Ways to Lose Your Belly Fat Naturally

Flat Belly Fix

In Flat Belly Fix program, you learn the easy, tested and trusted method that saved the creator of this program (Todd Lamb) beautiful wife Tara from a life battling Type 2 Diabetes and experiencing possibly death. It was a very nasty experience with the couple during those times, but with the determination of Todd, he labored ceaselessly to finding a way out for his depressed and unhappy wife. Now they live together both happy and contented. Having used the same technique for people around (seeing the wonders it did to his wife) and also recording so much success, Todd Lamb wants to relate this secret to the world, to create this same atmosphere of joy produced in his immediate environment. Hence, he was motivated to put together this workable program. You also get to learn the secret to having a flat belly, and a healthy and fit body that has been hidden from you for so long now. The creator if this program is positive about the efficacy of this program and is so excited for you to personally experience what happens when you apply The 21 Day Flat Belly Fix in your life. Read more here...

Flat Belly Fix Summary


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The writer presents a well detailed summery of the major headings. As a professional in this field, I must say that the points shared in this ebook are precise.

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Excessive Sympathetic Nervous System Output Is Detrimental to Health

Stimulation of the SNS is a hallmark of the acute stress response (Goldstein, 1987). SNS activation has many physiological consequences that work in concert to promote the fight-or-flight response (Jansen et al., 1995 Goldstein, 1996) and facilitate features of innate immunity (Campisi and Fleshner, 2003 Johnson et al., 2005). SNS activation is a powerful feature of the acute stress response that is adaptive when the response is acute and constrained. If, however, SNS activation is frequent or excessive, it can produce negative health consequences (Seals and Dinenno, 2004). For example, chronically elevated SNS responses are believed to mechanistically contribute to the etiology of metabolic syndrome, a key antecedent to clinical atherosclerotic diseases that includes visceral adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hypertension (Baron, 1990 Julius et al., 1992 Lind and Lithell, 1993). In addition, it has been reported in both the human and animal...

The contribution of reduced thermogenesis and fat oxidation to obesity and its metabolic complications

Besides and beyond contributing to increased fat mass (obesity), decreased fat oxidation and thermogenesis may result in an excess of available fatty acids to muscle, liver, pancreatic p cells and other non-adipose cells. Lipid accumulation can lead to functional impairments in these cells (lipotoxicity), and has been related to the development of insulin resistance, type 2 diabetes and other pathologies linked to obesity and the metabolic syndrome (reviewed in references 37 and 38). Because the activity of the UCPs may facilitate fat oxidation in the organism (see Section 4.2.1), it may help avoiding lipid accumulation in non-adipose cells and derived lipotoxic-ity. For instance, intramyocellular fat accumulation is highly correlated with

Other food and food components of interest

Suppression of abdominal fat accumulation after dietary supplementation with licorice194 and, in a human trial, licorice administration was found to reduce body fat mass, without changing body mass index, in 15 normal-weight subjects under free-living conditions (no caloric restriction).195 The mechanism of action, safety and efficacy of licorice for weight loss is unknown.

The Association Between Obesity And Type 2 Diabetes

Several mechanisms have been proposed to explain how excessive body weight is associated with Type 2 diabetes. In general, the accumulation of fat mass is associated with a decline in whole body insulin sensitivity. The distribution of obesity is important, with resistance to the action of insulin and glucose intolerance most closely associated with excess abdominal adipose tissue. As visceral adipose tissue increases plasma triglyceride (TG) concentrations are elevated, high-density lipoprotein (HDL) cholesterol decreases and low-density lipoprotein (LDL) cholesterol increases with a greater proportion of the more atherogenic small dense LDL particles (LDL subclass III). Other associated characteristics include an elevated plasma non-esterified fatty acid (NEFA) concentration, an increased plasminogen activator inhibitor 1 (PAI-1) concentration, hyperuricaemia and hypertension. Abdominal obesity is also associated with specific changes in skeletal muscle morphology, namely a...

Physical Activity for Obese Patients

Similar positive health benefits from walking were found in postmenopausal women, with a lower risk of hip fractures by 6 for each hourly increase in walking per week 30 , and in premenopausal women who maintained weight loss and decreased waist circumference with walking 2 to 3 hours per week 31 .

Approaches To Weight Management

Measurement of height and weight, in order to determine the BMI, is the initial step in the clinical assessment of obesity. Waist and hip circumference measurements provide information as to the distribution of weight, with a waist circumference measure of 102 cm in men and 88 cm in women associated with increased risk of CHD (39). More sophisticated measures of body fat can be made using other techniques such as bioelectrical impedance, dual energy X-ray absorptiometry, densitometry and isotope dilution, although these techniques tend to be expensive, complex and are generally confined to a research setting.

Pharmacological Management

Some evidence that the use of basal insulin as opposed to meal-time insulin will lessen the weight gain effect (85). Newer agents such as the thiozolidinedione insulin sensitisers remain controversial, as the impact of undesirable subcutaneous weight gain, despite reductions in the more harmful visceral fat, continues to be debated (8).

Health Impact of Obesity

An obese child's vascular system can be harmed in a variety of ways. Mild to moderately obese children have arterial endothelial dysfunction and an increased intima-media thickening 32 . Ultrasound studies have shown obese children's carotid arteries are thicker and stiffer than those of non-obese children 33 . Obese children have higher levels of lipoproteins, including the more atherogenic low-density lipoprotein (LDL) 34 , which may increase the child's risk for cardiovascular disease at a young age. The presence of the metabolic syndrome in the obese child may play an important role in development of cardiovascular disease therefore this syndrome deserves particular attention. A major metabolic impact of obesity is the development of insulin resistance that predisposes the child or adolescent to develop the metabolic syndrome. The components of the syndrome are glucose intolerance, a low HDL, elevated triglycerides, increased abdominal circumference, and elevated blood pressure....

