Recipe contributed by 125 Best Chinese Recipe1 By Bill Jones and Stephen Wong (Robert Rose)
5 lb. beef bone a(shine or neck)
3 large onion, peeled and roughly chopped
3 carrots, roughly chopped
3 stalks of celery, roughly chopped
1/2 garlic head
1/2 cup tomato paste
3 bay leaves
1 small handful thyme
1 small handful rosemary
1 small handful marjoram
1 bunch parsley stalks
5 whole pepper corns
20 cups water
1, Pace bone in a pan and roast until lightly golden, about 2 hours. Add vegetables and garlic; roast 1 hour. Add tomato paste, stirring to coat. roast 30 minutes.
1. Place roast bones and vegetables in a large stockpot, add remain ingredients. Add more water, if necessary to cover. Bring mixture to a broil; reduce heat and simmer gently for 8 hours, skimming occasionally to remove any foam or impurities that rise to the top. Try not to let the mixture boil or broth will be cloudy.
2. Strain in to container and cool to room temperature before refrigerating. (If hot stock is placed directly in the fridge, it will sometime sour). for a more intensely flavored stock, let liquid cool; return stock to pot and over low heat, simmer until volume is reduced by half.
Weight Loss the Easy Ways
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At Last! The Natural PCOS Diet
A Naturopath’s Easy Step-by-Step Guide to Overcome PCOS
by Qualified Australian Naturopath And Hormone Health Expert
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Sunday, 10 August 2014
4 someone who loves Walnuts: Hot and spicy Walnuts
Recipe attributed to Fresh and Easy Meals by Better Homes and Gardens
Nut hits the spot as snack, and this snack is loaded with them. walnuts have more heart-healthy Omega-3 fat than other nuts. Use canola oil in the recipe to boost it Omega 3 content even more.
Prep. 10 minutes
Bake 20 minutes
Cool 15 minutes
Oven 300 degree F
Make 8 (1/4 cup) servings
1 tsp. ground coriander
1 tsp. ground cumin
!/2 tsp. salt
1/4 tsp. freshly ground black pepper
1/2 tsp. cayenne pepper
2 cups walnuts halves
1 tsp. cooking oil
In a small bowl stir together coriander, cumin, salt, black pepper, and cayenne pepper; set aside. Place nuts in a 13x9x2 inch baking pan. Drizzle with the oil, stir to coat. Sprinkle with choice mixture; toss lightly.
Baking in a 300 degrees oven for 20 munities or until nuts are slightly toasted, stirring once or twice. Cool in pan for 15 minutes. Turn out onto paper towels; cool completely. Store, covered in a cool place.
Nutrition facts per serving: 214 Cal. 21 g total fat(2g sat. fat), O mg cholesterol, 147 mg sodium, 4g carbo, 2 g fiber, 5 g pro.
Daily value: 1% vitamin C, 3% calcium, 5% iron.
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Nut hits the spot as snack, and this snack is loaded with them. walnuts have more heart-healthy Omega-3 fat than other nuts. Use canola oil in the recipe to boost it Omega 3 content even more.
Prep. 10 minutes
Bake 20 minutes
Cool 15 minutes
Oven 300 degree F
Make 8 (1/4 cup) servings
1 tsp. ground coriander
1 tsp. ground cumin
!/2 tsp. salt
1/4 tsp. freshly ground black pepper
1/2 tsp. cayenne pepper
2 cups walnuts halves
1 tsp. cooking oil
In a small bowl stir together coriander, cumin, salt, black pepper, and cayenne pepper; set aside. Place nuts in a 13x9x2 inch baking pan. Drizzle with the oil, stir to coat. Sprinkle with choice mixture; toss lightly.
Baking in a 300 degrees oven for 20 munities or until nuts are slightly toasted, stirring once or twice. Cool in pan for 15 minutes. Turn out onto paper towels; cool completely. Store, covered in a cool place.
Nutrition facts per serving: 214 Cal. 21 g total fat(2g sat. fat), O mg cholesterol, 147 mg sodium, 4g carbo, 2 g fiber, 5 g pro.
Daily value: 1% vitamin C, 3% calcium, 5% iron.
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Obesity Complication of Pancreatitis
By Kyle J. Norton
Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
B. How to calculate your BMI index
BMI= weight (kg)/ height (m2)
C. Pancreatitis is defined as a condition of inflammation of the pancreas as its no longer function normally in secreting digestive juices, or enzymes. Pancreatitis can be acute or chronic.
D. How Obesity associates with Pancreatitis
1. According to the abstract of the study of "Influence of obesity on the severity and clinical outcome of acute pancreatitis" by Shin KY, Lee WS, Chung DW, Heo J, Jung MK, Tak WY, Kweon YO, Cho CM, posted in PubMed, researchers indicated that When compared with normal patients (BMI 18.5 to 22.9), all categories with a BMI ≥23 had an increased risk of developing a severe form of acute pancreatitis (p=0.003) and all categories with a BMI ≥25 significantly predicted severity (p<0.001). Patients with class 1 obesity (BMI 25 to 29.9) developed significantly more systemic and metabolic complications and concluded that Overweightedness and obesity were found to be associated with a higher risk of developing severe pancreatitis. Further studies are needed to establish the precise prognostic value of obesity in members of the population with low BMIs.
