Exercises to Burn Your Belly Fat in 4 Weeks

My Bikini Belly

If you are like most people, you are starting to worry that summer is around the corner and you don't look your best in a bikini Well don't you worry at all! There is actually a completely natural process that helps you lose belly fat and get the sexy body that you deserve this summer. Don't settle for looking a bit flabby around the middle or like the typical middle-aged woman You can get so much better! After you start reaching menopause, your molecules start to hold on to fat tighter than ever. However, specific workout that do NOT damage your menopause molecules. You have been taught the wrong sorts of exercise over the years; you may have noticed that you keep Gaining weight! But in this ebook, you will learn the exercises that truly give you the ability to lose weight and look your best! Read more...

My Bikini Belly Overview


4.8 stars out of 39 votes

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Martial Abs Discover How To Get Rid Of Belly Fat Once And For All

Step by step easy to follow video instructional from where ever you are. I go into the detailed approach on how to develop quicker than the others. Steal my knowledge and learn the best fat burning exercises all without equipment and can be done anywhere. I separate each section on three levels from beginner, intermediate and advanced so you keep progressing. Component 2: Follow Along Martial Ab Workout Videos (Value $47) So you never get confused or stuck on what exercise workout to do i have personally developed a easy to follow library of workout videos. Heres just some of what you will learn inside Separate difficulty level workouts to really test yourself. The forgotten old school martial arts core exercises that will get you burning fat in no time! Learn directly via video rather than trying to follow a complicated book full of pictures. Quick time workouts where you only need 10 minutes to get a killer workout. Component 3: What To Eat and What Not To Eat Audio (Value $27) Heres just some of what you will learn inside Learn what to eat, and what to avoid. We also cover one of the main foods that is locking in your belly fat very sneakily, and how you can prevent it. A non complicated approach which will keep you enjoying foods rather than having to starve yourself. Plus over 40 minutes of personal audio with me where i walk you through what you can eat and what you will want to avoid, plus my top favourite fat burning foods to get you started. Read more...

Martial Abs Discover How To Get Rid Of Belly Fat Once And For All Overview

Contents: Video Guide
Author: Richard Huntley
Official Website: martialabs.com
Price: $27.00

Personal Training Secrets To Lose Belly Fat And Get A Flat Stomach

Here's a sample of what you'll find in over 250 pages: The stress and cortisol belly fat connection The #1 Secret to a Beautiful Body The #1 Secret to increasing your metabolism and burning belly fat Foods that speed up your metabolism and help to burn belly fat More than 100 ab workout routines to add structure to your fitness program How to lose belly fat after pregnancy Secrets to never hit a weight loss plateau until you're at your goal The #1 myth many nutritionist are spreading that is keep you from having a thin waist How to develop motivation to help you reach your goals How to get flat abs after 50 The #1 trap mothers fall into that prevents losing baby fat on the abs The 5 biggest workout mistakes that prevent a flat stomach The 5 biggest lifestyle mistakes most women make that cause increased belly fat and body fat How many sit ups it takes to get a flat stomach Aerobic Exercise and Cardio Tips to Melt off Fat Hidden Secrets about how posture and flexibility affect your waistline How bad posture increases the size of your waist Key Stretches that can help you shrink your waistline 10 Top Weight Training exercises for a toned body and lean waist The unknown reason crunches are totally ineffective for most people. How slightly changing your crunch technique can triple the effectiveness The most important core muscle for a smaller waist and exercises that target it Learn about the stress and belly fat connection Learn easy ab exercises if you're a beginner Learn the best lower ab exercises and medicine ball ab exercises How much carbs is too much carbs Top exercises used by trainers and athletes

Personal Training Secrets To Lose Belly Fat And Get A Flat Stomach Overview

Contents: 250-page Ebook
Author: Charles Inniss
Official Website: www.ab-core-and-stomach-exercises.com
Price: $9.95