Obesity And Insulin Resistance

Obesity is the most common condition associated with insulin resistance (13). Obesity is a health problem reaching epidemic proportions in Western countries. In the UK alone some 16 of men and 18 of women are obese (14). Obesity can be defined as a body mass index (BMI) greater than 30kg m2. Insulin resistance is frequently observed in obese subjects and constitutes an independent risk factor for the development of Type 2 diabetes and atherosclerosis. The importance of increasing visceral fat (measured by waist hip ratio) as a risk factor for insulin resistance and cardiovascular disease has also been demonstrated (15).

Dietary fibres and food intake

Various types of DF may be of interest. Maeda et al. (2005) demonstrated that the addition of agar in the diet resulted in marked weight loss due to a reduction of food intake, and also improved cholesterol level, glucose and insulin response, and blood pressure. The Framingham Offspring Study reported that the prevalence of metabolic syndrome - defined following the National Cholesterol Education Program criteria - was improved by high cereal fibres intake (contributing to the beneficial effect of whole grain) (McKeown et al. 2004). Knowledge of the biochemical mechanism allowing DF to modulate satiety, glucose or lipid metabolism, and hypertension is essential when proposing key nutritional advice for specific disorders associated with the metabolic syndrome. In this context, the modulation of gastro-intestinal peptides by NDOs, such as fructans, is an interesting area of research, leading to an understanding of how events occurring in the gut participate in the control of food...

Treating Overweight Adolescents

Another issue regarding treatment of overweight adolescents is that there is no reimbursement. Unless the teenager meets the criteria for metabolic syndrome, third party payers do not cover clinic appointments for weight management, so payment is not provided for any treatment. Therefore, all the physician may be able to do to help the overweight adolescent is to encourage awareness of the weight trend and offer informational material and website addresses.

Immediate Questions

Is there a family history of hypertension or cardiovascular disease Ask about essential hypertension, metabolic syndrome (or syndrome X), and other familial forms of hypertension such as Alport syndrome, polycystic kidney disease, juvenile nephronephritis, glucocorticoid remediable aldosteronism, and Liddle syndrome, among others.

Obesity and Type 2 Diabetes

During the last 20 years, obesity has reached epidemic proportions in the United States and worldwide. Recent data from the National Center for Health Statistics indicate that 30 of U.S. adults 20 years of age and older (over 60 million people) are obese (Ogden, Carroll, Curtin, McDowell, Tabak, and Flegal 2006). Visceral obesity and three other pathologic conditions (dyslipidemia, hypertension, and insulin resistance) comprise the so-called metabolic syndrome, also known as Syndrome X. Syndrome X is a major risk factor for type 2 diabetes (T2D also called non-insulin-dependent diabetes mellitus, or NIDDM) (Haffner, Ruilope, Dahlof, Abadie, Kupfer, and Zannad 2006). A common feature of obesity, insulin resistance, and T2D is chronic, low-grade inflammation (Dandona, Aljada, and Bandyopadhyay 2004 Dandona, Aljada, Chaudhuri, Mohanty, and Garg 2005 Weisberg et al. 2006 Weisberg, McCann, Desai, Rosenbaum, Leibel, and Ferrante 2003 Wellen and Hotamisligil 2005). Markers of chronic...

Biological Effects

In contrast to MC4-R knockout mice, MC3-R knockouts exhibit an exclusively metabolic syndrome. Homozygous MCR3-R - - mice are not significantly overweight, but they exhibit an approximately 50-60 increase in fat mass and also exhibit an unusual increase in respiratory quotient when transferred onto high-fat diet, suggesting a reduced ratio of fat carbohydrate oxidation. Furthermore, these knockout mice also exhibit an approximately 50 reduction in locomotor behavior, indicating reduced energy expenditure. Additionally, MSH seems to play an important role during early neurogenesis and exhibits a peak around parturition. The latter has been interpreted to mean that MSH plays a signaling role in the initiation of parturition.

Determining the role of calcium in weight control

Zemel and co-workers (2000), who re-examined data from 380 women (of about 7000) from the NHANES III study, found less body fat and a lower risk for obesity in people with the highest calcium intake after controlling for energy intake and physical activity, and the risk of being in the highest BMI quartile was reduced by 85 at the highest quartile of calcium intake. The anti-obesity effect of calcium has been demonstrated in black and in white people of both sexes, although in the HERITAGE Family Study the strongest effects occurred in white women and black men (Loos et al., 2004) the former exhibited a significant inverse relationship between calcium and BMI, percentage body fat and total abdominal fat, the latter between calcium intake and leanness. Therefore it is particularly important that, in recent years, some studies have been published that test explicitly the effect of calcium on body weight, body fat and the efficacy of weight-reduction diets. An epidemio-logical,...