2. In a study of "The impact of obesity on the course and outcome of acute pancreatitis" by Abu Hilal M, Armstrong T., posted in PubMed, researchers filed the conclusion that This has led to proposed modifications of acute pancreatitis scoring systems to include obesity as an independent primary predictive factor of severe disease. Obesity is associated with a low-grade inflammatory state, which may predispose obese patients to such complications. Furthermore, visceral obesity and visceral adipose tissue may be particularly important in underlying the pathophysiology of these observations.
3. In another study of "Obesity: a risk factor for severe acute biliary and alcoholic pancreatitis" by Suazo-Baráhona J, Carmona-Sánchez R, Robles-Díaz G, Milke-García P, Vargas-Vorácková F, Uscanga-Domínguez L, Peláez-Luna M., posted in PubMed, researchers filed the result that Prevalence of obesity was 57%. Thirty-eight percent of the obese patients developed complications as compared with 21% of the nonobese (RR=1.74; 95% CI, 1-2.9). The risk for severe AP increased according to the degree of obesity. Pancreatic and peripancreatic necrosis was more common in obese patients (17.6% vs 6%), as was the incidence of infectious complications. The risk for severe AP was highest in obese patients with either alcoholic (RR=5.3; 95% CI, 1.2-23) or biliary etiology (RR=5.2, 95% CI, 1-26).
4. According to the abstract of the study of "Obesity: an important prognostic factor in acute pancreatitis" by Funnell IC, Bornman PC, Weakley SP, Terblanche J, Marks IN., posted in PubMed, researchers concluded that obesity had a sensitivity of 63 per cent and a specificity of 95 per cent for predicting disease severity. When five obese women with gallstone pancreatitis were excluded, the sensitivity of obesity increased to 86 per cent. Severe pancreatitis occurred in all eight obese patients with disease of an alcoholic aetiology. These data suggest that increased fat deposits in the peripancreatic and retroperitoneal spaces in obese patients may increase the risk of peripancreatic fat necrosis, abscess and death. Consideration should be given to including obesity as a prognostic factor in acute pancreatitis.
5. In the study of "Experimental evidence of obesity as a risk factor for severe acute pancreatitis" by Frossard JL, Lescuyer P, Pastor CM., posted in PubMed, researchers indicated that Several hypotheses have been suggested: (1) obese patients have an increased inflammation within the pancreas; (2) obese patients have an increased accumulation of fat within and around the pancreas where necrosis is often located; (3) increase in both peri- and intra-pancreatic fat and inflammatory cells explain the high incidence of pancreatic inflammation and necrosis in obese patients; (4) hepatic dysfunction associated with obesity might enhance the systemic inflammatory response by altering the detoxification of inflammatory mediators; and (5) ventilation/perfusion mismatch leading to hypoxia associated with a low pancreatic flow might reduce the pancreatic oxygenation and further enhance pancreatic injury. Recent experimental investigations also show an increased mortality and morbidity in obese rodents with acute pancreatitis and the implication of the adipokines leptin and adiponectin. Such models are important to investigate whether the inflammatory response of the disease is enhanced by obesity. It is exciting to speculate that manipulation of the adipokine milieu has the potential to influence the severity of acute pancreatitis.
6. Etc.
E. Treatments of Obesity and Pancreatitis
1, In the abstract of the study of "The influence of dietary restriction on the development of diabetes and pancreatitis in female WBN/Kob-fatty rats" by Akimoto T, Terada M, Shimizu A, Sawai N, Ozawa H., posted in PubMed, researchers stated that pathological changes of the pancreas were observed in female fatty rats. All female fatty rats showed severe interlobular, intra-lobular and intra-islet fibrosis. In female fatty rats of the restricted feeding group, pathological changes of the pancreas were milder those of the free-feeding fatty group. Although dietary restriction could not completely prevent pancreatitis in female fatty rats, the development of diabetes was inhibited by its reduction of the severity of pancreatitis.
2. According to the study of "Fat replacement of the malignant pancreatic tissue after neoadjuvant therapy" by Makay O, Kazimi M, Aydin U, Nart D, Yilmaz F, Zeytunlu M, Goker E, Coker A., posted in PubMed, researchers found that The tissue pathology revealed lipomatosis of the pancreas. He was disease-free and symptom-free at 1 year follow-up. To our knowledge, this is the first report in the literature of pancreatic head carcinoma with total fat replacement of the pancreas after neoadjuvant chemoradiotherapy.
3. In the study of "Pancreatic surgery" by Hines OJ, Reber HA., posted in PubMed, researcher indicated that Recent evidence suggests that obese patients with pancreatic cancer appear to have more advanced disease at the time of diagnosis and a worse outcome following resection. The issues surrounding adjuvant treatment for pancreatic cancer with chemotherapy and/or radiation therapy continue to be evaluated....... and summarized that each year more is learned about the natural history of pancreatic lesion. For those dedicated to the study and treatment of this gland, several new advances help the clinician with treatment decisions.