Scope of the Metabolic Syndrome Epidemic Prevalence and Risk

Estimates of MetS prevalence vary according to age, country, and ethnic group. Interpopulation comparisons have been complicated by the fact that it is probably inappropriate to use single threshold values for the defining quantitative traits. Abdominal obesity appears to be the most frequently found MetS component observed in a number of population-based studies, irrespective of ethnicity.8-10 There has been recent consideration of the appropriateness of uniform cutoff points for abdominal obesity, drawing attention to the need for ethnic-specific guidelines.11 Some investigators have already employed modified MetS criteria in order to identify better Asian individuals with MetS,12 yet clearly more investigation is required in this respect. Interestingly, other components, such as blood pressure, show distinctive variability between ethnic groups, being dominant features in African-American populations10 and Korean males.10 adults16 and in children with severe obesity.18 More...

Etiology of Metabolic Syndrome The Search for the Single Causal Mechanism

The recognition of the cluster of disorders characterizing MetS has sparked an ongoing examination of the potential for a single causal mechanism underlying the syndrome. This search for etiological mechanisms has largely focused on either the central role of insulin resistance and or the hormonal biochemical consequences of visceral obesity. The other major focus in the search for the single causal mechanism underlying MetS has been the cause consequences of visceral obesity. These relate to both hormonal and metabolic consequences of obesity. The impact of several adipocytokines has been examined for their roles as etiological factors in MetS. These include leptin, adiponectin, and resistin as well as inflammatory hormones (TNF-a) and additionally nonesterified free fatty acids.36 The pattern of endothelial dysfunction and sympathoadrenal activation has been linked to these mediators as well as the inflammatory phenotype characteristic of patients with MetS.

Obesity Overweight and Metabolic Syndrome

Include alterations in diet and nutrition and physical inactivity, both of which are also risk factors for CVD. Obesity not only increases the risk for the development of CVD but also for the development of type 2 diabetes. Thus, the risk factors for CVD can actually synergize with each other and produce greater changes in morbidity and mortality. The concept of synergy in combined risk factors is further reinforced when the metabolic syndrome is considered This disorder actually combines obesity, diabetes, and high blood pressure in such a way that an individual exhibiting two of the three of these disorders would be considered as part of the metabolic syndrome population. Additional discussion of the metabolic syndrome and the management of this complex disorder is available in this volume (see 6.17 Obesity Metabolic Syndrome Overview). While the obesity epidemic occurs worldwide, it is heavily concentrated in North America9 and especially in the USA where it is estimated that over...

Definition of Metabolic Syndrome

MetS is a commonly occurring cluster of clinical phenotypes that are individually and collectively strongly related to cardiovascular disease.2 MetS is characterized by disturbed carbohydrate and insulin metabolism, and is clinically defined by threshold values applied to indices of central obesity, dysglycemia, dyslipidemia, and or elevated blood pressure, which must be present concurrently in any one of a variety of combinations.2'3 The cardinal feature of MetS is abdominal obesity, as quantified most directly by increased waist circumference.4,5 Biochemically, MetS is characterized by insulin resistance - hyperinsulinemia - and by dyslipidemia - most typically raised triglycerides and or reduced HDL cholesterol. Additionally, a range of biochemical abnormalities have been secondarily associated, including increased serum concentrations of apolipoprotein B, fibrinogen, free fatty acids, C-reactive protein (CRP), tumor necrosis factor (TNF)-a, interleukin-6, and plasminogen activator...

Genes and the Metabolic Syndrome Monogenic Disorders

In addition to identifying genes for 'garden-variety' MetS, careful characterization of patients with rare monogenic disorders that recapitulate features of MetS have led to important insights that can be translated to the more common complex form. For instance, familial partial lipodystrophy (FPLD) syndromes are autosomal dominant disorders that occur with a frequency of perhaps 1 100 000 individuals in the general population.37-39 There are three distinct forms FPLD1, FPLD2, and FPLD3, of which the latter two have been found to be due to mutations, respectively, in the LMNA gene, encoding nuclear lamin A C and the PPAR-g gene, encoding peroxisome proliferator-g activated receptor (PPAR-g). Both FPLD2 and FPLD3 feature a loss of fat tissue in peripheral depots such as the extremities and gluteal region, with preservation of central and visceral fat stores. The infinite ratio of visceral to peripheral subcutaneous fat creates an extreme form of common visceral obesity, which leads to...