Sources of further information and advice

Almustafa m, doyle f h, gutteridge d h, hand d j, davis t m, spinks t j, freemantle c and joplin g f (1992), 'Effects of treatments by calcium and sex hormones on vertebral fracturing in osteoporosis', Q. J. Med., 83, 283-294. azadbakht l, mirmiran p, esmaillzadeh a and azizi f (2005), 'Dairy consumption is inversely associated with the prevalence of the metabolic syndrome in Tehranian adults', Am. J. Clin. Nutr., 82, 523-530. barger-lux m j, davies k m, heaney r p, chin b k and rafferty k (2001), 'Calcium supplementation may attenuate accumulation of fat in young women', J. Bone Miner. Res., 16, S219. barr s i (2004), 'Calcium and obesity', in Mela D. (Ed.), 'Food, Diet and Obesity',

Safety issues 1241 In animals

With subjects having type 2 diabetes, the quantity of 10t,12c isomer in plasma was inversely correlated with changes in body weight and in serum leptin. Unfortunately no information was available on body composition and insulin sensitivity. Concerns were raised by the findings of the group of Smedman, who carried out studies on a high-risk group of abdominally obese men. None of the studies carried out by this group showed any effects of CLA on body weight or BMI even if CLA resulted in a slight decrease in body fat, particularly of abdominal fat in obese men. On the contrary, CLA isomer induced lipid peroxidation, as reported in Fig. 12.6. Administration of a CLA mixture to obese men at 4.2 g day for 1 month resulted in an increase of both 8-isoprostaglandin F2a (PGF2a) and of 15-oxo dihydro-PGF2a as indicators of non-enzymic and enzymatic arachidonic acid oxidation, respectively, (Basu et al., 2000) as compared with the control group. However, these peroxidation parameters went back...

Examination of the obese patient

According to the NHLBI guidelines 5 , assessment of risk status due to overweight or obesity is based on the patient's body mass index (BMI), waist circumference and the overall risk status. BMI is calculated as weight (kg) height (m)2, or as weight (pounds) height (inches)2 x 703. A BMI table is more conveniently used for simple reference (see Table 9.1). Classifying obesity by BMI units replaces previous weight-height terminology such as percent ideal or desirable body weight. These previous terms were often difficult to interpret and difficult for patients to understand. BMI is recommended since it provides an estimate of body fat, is related to risk of disease and has been established as an independent risk factor for premature mortality 6 . A desirable or healthy BMI is 18.5 to 24.9kg m2, overweight is 25 to 29.9kg m2, and obesity is 30kg m2. Obesity is further sub-defined into class I (30.0-34.9kg m2), class II (35.0-39.9kg m2) and class III ( 40kg m2) (Table 9.2). Lower BMI...

Potential Mechanisms Responsible for Deficient Skin Vasodilatation to Mental Stress in Obesity

Adipose tissue has a local renin-angiotensin system. Angiotensinogen, angiotensin-converting enzyme, and AT1 and AT2 receptors are all present in human adipose tissue. Angiotensinogen expression in adipose tissue correlates with waist-to-hip ratio in obese humans. Central fat distribution is associated with increased systemic vascular resistance and hypertension. Increased activity of this local renin-angiotensin system may impair skin vasodilatation in obesity. Also, increased levels of proinflammatory cytokines might play a role, because chronic subclinical inflammation was shown to be a part of the insulin resistance syndrome. C-reactive protein has been shown to positively correlate with measures of obesity, such as body mass index and waist circumference. Tumor necrosis factor-a and interleukin-6 concentrations are higher in obese individuals. Weight loss leads to a decrease in the levels of these proinflammatory cytokines, along with a decrease in adhesion molecules and...

Prevalence Of Overweight And Obesity

This chapter focuses on the epidemiological evidence of obesity as a risk factor for various cancers. Most studies used BMI as an indicator of overall obesity, and some had other measures as well, such as waist circumference or waist-to-hip ratio (WHR) (an indicator of body fat distribution) to examine whether central obesity is a risk factor for cancer. Different cut points for BMI, waist circumference, and WHR were used in various studies. We identified studies published between 1966 and 2004 via the MEDLINE database. Included in this chapter are published reviews and meta-analyses as well as individual studies published since the reviews. For individual studies, only those with at least 100 cases were included however, all identified studies were included for less common cancers. When several articles were published from the same study, only the most recent is included. Most of the cohort and case-control studies, included in three published reviews, as well as studies published...

Laurence Moon syndrome

This syndrome was first described by John Zachariah Laurence. This is an autosomal recessive disorder associated with loci in chromosomes 11q13, 11q21, 15q22 and 3p13.(54 The syndrome is associated with mental retardation, short stature, spastic paraparesis, hypogenitalism, and red cone dystrophy leading to night blindness by mean age of 9 years and often being registered blind by mean age of 15 years. The prevalence varies between 1 in 125 000 and 1 in 160 000. The prevalence has been reported to be higher in Bedouins of Kuwait (1 in 13 500) and in Newfoundland (1 in 17 500), where a founder effect of a handful of families from the West Country of England in 1800s is thought to be responsible. (55 Laurence-Moon syndrome is usually considered together with Bardet-Biedl syndrome, although strictly this is a separate syndrome. Bardet-Biedl syndrome presents with mental retardation, hypogenitalism, and red cone dystrophy however, it differs in that central obesity and postaxial...

Dyslipidaemia And Other Cardiovascular Risk Factors

The dyslipidaemia of ESRF is characterised by raised plasma triglycerides with a normal cholesterol level. This form of dyslipidaemia becomes worse after starting CAPD. The lipid profile on CAPD is generally more atherogenic than with other dialysis modalities. A possible contributory factor for this atherogenic lipid profile is the glucose absorption from the dialysates giving rise to enhanced triglyceride synthesis. Chronic hyperinsulinaemia is a major component of the metabolic syndrome and a recognised risk factor for atherosclerosis (36). There is a preferential sieving of the smaller cardio-protective lipoprotein HDL-cholesterol among the proteins lost into the dialysate rather than that of other lipoproteins (37).