4. Etc.
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will Personally Coach You How to Get There The Easy Way
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and Keep Him/Her for Good,The Simple Way
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
B. How to calculate your BMI index
BMI= weight (kg)/ height (m2)
C. Pancreatitis is defined as a condition of inflammation of the pancreas as its no longer function normally in secreting digestive juices, or enzymes. Pancreatitis can be acute or chronic.
D. How Obesity associates with Pancreatitis
1. According to the abstract of the study of "Influence of obesity on the severity and clinical outcome of acute pancreatitis" by Shin KY, Lee WS, Chung DW, Heo J, Jung MK, Tak WY, Kweon YO, Cho CM, posted in PubMed, researchers indicated that When compared with normal patients (BMI 18.5 to 22.9), all categories with a BMI ≥23 had an increased risk of developing a severe form of acute pancreatitis (p=0.003) and all categories with a BMI ≥25 significantly predicted severity (p<0.001). Patients with class 1 obesity (BMI 25 to 29.9) developed significantly more systemic and metabolic complications and concluded that Overweightedness and obesity were found to be associated with a higher risk of developing severe pancreatitis. Further studies are needed to establish the precise prognostic value of obesity in members of the population with low BMIs.
2. In a study of "The impact of obesity on the course and outcome of acute pancreatitis" by Abu Hilal M, Armstrong T., posted in PubMed, researchers filed the conclusion that This has led to proposed modifications of acute pancreatitis scoring systems to include obesity as an independent primary predictive factor of severe disease. Obesity is associated with a low-grade inflammatory state, which may predispose obese patients to such complications. Furthermore, visceral obesity and visceral adipose tissue may be particularly important in underlying the pathophysiology of these observations.
3. In another study of "Obesity: a risk factor for severe acute biliary and alcoholic pancreatitis" by Suazo-Baráhona J, Carmona-Sánchez R, Robles-Díaz G, Milke-García P, Vargas-Vorácková F, Uscanga-Domínguez L, Peláez-Luna M., posted in PubMed, researchers filed the result that Prevalence of obesity was 57%. Thirty-eight percent of the obese patients developed complications as compared with 21% of the nonobese (RR=1.74; 95% CI, 1-2.9). The risk for severe AP increased according to the degree of obesity. Pancreatic and peripancreatic necrosis was more common in obese patients (17.6% vs 6%), as was the incidence of infectious complications. The risk for severe AP was highest in obese patients with either alcoholic (RR=5.3; 95% CI, 1.2-23) or biliary etiology (RR=5.2, 95% CI, 1-26).
4. According to the abstract of the study of "Obesity: an important prognostic factor in acute pancreatitis" by Funnell IC, Bornman PC, Weakley SP, Terblanche J, Marks IN., posted in PubMed, researchers concluded that obesity had a sensitivity of 63 per cent and a specificity of 95 per cent for predicting disease severity. When five obese women with gallstone pancreatitis were excluded, the sensitivity of obesity increased to 86 per cent. Severe pancreatitis occurred in all eight obese patients with disease of an alcoholic aetiology. These data suggest that increased fat deposits in the peripancreatic and retroperitoneal spaces in obese patients may increase the risk of peripancreatic fat necrosis, abscess and death. Consideration should be given to including obesity as a prognostic factor in acute pancreatitis.
5. In the study of "Experimental evidence of obesity as a risk factor for severe acute pancreatitis" by Frossard JL, Lescuyer P, Pastor CM., posted in PubMed, researchers indicated that Several hypotheses have been suggested: (1) obese patients have an increased inflammation within the pancreas; (2) obese patients have an increased accumulation of fat within and around the pancreas where necrosis is often located; (3) increase in both peri- and intra-pancreatic fat and inflammatory cells explain the high incidence of pancreatic inflammation and necrosis in obese patients; (4) hepatic dysfunction associated with obesity might enhance the systemic inflammatory response by altering the detoxification of inflammatory mediators; and (5) ventilation/perfusion mismatch leading to hypoxia associated with a low pancreatic flow might reduce the pancreatic oxygenation and further enhance pancreatic injury. Recent experimental investigations also show an increased mortality and morbidity in obese rodents with acute pancreatitis and the implication of the adipokines leptin and adiponectin. Such models are important to investigate whether the inflammatory response of the disease is enhanced by obesity. It is exciting to speculate that manipulation of the adipokine milieu has the potential to influence the severity of acute pancreatitis.
6. Etc.
E. Treatments of Obesity and Pancreatitis
1, In the abstract of the study of "The influence of dietary restriction on the development of diabetes and pancreatitis in female WBN/Kob-fatty rats" by Akimoto T, Terada M, Shimizu A, Sawai N, Ozawa H., posted in PubMed, researchers stated that pathological changes of the pancreas were observed in female fatty rats. All female fatty rats showed severe interlobular, intra-lobular and intra-islet fibrosis. In female fatty rats of the restricted feeding group, pathological changes of the pancreas were milder those of the free-feeding fatty group. Although dietary restriction could not completely prevent pancreatitis in female fatty rats, the development of diabetes was inhibited by its reduction of the severity of pancreatitis.
2. According to the study of "Fat replacement of the malignant pancreatic tissue after neoadjuvant therapy" by Makay O, Kazimi M, Aydin U, Nart D, Yilmaz F, Zeytunlu M, Goker E, Coker A., posted in PubMed, researchers found that The tissue pathology revealed lipomatosis of the pancreas. He was disease-free and symptom-free at 1 year follow-up. To our knowledge, this is the first report in the literature of pancreatic head carcinoma with total fat replacement of the pancreas after neoadjuvant chemoradiotherapy.