Metabolic syndrome

Effects for drugs that are used chronically. However, metabolic syndrome, including abdominal obesity, dyslipidemia, hypertension, and insulin resistance, have an increased prevalence in schizophrenics63 which may be genetically related. Weight gain in schizophrenics has been associated with the histamine H1 receptor affinity of antipyschotic medications86 with clozapine and olanazepine being the most potent of the current medications (Ki 1nM) and haloperidol (Ki 1800 nM, the least). The CATIE study55 noted that olanzapine, of the four atypical antipsychotics studied, was associated with the greatest incidence of weight gain (0.9 kg month_ 1) with greater increases in glycosylated hemoglobin, total cholesterol, and triglycerides, effects consistent with the development of metabolic syndrome.

Clinical manifestation

Skin changes facial plethora striae ecchymoses and purpura telangiectasias skin atrophy hirsutism and male pattern balding in women increased lanugo facial hair steroid acne acanthosis nigricans Central obesity increased adipose tissue in the face (moon facies), upper back at the base of neck (buffalo hump), and above the clavicles

And Insulin Sensitivity

In experimental rodent models, ACE inhibition has been shown to enhance glucose transport skeletal muscle and adipose tissue in insulin-resistant obese Zucker rats and spontaneously hypertensive rats (147-150). Angiotensin ATI receptor antagonism has been shown to improve insulin sensitivity and glucose uptake in skeletal muscle of normotensive diabetic KK-Ay mice (151), partially reduce insulin resistance in Wistar fatty rats (114), and increase 2DG uptake and GLUT-4 expression in skeletal muscle in obese Zucker rats (152). Because insulin resistance and the metabolic syndrome accelerate CVD (153) inhibition of the RAS may improve cardiovascular outcomes, in part, by increasing insulin sensitivity and improving metabolic control.

Clinical Trial Issues

While BMI is the most commonly used measure to assess the degree of overweight, there are concerns about how well it defines adiposity among different body types, between the genders, and among different racial and age groups. Since BMI does not really measure body composition, obesity trials may include other measures. For example, accumulation of central or visceral fat might be a better index of the overall association of obesity with morbidity, and therefore, a measure of waist-to-hip ratio may be appropriate in addition to calculating BMI. Noninvasive methods of measuring body composition in humans are available, e.g., DEXA and hydrostatic weighing. However, these can add substantially to trial costs and may not be readily available at most clinical trial sites.

Inner Ear Visible In

Classification Tympanic Atelectatic

To the level of the temporomandibular joint. The cavity can be exteriorized or obliterated with abdominal fat and the external auditory canal closed as cul-de-sac. When indicated, the resection can include a superficial parotidectomy, resection of the mandibular condyle, and or neck dissection. When the tumor has a deeper extension towards the middle ear, en-bloc subtotal resection of the temporal bone is indicated. In such cases, a middle and posterior fossa craniotomy is necessary. Bone removal is performed up to the level of the medial third of the petrous apex and the internal carotid artery. The facial nerve and inner ear are sacrificed. A more extended procedure is total en-bloc resection of the temporal bone entailing, in addition, the sacrifice of the internal carotid artery, closure of the sig-moid sinus and jugular bulb, and in some cases a total parotidectomy and neck dissection.

Effects of Estrogen on Risk Factors for Diabetes

The changes in lipid metabolism that occur with the menopause, including increased total and LDLC, triglycerides and Lp(a), and decreased HDL-C, resemble those of type 2 diabetes and the metabolic syndrome (12). Adverse changes in carbohydrate metabolism also emerge with the menopause including decreased insulin sensitivity and insulin secretion (128). These together with increased central adiposity contribute to the increased risk of CVD in postmenopausal women. The effects of estrogen on lipid parameters are discussed in detail in the first part of this chapter. A number of observational studies have also reported that estrogen improves insulin resistance in postmenopausal women, a factor that is predictive for the development of type 2 diabetes (125,129). Estrogen therapy also appears to prevent central fat distribution, a factor that is strongly associated with insulin resistance (126). Thus, estrogen can potentially prevent the insulin resistance associated with central obesity...

