceral fat accumulation causes dysfunction of adipocytes and results in the development of a variety of metabolic and circulatory diseases through the abnormal secretion of adipocytokines” (p.59). Hotamisligil agrees that adipose tissue may produce increased levels of cellular, hormone-like substances—cytokines and other bioactive substances referred to as adipocytokines (Hotamisligil, 2004). As a result of the above vicious circle, insulin sensitivity in organs like muscle and liver is decreasing (Matsuzawa, Funahashi, Kihara & Shimomura, 2004). It is also hypothesized that secondary factors as nonesterified fatty acid liberation and adipokine (e.g., adiponectin) production (Carr et al., 2004) as well as other risk factors (Egan & Julius, 2004; Janssen, Debets, Leenders & Smits, 2002) may also play a major role in metabolic syndrome pathogenesis.
Obviously the conglomeration of all the above risk factors elevates the risk for metabolic syndrome (Pladevall et al., 2006). While central obesity is likely to be the main culprit and contributor, other major factors are: hypertension, glucose intolerance (insulin resistance), and dyslipidemia (Fisman, Esper & Tenenbaum, 2005). Blood pressure consequently rises, blood glucose levels and very low density cholesterol (VLDL) levels elevate, while HDL cholesterol drops precipitously. Some authors make statement that in metabolic syndrome it is important to recognize and to know that on a whole-body level, lipid and glucose metabolisms interact intimately (Fisman, Adler & Tenenbaum 2004).
Decades of research show that poor lifestyle choices, aging, and nutritional deficiency beginning in childhood are the main causes of metabolic syndrome. The prevalence of metabolic syndrome increases with age, affecting less than 10 % of people in their 20s and 40 % of people in their 60s (Camardella, 2007; Ford et al., 2004). The prevalence of metabolic syndrome in U.S. adolescents is reported by two independent teams (DeFeranti, Gauvreau, Ludwig, Neufeld & Jane, 2004; Messiah, 2008). Major risk factors, such as lack of exercise, poor fluid intake, general and mercury toxicity, bacterial and viral infections combined with chronic stress close the vicious circle of the disorder. Others, as long term untreated hypertension or difficult to treat— “malignant hypertension," smoking, increased intake of saturated fats and simple carbohydrates, lack of essential antioxidants, excessive exposure to free radicals via pesticides, chlorinated water, air pollutants and other toxic chemicals, elevated bad cholesterol, convenience lifestyle (i.e., reduced exercise) and genetic predisposition are blamed for metabolic syndrome pandemic rate. Coffee is proven to decrease HGH secretion, to increase insulin secretion, and to provoke insulin resistance if used in over plus (Salazar-Martrinez et al, 2004).
Syndrome X is frequently associated with a state of low-grade systemic, chronic inflammation, induced by abdominal obesity that can secondarily exacerbate the syndrome and induce insulin resistance (Reaven & Laws, 1999). Other study shows results that adults with metabolic syndrome show evidence of a low-grade, despite persistent inflammation (Challem, 2003). First who speaks on the role of insulin resistance in humans and its connection with disease appearance is Reaven (1988). The main pro-inflammatory component in metabolic syndrome pathophysiology represents a combination of vascular dysfunction (endothelial dysfunction and microalbuminuria), a proinflammatory state (elevated CRP, elevated cytokines TNF-a, IL-6), decreased adiponektin levels, and a prothrombotic state (increased fibrinogen, and antifibrinolytic factors) with insulin resistance and visceral adiposity (Bechmann, Libby & Creager, 2005). The circulating levels of inflammatory cytokines- tumor necrosis factor (TNF) and interleukin-6 and their receptors are evaluated in a multicenter clinical trial in 1,200 patients with advanced heart failure (Deswal et al., 2001). Their conclusion is that cytokines and cytokine receptors are independent predictors of mortality in patients with advanced heart failure.
Another study has shown that even children and adolescents with metabolic syndrome are more likely to show evidence of low-grade inflammation than those without metabolic syndrome. The researchers claim that percentage of children and adolescents with elevated concentration of CRP (>3.0 mg/ l) is almost four times higher among those with the metabolic syndrome compared to those who did not have the syndrome. An association between obesity and elevated concentrations of CRP in children and adolescents has been clearly established (Earl et al, 2002; Ford et al., 2004). Several other authors speculate on the cascade of disorders or abnormalities in which excess fat promotes increased insulin resistance that in turn promotes even more fat formation (Wood, 2006). The author explains that “adipose tissue is not a passive but an active endocrine organ, and sends us signals while secreting fatty acids and peptide hormones (cytokines), called collectively – adipocytokines (p.10). Adipocytokines act locally or peripherally to influence glucose and fatty acid metabolism, insulin sensitivity, adipocyte differentiation, chronic inflammation, and the immune response. In extremely obese individuals, adipose tissue produces excessive amount of cytokines, and the output of adiponectin is diminished. Chronic inflammation based on the excess of inflammatory cytokines reportedly induces higher insulin resistance in adipose tissue and muscles. All of the above creates a vicious circle which appears to heighten the connection between obesity and inflammation (Armstrong, 2006).