3. In the study of "Pancreatic surgery" by Hines OJ, Reber HA., posted in PubMed, researcher indicated that Recent evidence suggests that obese patients with pancreatic cancer appear to have more advanced disease at the time of diagnosis and a worse outcome following resection. The issues surrounding adjuvant treatment for pancreatic cancer with chemotherapy and/or radiation therapy continue to be evaluated....... and summarized that each year more is learned about the natural history of pancreatic lesion. For those dedicated to the study and treatment of this gland, several new advances help the clinician with treatment decisions.
4. Etc.
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Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
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Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
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Saturday, 9 August 2014
Obesity Complication of Type II Diabetes
By Kyle J. Norton
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
Type II diabetesDiabetes is defined as a medical condition of insufficient insulin entering the bloodstream to regulate the glucose. It is either caused by cells in the pancreas dying off or receptor sites clogged up by the accumulation of fat and cholesterol. In some case, diabetes is also caused by allergy reactions of cells in our body.
How do calculate your BMI indexBMI= weight (kg)/ height (m2)
How obesity cause type II diabetes
Type II diabetes is a result of insulin resistance and obesity is considered as a risk factor for developing insulin resistance.
1. According to the article of "Obesity and insulin resistance" by Barbara B. Kahn and Jeffrey S. Flier (1), researchers indicated that the association of obesity with type 2 diabetes has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance. Insulin resistance is a fundamental aspect of the etiology of type 2 diabetes and is also linked to a wide array of other pathophysiologic sequelae including hypertension, hyperlipidemia, atherosclerosis (i.e., the metabolic syndrome, or syndrome X), and polycystic ovarian disease.
1. Can Gene and Inherited factor cause of Obesity and type II diabetes be changed
Obesity and type II diabetes as a result of genetic susceptible or heredity can be prevented, according to the study of " Lifestyle and Genetics in Obesity and type 2 Diabetes." by Temelkova-Kurktschiev T, Stefanov T. (Source from Medicobiological Unit.) posted in PubMed, researchers found that gene-lifestyle interaction studies suggest that
a. Genetic susceptibility to obesity and type 2 diabetes may be partially or totally kept under control by healthy lifestyle or lifestyle modification and that lifestyle determines whether an individual is likely to develop the disease.
b. Inherited factors, however, seem to influence individual response to a lifestyle intervention program and even the motivation for lifestyle change. Personalized interventions according to genotype may be, therefore, considered in the future.
By then lifestyle modification targeting dietary change and increased physical activity may be recommended for successful obesity and type 2 diabetes prevention irrespectively of genetic susceptibility.
2. Leptin and Obesity and Type 2 Diabetes
Since leptin is the protein product of the obese gene, many researchers have tries to develop the mew approach to treat obesity and type 2 diabetes. In a study of " Novel Approaches to the Treatment of Obesity and Type 2 Diabetes Mellitus: Bioactive Leptin-Related Synthetic Peptide Analogs." by Grasso P. (Source from Department of Medicine, Division of Endocrinology and Metabolism Albany Medical College, MC 141, Albany, NY 12208, USA. grassop@mail.amc.edu), posted in PubMed, researches indicated that The pleiotropic nature of leptin has been confirmed by demonstration of a role for leptin in hematopoiesis, angiogenesis, immune function, osteogenesis, reproduction, and wound healing. Unfortunately, the results of the majority of clinical trials with recombinant human leptin indicated that its effectiveness in restoring energy balance and correcting obesity-related endocrinopathies in genetically obese rodent models extended only to the management of those rare forms of human obesity caused by mutation in the ob gene. Failure of leptin in the clinic, and withdrawal of fenfluramine, phentermine, and sibutrimine from clinical use in the United States, have stimulated new approaches in the development of anti-obesity and anti-diabetes pharmacophores.
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will Personally Coach You How to Get There The Easy Way
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and Keep Him/Her for Good,The Simple Way
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(1) Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USAAddress correspondence to: Barbara B. Kahn, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: (617) 667-5422; Fax: (617) 667-2927; E-mail: bkahn@caregroup.harvard.edu. The Journal of Clinical investigation
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
Type II diabetesDiabetes is defined as a medical condition of insufficient insulin entering the bloodstream to regulate the glucose. It is either caused by cells in the pancreas dying off or receptor sites clogged up by the accumulation of fat and cholesterol. In some case, diabetes is also caused by allergy reactions of cells in our body.
How do calculate your BMI indexBMI= weight (kg)/ height (m2)
How obesity cause type II diabetes
Type II diabetes is a result of insulin resistance and obesity is considered as a risk factor for developing insulin resistance.
1. According to the article of "Obesity and insulin resistance" by Barbara B. Kahn and Jeffrey S. Flier (1), researchers indicated that the association of obesity with type 2 diabetes has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance. Insulin resistance is a fundamental aspect of the etiology of type 2 diabetes and is also linked to a wide array of other pathophysiologic sequelae including hypertension, hyperlipidemia, atherosclerosis (i.e., the metabolic syndrome, or syndrome X), and polycystic ovarian disease.