Key Issues in the Treatment Strategy

The novel classes of antidiabetic agents, incretin mimetics and DPP-4 inhibitors, may hold two additional promises A reduction in cardiovascular complications typically associated with type 2 diabetes 188 and the metabolic syndrome, and a positive influence on the natural history of type 2 diabetes, which with current treatment options is characterized by a steady loss of P-cell function 189,190 , which in turn determines a rather short durability of successful glycemic control with any choice of antidiabetic agents 191,192 .

Mastoidectomy Facial Recess Approach and Cochleostomy Techniques

Facial Nerve Recess Cochlear Implant

For those individuals who have undergone a canal-wall-down mastoidectomy procedure in the past and require cochlear implantation to rehabilitate their hearing loss, a two-stage procedure is required. First, mastoid obliteration with removal of all epithelium, oversewing the external auditory canal, and filling the resulting dead space with abdominal fat is performed. Three to 6 months later, cochlear implantation can be undertaken. If no active disease is present, a one-stage procedure may be considered however, this is not recommended due to the risk of bacterial contamination.

The Molecular Endocrinology Of Diabetes Mellitus

Diabetes mellitus is a metabolic syndrome characterized by hyperglycemia resulting from variable defects in insulin secretion and action. Traditionally, diabetes mellitus has been divided into four categories Type 1 diabetes, characterized by absolute insulin deficiency and requirement of insulin therapy to sustain life Type 2 diabetes, characterized by variable defects in insulin secretion and action, without an absolute need for insulin therapy (although insulin might be necessary for adequate control of hyperglycemia) other specific types of diabetes and gesta-tional diabetes. Type 1 diabetes is further subdivided into Type 1A, or autoimmune, diabetes and Type 1B, or idiopathic diabetes. The other category is very large, encompassing diabetes resulting from other illness or medications (such as cystic fibrosis-related diabetes) as well as many genetic syndromes that include diabetes (101). It is becoming increasingly apparent, however, that these categories are artificial and that...

Suggested Daily Intravenous Intake of Essential Trace Elements

Studies show that people with type 2 diabetes have lower blood levels of chromium than those without the disease. Insulin resistance is the common denominator in a cluster of cardiovascular disease risk factors. One out of every five Americans has metabolic syndrome. It affects 40 of people in their 60s and 70s. Insulin resistance, with or without the presence of metabolic syndrome, significantly increases the risk of cardiovascular disease. Insulin resistance is present in two serious health problems in women polycystic ovarian syndrome (PCOS) and gestational diabetes. Several studies have demonstrated that chromium supplements enhance the metabolic action of insulin and lower some of the risk factors for cardiovascular disease, particularly in overweight individuals. Chromium picolinate, specifically, has been shown to reduce insulin resistance and to help reduce the risk of cardiovascular disease and type 2 diabetes. It must be remembered that dietary chromium is poorly absorbed,...

Substances reducing the rate of de novo lipogenesis and their possible therapeutic potential for the control of obesity

Therefore, whereas a reduction in food intake and body weight by HCA was shown in many rodent studies, the efficacy of HCA in humans appears to be inconsistent and variable effects of HCA on food intake, body weight, visceral fat accumulation or fatty acid oxidation have been reported in some (Lim et al. 2002, 2003 Westerterp-Plantenga and Kovacs 2002 Hayamizu et al. 2003 Tomita et al. 2003 Preuss et al. 2004), but not all (Kriketos et al. 1999 Mattes and Bormann 2000 van Loon et al. 2000 Kovacs et al. 2001a,b), studies. Different experimental designs or differences in the HCA preparations employed might explain the discrepant findings. For example, the bioavailability of various HCA preparations differs (Lim et al. 2005).

Metaiodobenzylguanidine MIBG radionuclide scan If

The 13-year-old girl had modest BP elevation, which might be attributed to office hypertension, essential hypertension, or metabolic syndrome. Further investigation showed multiple high BP readings had been obtained by school nurse, and patient also had a strong family history of hypertension. Diagnosis of essential hypertension was made, and patient's BP was well controlled on salt restriction and hydrochlorothiazide, 25 mg daily.

Carbohydrate type glycaemic response and weight control

GI of the diet by giving brief instructions and a handout about dietary changes to the parents, resulted in a reduction of body mass index (BMI) Z-scores of the children (Young et al., 2004). A 5-week study in healthy men allocated to a high- or a low-GI diet reported both groups experienced an increase in lean body mass but no changes in BMI after the low-GI period (Bouche et al., 2002). A more marked effect was reported in a study of men with abdominal obesity given an ad libitum low glycaemic load or low-fat diet for 6 days there was a reduction in energy intake, bodyweight, and waist and hip circumference with the low glycemic load diet, but not with the low-fat diet (Dumesnil et al., 2001). Although these findings suggest a potential advantage of low-GI or low-GL diets, the definitive long-term study, where ad libitum intake is permitted but diets are similar in all aspects except the GI, has not yet been done.

The Il6 Response To Exercise

Today, interleukin IL-6 is thought by many authors to be the link between inflammation, obesity, stress and coronary heart disease 71 . However, given the finding that working muscles produce and release IL-6 in large amounts and the many beneficial effects of physical exercise on health 30 , it is hard to believe that muscle-derived IL-6 is detrimental to health. An alternative explanation is that TNF-a, rather than IL-6, is the actual driver behind the metabolic syndrome. Thus, since TNF induces the production of IL-6, a high concentration of TNF will induce a high production of IL-6. Increased levels of both TNF-a and IL-6 have been observed in ageing 72 , in obese individuals 73 and in non-insulin-dependent diabetes mellitus 74-77 . Furthermore, in several population-based studies, plasma concentrations of IL-6 have been shown to predict total and cardiovascular mortality 78 , Nevertheless, although adipose tissue produces and releases both TNF-a and IL-6 79,80 , there is...