Multiple markers of chronic systemic inflammation, including C-reactive protein (CRP), are often increased as fibrinogen, interleukin 6 (IL–6), and tumor necrosis factor-alpha (TNFα). Many authors have pointed out to oxidative stress as a common link in metabolic syndrome pathogenesis as a consequence of increased uric acid levels caused by dietary fructose (Temelkova-Kurktschiev et al., 2002). The cellular mechanisms behind insulin resistance appearance as potential link to inflammation are studied by (Perseghin, Petersen & Shulman, 2003). Researchers are linking levels of the C-reactive protein that indicates tissue inflammation in the body to future risk of heart attack, stroke, cancer and chronic lung disease. The molecule, known as C-reactive protein (CRP), is produced by the liver and indicates that tissues are inflamed because of injury. Some research has suggested that CRP levels might be as important a cause of heart attacks as cholesterol in the blood. In a new study published Dec. 22 in The Lancet (2009), researchers led by John Danesh of the University of Cambridge looked over findings from 54 research projects that analyzed more than 160,000 people in 18 countries. But the association may be the result of other risk factors related to heart disease, such as smoking, rather than the protein itself, researchers said. The researchers report that other factors -- such as smoking, obesity and cholesterol levels better explain links between CRP and heart disease. More research is needed, they write, partly "to assess whether evidence of low-grade inflammation mainly indicates external triggers (e.g., socioeconomic position or infection), insulin resistance, hereditary predisposition, or some combination of such factors." Matsusawa (2007), writes,” Recently, adipocytes have been shown to be recognized as endocrine cells that secrete a variety of bioactive substances known as adipocytokines, among which, adiponectin, a newly found adipose tissue-specific collagen-like protein has been noted as an important antiatherogenic and antidiabetic protein and then proceeds, “Visceral fat accumulation causes dysfunction of adipocytes and results in the development of a variety of metabolic and circulatory diseases through the abnormal secretion of adipocytokines” (p.59). Hotamisligil agrees that adipose tissue may produce increased levels of cellular, hormone-like substances—cytokines and other bioactive substances referred to as adipocytokines (Hotamisligil, 2004). As a result of the above vicious circle, insulin sensitivity in organs like muscle and liver is decreasing (Matsuzawa, Funahashi, Kihara & Shimomura, 2004). It is also hypothesized that secondary factors as nonesterified fatty acid liberation and adipokine (e.g., adiponectin) production (Carr et al., 2004) as well as other risk factors (Egan & Julius, 2004; Janssen, Debets, Leenders & Smits, 2002) may also play a major role in metabolic syndrome pathogenesis.
Obviously the conglomeration of all the above risk factors elevates the risk for metabolic syndrome (Pladevall et al., 2006). While central obesity is likely to be the main culprit and contributor, other major factors are: hypertension, glucose intolerance (insulin resistance), and dyslipidemia (Fisman, Esper & Tenenbaum, 2005). Blood pressure consequently rises, blood glucose levels and very low density cholesterol (VLDL) levels elevate, while HDL cholesterol drops precipitously. Some authors make statement that in metabolic syndrome it is important to recognize and to know that on a whole-body level, lipid and glucose metabolisms interact intimately (Fisman, Adler & Tenenbaum 2004).
Decades of research show that poor lifestyle choices, aging, and nutritional deficiency beginning in childhood are the main causes of metabolic syndrome. The prevalence of metabolic syndrome increases with age, affecting less than 10 % of people in their 20s and 40 % of people in their 60s (Camardella, 2007; Ford et al., 2004). The prevalence of metabolic syndrome in U.S. adolescents is reported by two independent teams (DeFeranti, Gauvreau, Ludwig, Neufeld & Jane, 2004; Messiah, 2008). Major risk factors, such as lack of exercise, poor fluid intake, general and mercury toxicity, bacterial and viral infections combined with chronic stress close the vicious circle of the disorder. Others, as long term untreated hypertension or difficult to treat— “malignant hypertension," smoking, increased intake of saturated fats and simple carbohydrates, lack of essential antioxidants, excessive exposure to free radicals via pesticides, chlorinated water, air pollutants and other toxic chemicals, elevated bad cholesterol, convenience lifestyle (i.e., reduced exercise) and genetic predisposition are blamed for metabolic syndrome pandemic rate. Coffee is proven to decrease HGH secretion, to increase insulin secretion, and to provoke insulin resistance if used in over plus (Salazar-Martrinez et al, 2004).
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These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.
These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.
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