1. Can Gene and Inherited factor cause of Obesity and type II diabetes be changed
Obesity and type II diabetes as a result of genetic susceptible or heredity can be prevented, according to the study of " Lifestyle and Genetics in Obesity and type 2 Diabetes." by Temelkova-Kurktschiev T, Stefanov T. (Source from Medicobiological Unit.) posted in PubMed, researchers found that gene-lifestyle interaction studies suggest that
a. Genetic susceptibility to obesity and type 2 diabetes may be partially or totally kept under control by healthy lifestyle or lifestyle modification and that lifestyle determines whether an individual is likely to develop the disease.
b. Inherited factors, however, seem to influence individual response to a lifestyle intervention program and even the motivation for lifestyle change. Personalized interventions according to genotype may be, therefore, considered in the future.
By then lifestyle modification targeting dietary change and increased physical activity may be recommended for successful obesity and type 2 diabetes prevention irrespectively of genetic susceptibility.
2. Leptin and Obesity and Type 2 Diabetes
Since leptin is the protein product of the obese gene, many researchers have tries to develop the mew approach to treat obesity and type 2 diabetes. In a study of " Novel Approaches to the Treatment of Obesity and Type 2 Diabetes Mellitus: Bioactive Leptin-Related Synthetic Peptide Analogs." by Grasso P. (Source from Department of Medicine, Division of Endocrinology and Metabolism Albany Medical College, MC 141, Albany, NY 12208, USA. grassop@mail.amc.edu), posted in PubMed, researches indicated that The pleiotropic nature of leptin has been confirmed by demonstration of a role for leptin in hematopoiesis, angiogenesis, immune function, osteogenesis, reproduction, and wound healing. Unfortunately, the results of the majority of clinical trials with recombinant human leptin indicated that its effectiveness in restoring energy balance and correcting obesity-related endocrinopathies in genetically obese rodent models extended only to the management of those rare forms of human obesity caused by mutation in the ob gene. Failure of leptin in the clinic, and withdrawal of fenfluramine, phentermine, and sibutrimine from clinical use in the United States, have stimulated new approaches in the development of anti-obesity and anti-diabetes pharmacophores.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
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(1) Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USAAddress correspondence to: Barbara B. Kahn, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: (617) 667-5422; Fax: (617) 667-2927; E-mail: bkahn@caregroup.harvard.edu. The Journal of Clinical investigation
The recipe 4 nut and seed lovers: Spiced chili nuts and seeds
Recipe contributed by Fresh and Easy Meals by Better Homes and Gardens
Pick your favorite nuts and seed for this snack recipe. Orange juice concentration spiked with piquant spices gives the mixture a burst of favor.
Prep. 10 minutes
Bake 15 minutes
Oven 300 degrees F
Make 16 (1/4 cup) serving
2 tsp. frozen orange juice concentrate thawed.
2 tsp. Worcestershire sauce
1 tsp. garlic powder
1 tsp. ground cumin
1 tsp. chili powder
1/2 tsp. cayenne pepper
1/4 tsp. salt
1/4 tsp. ground allspice
1.4 tsp. onion salt
2 cups unsalted peanuts, hazelnuts, and/or Brazil nuts
1 cup pecan halves
6 tsp. unsalted shelled sunflower seeds
2 tsp. sesame seeds
Non stick cooking tray
In a large bowl, combined orange juice concentrate, Worcestershire sauce, garlic powder, cumin, chili powder, cayenne pepper,salt, allspice, black pepper and onion salt. Stir in nuts and seeds; toss to coat.
Line a 15x10x1 inch baking pan with foil; slightly coat with nonstick cooking spray. Spread nuts and seed on foil. Bake in a300 degrees oven for 15 to 20 minutes or until toasted, stirring once. Cool. Store in an airtight container at room temperature for up to 1 week.
Nutrition facts per serving: 186Cal, 16 g total fat(2 g sat. fat), 0mg cholesterol, 59 sodium, 7 g carbo, 3 g fiber, 6 g pro.
daily value: 2% vitamin A, 6% vitamin C, 2% calcium, 5% iron.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Pick your favorite nuts and seed for this snack recipe. Orange juice concentration spiked with piquant spices gives the mixture a burst of favor.
Prep. 10 minutes
Bake 15 minutes
Oven 300 degrees F
Make 16 (1/4 cup) serving
2 tsp. frozen orange juice concentrate thawed.
2 tsp. Worcestershire sauce
1 tsp. garlic powder
1 tsp. ground cumin
1 tsp. chili powder
1/2 tsp. cayenne pepper
1/4 tsp. salt
1/4 tsp. ground allspice
1.4 tsp. onion salt
2 cups unsalted peanuts, hazelnuts, and/or Brazil nuts
1 cup pecan halves
6 tsp. unsalted shelled sunflower seeds
2 tsp. sesame seeds
Non stick cooking tray
In a large bowl, combined orange juice concentrate, Worcestershire sauce, garlic powder, cumin, chili powder, cayenne pepper,salt, allspice, black pepper and onion salt. Stir in nuts and seeds; toss to coat.