Establishing a Third Category IFG Why and What is IFG

As already discussed, the DECODE-study showed that while IGT is associated with an increased risk of developing CVD this is only the case in IFG-individuals if they also have abnormal 2-h glucose values 11,13 . In other words, isolated IFG is not associated with increased risk of CVD or increased all cause mortality. It has also been shown that while IGT is often associated with other abnormalities associated with the metabolic syndrome as dyslipidemia and hypertension, this is not the case for isolated IFG (at least not to the same extent) 18 .

Low Carbohydrate Versus Low Fat Diets

A study at the Philadelphia Veterans Affairs Hospital evaluated weight loss and lipid changes among severely obese (BMI 35) patients of whom 39 had diabetes and 43 had metabolic syndrome. The 6-month study started with 132 patients. The low-carbohydrate group (N 68) consumed less than 30g of carbohydrates per day, while the low-fat, low-calorie group (N 64) reduced their caloric intake by 500 calories per day with less than 30 of total calories from fat. At 6 months, the results favored a low-carbohydrate diet with a mean weight loss of 5.1kg compared to a mean loss of 1.9kg for the reduced calorie, low-fat group. Triglyceride levels fell by 20 and insulin sensitivity improved by 6 for the low-carbohydrate group compared to only a 4 drop in triglyceride levels and a 3 reduction in insulin sensitivity for the low-fat group. An attrition rate of 47 at 6 months was a significant limitation of the study 8 .

Using food and food components to control lipogenesis and thermogenesis

Studies in rodents have consistently reported that intake of n-3 PUFAs reduces adipose mass, preferentially visceral fat, in general without affecting body weight (see references in reference 87). Some studies in humans also reported an effect of dietary fish oil consumption increasing whole-body lipid oxidation and decreasing total body fat content,96 and specifically abdominal fat content.97 Most human studies, however, have so far examined the effect of PUFA intake on end-points related to cardiovascular health and insulin sensitivity, rather than to body weight and body fat control. There is a paucity of human studies specifically designed to ascertain whether the intake of PUFAs (or PUFA-rich foods such as fish oils and nuts) can assist in weight loss and or in weight maintenance after weight loss in the long-term. Studies in humans support the potential value of diacylglycerol for the management of excess body weight and related disorders. In one study, carried out in 38 healthy...

Effects of structured lipids related to weight control

Human studies have been conducted with a variety of structured lipids as demonstrated in Table 14.3. Matsuo et al. (2001) examined the effects of a liquid diet supplement containing structured lipid composed of 10 MCFA and 90 LCFA as compared with a liquid formula containing LCT in 13 healthy male volunteers. Although body weight increased non-significantly in both groups, the rates of variation in body fat percentage were lower in the structured lipid group than in the LCT group throughout the 12-week study. Despite this, in another 12-week study comparing LCT with a diet supplemented with 14 g of structured fat containing only 1.7 g MCFA, results showed decreases in body weight, including subcutaneous and visceral fat as measured by air displacement methods (Kasai et al., 2003). Similarly, Takeuchi et al. (2002) examined the effects of 20 g of structured lipid containing MCFA and LCFA versus the same quantity of soybean oil for 3 weeks in 6 young men. The rate of variation in body...

Effects of mediumchain triglycerides on body weight and body fat

The addition of MCT to hypocaloric diets displays variable effects. Yost and Eckel (1989) compared MCT and LCT feedings during and after 4 or 12 weeks of hypocaloric feedings in 16 obese women. It was concluded that MCT are safe, but fail to increase the rate or amount of weight loss. However, a major drawback in this study was that the authors did not measure EE or body composition. Another study tested the effects of a very low calorie diet supplemented with MCT versus a low-fat, high-carbohydrate regimen over 4 weeks (Krotkiewski, 2001). The MCT group showed a significantly greater decrease in body weight during the first 2 weeks compared with the group consuming the low-fat, high-carbohydrate diet. The contribution of body fat to the total weight loss was also higher while the contribution of fat-free mass was lower, as measured by dual-energy x-ray absorptiometry. Similarly, Nosaka et al. (2003) randomized 73 subjects into two groups and provided them with 2100-2400 kcal day of...

Surgical Technique

If a pressure equalizing (PE) tube has been placed previously for any reason, it is removed now. A complete mastoidectomy is performed and the teg-men and perilabyrinthine air cells carefully examined for CSF leakage. The extent of surgical exposure depends on the location and size of the dural defect and the status of hearing. If the leak occurs in a deaf ear, it is repaired through a transmastoid approach by direct reinforcement with fascia or other connective tissue, and by obliteration of the mastoid with abdominal fat, and of the middle ear and eustachian tube with temporalis muscle. Removing the incus, opening the facial recess, and transecting the tensor tympani tendon facilitate exposure of the eustachian tube. If hearing is good, the initial approach is again transmastoid. If the dural defect is less than 1 cm and posteriorly located along the mastoid tegmen or posterior fossa, it can be sealed with fascia, the mastoid can be obliterated with abdominal fat in a similar...