Line a 15x10x1 inch baking pan with foil; slightly coat with nonstick cooking spray. Spread nuts and seed on foil. Bake in a300 degrees oven for 15 to 20 minutes or until toasted, stirring once. Cool. Store in an airtight container at room temperature for up to 1 week.
Nutrition facts per serving: 186Cal, 16 g total fat(2 g sat. fat), 0mg cholesterol, 59 sodium, 7 g carbo, 3 g fiber, 6 g pro.
daily value: 2% vitamin A, 6% vitamin C, 2% calcium, 5% iron.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
4 the best soup with Vegetable stock
Recipe contributed by 125 Chinese recipes with Bill Jones and Stephen Wong
4 large onions, peeled and roughly chopped
2 leeks, washed and roughly chopped
5 stalks of celery, roughly chopped
3 bay leaves
1 small mixed herb (cilantro, basil, etc.)
10 whole pepper corns
1/2 head garlic
2 ginger slices
1 tsp. fennel seed
1 tsp. whole allspice
1 tsp. whole coriander seed
2 cups white wine
20 cups water
1. Place ingredients in a large stockpot, adding more water, if necessary to cover. Bring mixture to a broil; reduce heat and simmer gently for 2 hours, skimming occasionally to remove any foam or impurities that rise to the top. Try not to let the mixture boil or broth will be cloudy.
2. strain in to container and cool to room temperature before refrigerating. (If hot stock is placed directly in the fridge, it will sometime sour). for a more intensely flavored stock, let liquid cool; return stock to pot and over low heat, simmer until volume is reduced by half.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
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and Keep Him/Her for Good,The Simple WaySuper foods Library, Eat Yourself Healthy With The Best of the Best Nature Has to Offer
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4 large onions, peeled and roughly chopped
2 leeks, washed and roughly chopped
5 stalks of celery, roughly chopped
3 bay leaves
1 small mixed herb (cilantro, basil, etc.)
10 whole pepper corns
1/2 head garlic
2 ginger slices
1 tsp. fennel seed
1 tsp. whole allspice
1 tsp. whole coriander seed
2 cups white wine
20 cups water
1. Place ingredients in a large stockpot, adding more water, if necessary to cover. Bring mixture to a broil; reduce heat and simmer gently for 2 hours, skimming occasionally to remove any foam or impurities that rise to the top. Try not to let the mixture boil or broth will be cloudy.
2. strain in to container and cool to room temperature before refrigerating. (If hot stock is placed directly in the fridge, it will sometime sour). for a more intensely flavored stock, let liquid cool; return stock to pot and over low heat, simmer until volume is reduced by half.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple WaySuper foods Library, Eat Yourself Healthy With The Best of the Best Nature Has to Offer
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
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Friday, 8 August 2014
Obesity Complication of Insulin Resistance
By Kyle j. Norton
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
How to calculate your BMI index
BMI= weight (kg)/ height (m2)
Insulin Resistance is defined as condition of the pancreas has become less effective in lowering the glucose in the blood that can lead to diabetes and other health problems, such as coronary artery disease, stroke, and type 2 diabetes.
How Obesity associates with Insulin Resistance
1. According to the study of "Inflammatory mediators and insulin resistance in obesity: role of nuclear receptor signaling in macrophages?" by Fuentes L, Roszer T, Ricote M., posted in PubMed, researchers found that Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.
2. In the study of "Association studies of novel obesity-related gene variants with quantitative metabolic phenotypes in a population-based sample of 6,039 Danish individuals" by Burgdorf KS, Gjesing AP, Grarup N, Justesen JM, Sandholt CH, Witte DR, Jørgensen T, Madsbad S, Hansen T, Pedersen O., posted in PubMed, researchers found that Our correlative findings from analysing single-locus data suggest that some variation in validated BMI and WHR loci are associated with either increased or decreased insulin sensitivity and thereby potentially with metabolically healthy or metabolically unhealthy subsets of obesity. The results call for testing in larger study samples and for further physiological exploration of the possible metabolic implications of these loci.
3. According to the abstract of the study of 'Polymorphisms in the adiponutrin gene are associated with increased insulin secretion and obesity" by Johansson LE, Lindblad U, Larsson CA, Råstam L, Ridderstråle M., posted in PubMed, researchers concluded that We confirm the association between PNPLA3 and obesity. In addition, the rs738409 variant was associated with insulin secretion. There seems to be a differential effect of the Ile-allele depending on the degree of obesity, possibly as a consequence of insulin resistance.
4. In the study of "Association analysis indicates that a variant GATA-binding site in the PIK3CB promoter is a Cis-acting expression quantitative trait locus for this gene and attenuates insulin resistance in obese children" by Le Stunff C, Dechartres A, Mariot V, Lotton C, Trainor C, Miraglia Del Giudice E, Meyre D, Bieche I, Laurendeau I, Froguel P, Zelenika D, Fallin D, Lathrop M, Roméo PH, Bougnères P., posted in PubMed, researchers filed the conclusion that the C allele of rs361072 is a causal variant capable of attenuating insulin resistance in obese children through increased expression of p110beta.
5. According to the study of "Genetics of insulin resistance" by Pedersen O., posted in PubMed, researcher indicated that Even among young, healthy individuals, there is more than a 10-fold variation in insulin sensitivity; however, taken in combination, all the known modifiers of insulin sensitivity - including obesity and a variety of environmental factors - explain less than one third of this variation........ and concluded that It is likely that inherited insulin resistance will eventually prove to be related to subtle mutations in many such genes of the insulin signalling network and the numerous genetic components controlling energy metabolism.
6. In another study of "Insulin resistance: interactions between obesity and a common variant of insulin receptor substrate-1" by Clausen JO, Hansen T, Bjørbaek C, Echwald SM, Urhammer SA, Rasmussen S, Andersen CB, Hansen L, Almind K, Winther K, et al., posted in PubMed, researchers found that The obese carriers of the codon-972 variant were also characterised by a clustering of metabolic cardiovascular risk factors, with raised fasting concentrations of plasma glucose, serum triglyceride, and plasma tissue-plasminogen-activator and its fast-acting inhibitor. With adjustment for known modulators of insulin sensitivity, multivariate analyses showed that the combination of obesity and the codon-972 variant was associated with a 50% reduction in insulin sensitivity (p = 0.0008). Our results suggest that the codon-972 IRS-1 gene variant may interact with obesity in the pathogenesis of common insulin-resistant disorders.
7. Etc.
Treatments of Obesity and Insulin Resistance
1. In the abstract of the study of "Molecular mechanism of insulin resistance in obesity and type 2 diabetes" by Choi K, Kim YB., posted in PubMed, researchers indicated that Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired insulin-dependent PI3K activation and downstream signaling. This review focuses on the molecular basis of skeletal muscle insulin resistance in obesity and type 2 diabetes. In addition, the effects of insulin-sensitizing agent treatment and lifestyle intervention of human insulin-resistant subjects on insulin signaling cascade are discussed. Furthermore, the role of Rho-kinase, a newly identified regulator of insulin action in insulin control of metabolism, is addressed.
2. In a study of "Insulin resistance and improvements in signal transduction" by Musi N, Goodyear LJ., posted in PubMed, researchers stated that A different strategy to increase muscle glucose disposal is by stimulating insulin-independent glucose transport. AMP-activated protein kinase (AMPK) is an enzyme that works as a fuel gauge and becomes activated in situations of energy consumption, such as muscle contraction. Several studies have shown that pharmacologic activation of AMPK increases glucose transport in muscle, independent of the actions of insulin. AMPK activation is also involved in the mechanism of action of metformin and adiponectin. Moreover, in the hypothalamus, AMPK regulates appetite and body weight. The effect of AMPK to stimulate muscle glucose disposal and to control appetite makes it an important pharmacologic target for the treatment of type 2 diabetes and obesity.
3. According to another study of "Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance" by Hawley JA., posted in PubMed, researcher indicated that During the past half-century, there has been a dramatic increase in the incidence of obesity, insulin resistance and type 2 diabetes....... Several putative mechanisms for enhanced glucose uptake after exercise training will be discussed. A determination of the underlying biological mechanisms that result from exercise training is essential in order to define the precise variations in physical activity that result in the most desired effects on targeted risk factors, and to aid in the development of such interventions.
4. In a study of "Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance" by Trovato GM, Martines GF, Trovato FM, Pirri C, Pace P, Garozzo A, Castro A, Catalano D., posted in PubMed, researchers concluded that Ad36 previous infection is significantly associated with enhanced weight loss, bright liver disappearance, and recovery of insulin sensitivity through the chosen tailored nutritional interventional treatment. Nonetheless, Ad36 seronegative NAFLD patients' fatty liver pattern improves, at a lower extent, also without significant weight loss: an effect of dietary changes profile, Mediterranean diet, not only of lowered food caloric intake, is conceivably operating.
5. Etc.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
Obesity is defined as a medical condition of excess body fat accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
How to calculate your BMI index
BMI= weight (kg)/ height (m2)
Insulin Resistance is defined as condition of the pancreas has become less effective in lowering the glucose in the blood that can lead to diabetes and other health problems, such as coronary artery disease, stroke, and type 2 diabetes.
How Obesity associates with Insulin Resistance
1. According to the study of "Inflammatory mediators and insulin resistance in obesity: role of nuclear receptor signaling in macrophages?" by Fuentes L, Roszer T, Ricote M., posted in PubMed, researchers found that Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.
2. In the study of "Association studies of novel obesity-related gene variants with quantitative metabolic phenotypes in a population-based sample of 6,039 Danish individuals" by Burgdorf KS, Gjesing AP, Grarup N, Justesen JM, Sandholt CH, Witte DR, Jørgensen T, Madsbad S, Hansen T, Pedersen O., posted in PubMed, researchers found that Our correlative findings from analysing single-locus data suggest that some variation in validated BMI and WHR loci are associated with either increased or decreased insulin sensitivity and thereby potentially with metabolically healthy or metabolically unhealthy subsets of obesity. The results call for testing in larger study samples and for further physiological exploration of the possible metabolic implications of these loci.
3. According to the abstract of the study of 'Polymorphisms in the adiponutrin gene are associated with increased insulin secretion and obesity" by Johansson LE, Lindblad U, Larsson CA, Råstam L, Ridderstråle M., posted in PubMed, researchers concluded that We confirm the association between PNPLA3 and obesity. In addition, the rs738409 variant was associated with insulin secretion. There seems to be a differential effect of the Ile-allele depending on the degree of obesity, possibly as a consequence of insulin resistance.