Lifestyle Modification Works

The DPP researchers also reported results on the 53 of participants (n 1,711) who had the metabolic syndrome at baseline. The incidence of the metabolic syndrome was reduced by 41 in the lifestyle group and by 17 in the metformin group, compared with placebo 14 . The researchers attributed the dramatic effect of lifestyle modification on both the prevention of incident metabolic syndrome and a reduction of its overall prevalence primarily to reductions in waist circumference and in blood pressure. They concluded that their results demonstrate the value of lifestyle intervention in both the prevention and treatment of the syndrome, above and beyond improvement in glycemia alone and that lifestyle intervention may reduce risk in individuals with impaired glucose tolerance.

Role of resistant starch in weight management 831 Weight management direct evidence

RS is associated with nutritional, metabolic and physiological changes that make it an attractive ingredient not only for weight management (Table 8.1), but also for other chronic diseases associated with the metabolic syndrome such as dyslipidemia, insulin resistance, type 2 diabetes, hypertension and coronary heart disease (Higgins, 2004). Previously a role for RS was attributed to reduced digestibility, and the impact of lower glucose absorption. More recent research, however, indicates a broader health impact of RS on metabolism, via fermentation of RS to SCFAs in the large bowel. Fermentable carbohydrates have their own unique fermentation profile, in terms of relative type and amount of SCFAs. Hence the metabolic impact of fermentation will differ between RS and other fiber types. The hypothesized interaction between fermentation by-products and target metabolic tissues will evolve as more mechanistic information becomes available. Insulin sensitivity Insulin is an important...

Thrifty Phenotype Hypothesis

The structural and metabolic alternations induced in utero by adverse environment entrain both selective preservation of key organs and metabolic adaptations that are of advantage in a restricted postnatal life. If nutrition becomes plentiful postnatally, these changes predispose to obesity and impaired glucose tolerance. This has been substantiated by the Dutch Famine study in which poor nutrition in the first trimester was associated with increased obesity in 19-year-old males.197 This obesity and the consequent metabolic syndrome predispose an individual to coronary heart disease later in life.

Immune Function in Sleep Disorders

Recurrent nocturnal hypoxia and sleep fragmentation are related to obstructive sleep apnea, and these are also associated with increased activation of the HPA and the sympathetic systems. Ultimately, the latter alteration is regarded as one of the mechanisms responsible for hypertension that are commonly associated with to obstructive sleep apnea (Waradekar, Sinoway, Zwillich, and Leuenberger 1996). Patients with sleep apnea show higher nocturnal urinary and plasma catecholamine levels than healthy individuals (Fletcher, Miller, Schaaf, and Fletcher 1987). Although the assessment of the HPA axis activity in these patients is scarce, there is a study that shows a greater tryptophan-induced cortisol response, indicating augmented sensitivity of the axis (Hudgel and Gordon 1997). Despite this scarcity, increased sympathetic tonus and especially, augmented sleep fragmentation are connected to increased stress response and it seems unquestionable that such poor sleep quality leads to...

Causes of Overweight and Obesity

The primary care physician must consider genetic syndromes and endocrine conditions as possible explanations for a child's obesity. Prader-Willi syndrome is characterized by a rapid increase in weight from ages 1 to 6, hypotonia and poor feeding in infancy, hypogonadism, and cognitive delay 13 . The majority of children with Cushing syndrome are obese and short in stature 14 , which contrasts with children who are obese from eating excess calories and are commonly taller than their peers. Other medical conditions like hypothyroidism or growth hormone deficiency can cause a child to be obese, which would be suggested by clinical findings like a goiter, short stature, or delayed puberty. After a complete history and physical examination, in the vast majority of obese patients the physician can reassure the parents that their child does not have a genetic disorder or a metabolic syndrome. The one laboratory test all obese patients need is a thyroid-stimulating hormone (TSH) test....

Adipose tissue

White adipose tissue was long seen as a passive reservoir for the storage of fat derived from the diet or from endogenous synthesis. Meanwhile it is clear that white adipose tissue is also an important endocrine organ for review see Kershaw and Flier (2004) . The proteins that are produced and released by adipose tissue are called adipokines. It is important to note that white adipose tissue is not a homogeneous organ. The two best-described adipose tissue depots are subcutaneous and visceral adipose tissues. FFA, glycerol and hormones from visceral adipose tissue are directly released into the hepatic portal vein and thus have direct access to the liver, whereas the subcutaneous fat depots release their adipokines and metabolites into the systemic circulation. Therefore it is clear that visceral adipose tissue has a greater effect on hepatic metabolism than subcutaneous adipose tissue. Finally, the two adipose tissues have different adipokine secretion patterns, with visceral adipose...

Knut Borch Johnsen

In 1980, the World Health Organisation (WHO) ended a long phase of confusion by providing international standards for diagnosis and classification of diabetes 1 . Before this, confusion existed with respect to the glucose threshold for diagnosis of diabetes and other categories of glucose intolerance as well as the glucose load used for the oral glucose tolerance test. As always, however, new scientific data and insight combined with health political issues have led to several revisions of the diagnostic criteria and classification of patients with diabetes as well as with other categories of glucose intolerance. The first revision was made in 1985 2 , the second in 1999 3 and most recently the third revision came out in 2006 4 based on a collaborative effort between WHO and the International Diabetes Federation (IDF). In addition to these global definitions, national agencies like the American Diabetes Association (ADA) 5,6 as well as international organizations such as the IDF 7...