4. In the study of "Association analysis indicates that a variant GATA-binding site in the PIK3CB promoter is a Cis-acting expression quantitative trait locus for this gene and attenuates insulin resistance in obese children" by Le Stunff C, Dechartres A, Mariot V, Lotton C, Trainor C, Miraglia Del Giudice E, Meyre D, Bieche I, Laurendeau I, Froguel P, Zelenika D, Fallin D, Lathrop M, Roméo PH, Bougnères P., posted in PubMed, researchers filed the conclusion that the C allele of rs361072 is a causal variant capable of attenuating insulin resistance in obese children through increased expression of p110beta.
5. According to the study of "Genetics of insulin resistance" by Pedersen O., posted in PubMed, researcher indicated that Even among young, healthy individuals, there is more than a 10-fold variation in insulin sensitivity; however, taken in combination, all the known modifiers of insulin sensitivity - including obesity and a variety of environmental factors - explain less than one third of this variation........ and concluded that It is likely that inherited insulin resistance will eventually prove to be related to subtle mutations in many such genes of the insulin signalling network and the numerous genetic components controlling energy metabolism.
6. In another study of "Insulin resistance: interactions between obesity and a common variant of insulin receptor substrate-1" by Clausen JO, Hansen T, Bjørbaek C, Echwald SM, Urhammer SA, Rasmussen S, Andersen CB, Hansen L, Almind K, Winther K, et al., posted in PubMed, researchers found that The obese carriers of the codon-972 variant were also characterised by a clustering of metabolic cardiovascular risk factors, with raised fasting concentrations of plasma glucose, serum triglyceride, and plasma tissue-plasminogen-activator and its fast-acting inhibitor. With adjustment for known modulators of insulin sensitivity, multivariate analyses showed that the combination of obesity and the codon-972 variant was associated with a 50% reduction in insulin sensitivity (p = 0.0008). Our results suggest that the codon-972 IRS-1 gene variant may interact with obesity in the pathogenesis of common insulin-resistant disorders.
7. Etc.
Treatments of Obesity and Insulin Resistance
1. In the abstract of the study of "Molecular mechanism of insulin resistance in obesity and type 2 diabetes" by Choi K, Kim YB., posted in PubMed, researchers indicated that Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired insulin-dependent PI3K activation and downstream signaling. This review focuses on the molecular basis of skeletal muscle insulin resistance in obesity and type 2 diabetes. In addition, the effects of insulin-sensitizing agent treatment and lifestyle intervention of human insulin-resistant subjects on insulin signaling cascade are discussed. Furthermore, the role of Rho-kinase, a newly identified regulator of insulin action in insulin control of metabolism, is addressed.
2. In a study of "Insulin resistance and improvements in signal transduction" by Musi N, Goodyear LJ., posted in PubMed, researchers stated that A different strategy to increase muscle glucose disposal is by stimulating insulin-independent glucose transport. AMP-activated protein kinase (AMPK) is an enzyme that works as a fuel gauge and becomes activated in situations of energy consumption, such as muscle contraction. Several studies have shown that pharmacologic activation of AMPK increases glucose transport in muscle, independent of the actions of insulin. AMPK activation is also involved in the mechanism of action of metformin and adiponectin. Moreover, in the hypothalamus, AMPK regulates appetite and body weight. The effect of AMPK to stimulate muscle glucose disposal and to control appetite makes it an important pharmacologic target for the treatment of type 2 diabetes and obesity.
3. According to another study of "Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance" by Hawley JA., posted in PubMed, researcher indicated that During the past half-century, there has been a dramatic increase in the incidence of obesity, insulin resistance and type 2 diabetes....... Several putative mechanisms for enhanced glucose uptake after exercise training will be discussed. A determination of the underlying biological mechanisms that result from exercise training is essential in order to define the precise variations in physical activity that result in the most desired effects on targeted risk factors, and to aid in the development of such interventions.
4. In a study of "Adenovirus-36 Seropositivity Enhances Effects of Nutritional Intervention on Obesity, Bright Liver, and Insulin Resistance" by Trovato GM, Martines GF, Trovato FM, Pirri C, Pace P, Garozzo A, Castro A, Catalano D., posted in PubMed, researchers concluded that Ad36 previous infection is significantly associated with enhanced weight loss, bright liver disappearance, and recovery of insulin sensitivity through the chosen tailored nutritional interventional treatment. Nonetheless, Ad36 seronegative NAFLD patients' fatty liver pattern improves, at a lower extent, also without significant weight loss: an effect of dietary changes profile, Mediterranean diet, not only of lowered food caloric intake, is conceivably operating.
5. Etc.
Weight Loss the Easy Ways
Andrea Albright Featured on Health and Fitness Jan. 2015
will Personally Coach You How to Get There The Easy Way
If You Are Looking For a SoulMate
Celebrity Patti Stanger Will Coach You To Get Him/Her
and Keep Him/Her for Good,The Simple Way
Back to Obesity's Complications http://kylejnorton.blogspot.ca/p/obesitys-complications.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca
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