Sedative drugs that decrease ICP via an effect on cerebral metabolism and CBF include most of the intravenous anesthetic agents except keta-mine. All have a depressant effect on the central nervous system, resulting in a dose-related decrease in level of consciousness and metabolic rate. Propofol has a similar metabolic and vascular profile to barbiturates, causing a dose-related decrease in cerebral metabolic rate and coupled decrease in CBF, resulting in a reduction in ICP in patients with cerebral metabolic activity. However, in some studies the decrease in CBF exceeded the concomitant decrease in metabolic rate. Its pharmacokinetic profile, with a short half-life, makes it a particularly suitable sedative agent in neurosurgical patients, allowing prompt neurological assessment within 2-3 hours of discontinuation of the infusion in usual doses (50-150 g kg min). In a multicenter trial, propofol was efficacious in reducing ICP although the study failed to show an improvement in...

Lipid Metabolism

Adipose tissue is present in regional depots such as subcutaneous upper and lower body and visceral fat 11 . Apart from these classic depots fat is present in most other tissues, for example, connective tissue, bone marrow, liver and muscle. The picture is further complicated by the fact that within each tissue fat is distributed in compartments. In muscle for instance fat is present intramyocellularly, intermyocellularly and inter-muscularly. Under physiological conditions lipolysis

Insulin Therapy

As a consequence of the relentless deterioration in beta cell function in Type 2 diabetic patients with little, if any, improvement in insulin resistance with time exogenous insulin therapy is required to achieve adequate glycaemic control. During the UKPDS approximately 30 of obese and 22 of non-obese Type 2 DM patients required insulin within six years of diagnosis 1 . The introduction of insulin in Type 2 DM patients is however associated with weight gain which itself is likely to be detrimental to the underlying metabolic syndrome, glycaemic control and cardiac risk.


(1) There is a large bulk of evidence that using low GI foods has a greatly significant impact on the amelioration of the metabolic disturbances observed in diabetic and or hyperlipidemic patients and in subjects affected by the metabolic syndrome. Studies showing convincing evidence against this concept are very rare if any.

The Hypothesis

Insulin dependency is the end stage towards which all diabetes moves, the rate dependent on the accelerators present, and the notions of type 1 and type 2, insulin- and non-insulin-dependent, are consequently artificial. The development of diabetes is just a matter of time, and tempo is the only feature that distinguishes one type from another. Of the three accelerators, the first is intrinsic and others acquired. Insulin resistance, the second accelerator, is associated with visceral fat mass and is widely believed to explain the epidemic rise of type-2 diabetes in the industrially developed world 14 . The accelerator hypothesis argues that visceral weight gain is also central to type-1 diabetes, as much responsible for its rising incidence as for that of type 2, and the environmental factor in type-1 diabetes that has eluded epidemiology for so long.

Learning Elements

Improvement in the insulin resistance that underlies the pathogenesis of type 2 diabetes and the metabolic syndrome leads to pleiotropic effects, including reduced glycemia, enhanced beta cell function, reduction in the inflammatory milieu, improvement in dyslipidemia and blood pressure vascular endothelial function, cardiovascular risk reduction, and in the prevention of diabetes.

Diabetes Mellitus

DM is an increasing global health burden affecting more than 150 million people worldwide, with an ever increasing incidence and a prevalence that varies from population to population (1). The vast majority of patients suffering from DM have type 2 DM, a multi-faceted and heterogeneous metabolic syndrome characterized by fasting and postprandial hyperglycemia-due to peripheral insulin resistance resulting in a decreased insulinmediated glucose disposal, increased endogenous glucose production (mainly from the liver), and impaired pancreatic insulin secretion (2-4). Insulin resistance, or reduced responsiveness to circulating concentrations of insulin, is an early defect in type 2 DM and is often present years before the onset of hyperglycemia and the clinical diagnosis of diabetes (5). Therapeutic strategies with single or combination therapy have targeted the metabolic defects seen in type 2 DM either individually or in concert.

Subject Index

Lipoprotein Triglycerides Dysmetabolic syndrome, see Metabolic syndrome dietary fiber hypothesis 43, 44 effects in diet 100 Free fatty acids (FFAs) low glycemic index food effects 46, 47 metabolic syndrome levels 5-7, 10-12 Fructose bariatric surgery effects 10 metabolic syndrome 12

Weight Gain

Fluid retention, and increased appetite 65 . In general, improvement in glycemic control with decreased glycosuria and caloric retention and storage may result in expanded adipose tissue and body weight. Several studies have shown that the weight gain with TZDs may be associated with an increase in subcutaneous fat. However, at the same time, there is a reduction in visceral fat and an overall decrease in the ratio of visceral to subcutaneous fat. This change in fat distribution seems to underlie the improvement in glycemic control despite an overall increase in body weight.

Cytokines in OSA

OSA is commonly associated with obesity, and abdominal fat is a major reservoir of cytokines. OSA is commonly seen in middle-aged obese men. Vgontzas and colleagues (1997) showed that OSA patients have a greater amount of visceral fat compared to obese non-OSA controls and higher levels of the adipose tissue-derived hormone leptin. The authors concluded that there is a strong independent association among OSA, visceral obesity, and elevated IL-6, TNF-a levels. Other findings from these investigators support the view that sleep apnea in obese patients may be a manifestation of the Metabolic Syndrome, in that cytokines and insulin resistance are mediators of excessive daytime sleepiness and sleep apnea in humans. They propose a model of a bi-directional, feed forward, pernicious association between sleep apnea, sleepiness, inflammation, and insulin resistance, all promoting atherosclerosis and cardiovascular disease (Vgontzas, Bixler, and Chrousos 2005).

John F Beltrame

Syndrome X is the most extensively investigated coronary microvascular disorder and must be delineated from the metabolic syndrome X. The term was first coined by Kemp in 1973, in an accompanying editorial to a study by Arbogast and Bourassa. This landmark study demonstrated both ST segment depression and myocardial lactate production during rapid atrial pacing in 11 patients with angio-graphic obstructive epicardial coronary artery disease (group C) and also in 10 patients with angina but no epicar-dial coronary disease (group X). Today, syndrome X is broadly defined as chronic angina occurring in the absence of fixed or dynamic flow-limiting epicardial coronary obstructions on angiography. The diagnosis is most frequently made in patients with exertional angina, ST segment depression on exercise stress testing, and angiographically normal epicardial coronary arteries.


In another leptin mutant, the hyperphagic Zucker (fa fa) rat, ACS1 activity and mRNA have been shown to be 3.3- and 3.9-fold higher, respectively, in abdominal subcutaneous adipose tissue than in lean controls, and mesenteric ACS1 activity and mRNA concentrations were elevated 2.0- and 2.2-fold, respectively.58 These data are consistent with the greatly increased adipose lipid synthesis and storage characteristic of the Zucker (fa fa) rat. Liver ACS1 activity and mRNA levels were only modestly increased, but another previous study reported that in Zucker (fa fa) liver acyl-CoA is much more utilized for esterification to triacylglycerol than for P-oxidation (80 vs. 20 , respectively), compared with lean control rats (40 vs. 60 ).59 These observations are also consistent with a subcompartmental shift of ACS1 enzyme activity from mitochondria to microsomes.59 The mechanisms for the increased expression of the ACS1 gene in these animal models is unknown. Potential regulatory signals could...

Cancer Cachexia

Weight loss and malnutrition are problematic causes of symptom distress in cancer patients. Anorexia, weight loss and the associated fatigue as well as changes in body image can contribute to depression and decreased social interactions 59, 60 . It is especially relevant in relation to cancer patients to keep in mind that poor intake is rarely the most important cause of cancer-induced weight loss. Patients fed intravenously generally still lose weight, despite intake of adequate or even supraphysiologic calories. CCS is a metabolic syndrome that affects intermediary metabolism and substrate utilization, not just appetite. Therefore, particularly in patients with primary GI tract malignancies, it is rarely appropriate to undertake specialized nutrition support for anorexia or even GI obstruction unless there is a plan in place to treat the obstruction and the underlying cancer.


Syndrome ranging from steatosis to cirrhosis it affects 10-25 of people in the U.S. 18-20 . Nonalcoholic steatohepatitis (NASH) is the most severe form of NAFLD it is characterized by fatty liver, inflammation, necrosis and fibrosis and occurs in 50 of the obese population, but in only 3 of lean individuals 20 . Like many other chronic diseases, NASH is associated with metabolic syndrome 21, 22 . Obesity, dyslipidemia, hypertension, diabetes mellitus, hyperinsu-linemia and insulin resistance are common problems linked with the metabolic syndrome and NASH. Treatment of NAFLD includes diet changes, weight loss and insulin-sensitizing drugs 23 .

HP Sauerwein

The metabolic syndrome is a common metabolic disorder that results from the increasing prevalence of obesity. It also refers to a clustering of specific cardiovascular disease risk factors whose underlying pathophysiology is thought to be related to insulin resistance with an excessive flux of fatty acids implicated. Opinions have varied as to whether the metabolic syndrome should be defined to indicate mainly insulin resistance, the metabolic consequences of obesity, risk of cardiovascular disease, or simply a collection of statistically related factors. Based on these different viewpoints 4 definition sets of the metabolic syndrome are formulated. The pros and cons of each of them are extensively discussed. A major role in the etiology of the metabolic syndrome is ascribed to the occurrence of insulin resistance. Data are provided that insulin resistance can worsen the expression of this syndrome, but cannot have a primary role. Therefore, insulin resistance is not the main player...

Hormonal Effects

Hormone excess (unknown mechanism) Increases REM density Increases central obesity Leptin is a hormone recently identified to be associated with obesity and ventilatory control. Produced by subcutaneous adipocytes and to a lesser degree visceral adipocytes, leptin acts directly on the hypothalamus to reduce appetite and increase energy consumption (50). It also may have indirect effects on levels of reproductive hormones (51). Leptin has been shown to stimulate breathing, which in the face of increased work of breathing with obesity, may serve to preserve ventilation (29). Circulating levels of leptin are higher in women than men, which may be related to the distribution of adiposity and the higher relative contribution of subcutaneous fat versus visceral fat to leptin synthesis. In animal models, leptin has been shown to have a greater role in ventilatory control in obese female than in obese male mice during wake and NREM sleep (52). Thus, differences in leptin levels and function...

General Conclusions

These data support the hypothesis that exposure to intense acute stressor activates a cascade of physiological responses that work together to promote host survival. Here we suggest that in addition to classically associated consequences of activation of the SNS (i.e., pupil dilation, increased heart rate, increased respiration, increased muscular blood flow, etc.), the release of endogenous danger signals that prime immunity also occur. Thus we propose that SNS-induced release of eHsp72 should be considered a normal and adaptive feature of the stress response. If, however, SNS activation is chronic or excessive, then the response is maladaptive contributing to a plethora of negative effects such as immunosuppression and metabolic syndrome, a key antecedent to clinical atherosclerotic diseases and immunosuppression (Irwin, 1993 Kennedy et al., 2005b).

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