Polycystic Ovary Syndrome and Cardiovascular Risk

PAI-1 concentrations in blood are higher in women with PCOS as compared to those not affected. PAI-1 levels have been shown to be positively correlated with triglycerides, basal insulin and abdominal obesity (193). It was shown that impaired fibrinolysis and particularly the high levels of PAI-1 in selected groups of patients with CHD, is not a consequence of the coronary disease itself but it is rather related to the metabolic risk factors of atherosclerosis (194).

Dissect colon and wash out contents

Open the abdominal cavity of mice treated with TNBS longitudinally. Place the bladder and abdominal fat to the side. Identify the rectal area in the posterior cavity. Cut the area where the distal colon inserts into the rectum and slowly pass the colon tissue out of the abdominal cavity with forceps.

Other Potential Therapeutic Targets

Protein tyrosine phosphatase-1B (PTP1B) dephosphorylates the insulin receptor, thus blunting its ability to initiate the signal transduction cascade upon insulin binding.92 Genetically modified mice that lack PTP1B protein expression and animals treated with a specific PTP1B antisense oligonucleotide inhibit PTP1B and thereby restore activity to the insulin receptor, resulting in increased insulin sensitivity, improved glycemic control, and resistance to diet-induced obesity. PTP1B inhibition also reduces adipose tissue storage of triglyceride under conditions of overnutrition, and was not associated with any obvious toxicity. The effects of the loss of PTP1B in vivo were also remarkably specific for components of the insulin action cascade, in spite of cell studies suggesting that PTP1B may exert a regulatory influence on a variety of other signaling pathways. Overall, these studies have paved the way for the commercial development of PTP1B inhibitors, which may serve as a novel type...

Diabetes and Insulin Resistance

In humans, type 2 diabetes has been associated with decreased levels of adiponectin (14). In several studies, adiponectin has a negative correlation with fasting glucose, insulin, and insulin resistance and a positive association with insulin sensitivity, independent of BMI (9,14,44). One study demonstrated that adjusting for central obesity renders the negative correlation between adiponectin and insulin resistance no longer significant, suggesting that adiponectin may mediate the relationship between central obesity and insulin resistance (19). In studies involving Pima Indians, Japanese people, and Europeans, subjects with lower adiponectin were more likely to develop type 2 diabetes, independent of adiposity parameters (45-47). In contrast, type 1 diabetic patients have elevated adiponectin levels compared to nondiabetic individuals, and chronically administered insulin does not have an effect on adiponectin levels (48).

Mechanisms of Renal Dysfunction

Inflammation is an important contributor to the renal injury and endothelial dysfunction observed in hypertension and obesity. Elevated circulating levels of IL6 and TNF-a are observed in obesity and metabolic syndrome patients. IL6 stimulates the central and the sympathetic nervous system, which may result in hypertension.30 IL6 induces increases in hepatic triglyceride secretion in rats. IL6 also stimulates the production of C-reactive protein in liver and plasma levels of this protein are a good predictor of vascular inflammation. Another cytokine linked to obesity is TNF-a. TNF-a is overexpressed in the adipose tissue of obese patients, as compared with tissues from lean individuals. A positive correlation has been found between serum TNF-a concentration and both systolic blood pressure and insulin resistance in subjects with a wide range of adiposity. TNF- a acutely raises serum triglyceride levels in vivo by stimulating very low-density lipoprotein (VLDL) production and hence it...

ACE Inhibitors and Aldosterone Receptor Antagonism

Inhibition of ACE activity decreases the formation of AT-II and aldosterone and potentiates the vasodilatory effects of bradykinin. As a result, ACE inhibitors are used widely to treat hypertension. These agents reduce proteinuria and delay the progression of renal disease in patients with diabetic nephropathy or nondiabetic kidney disease. ACE inhibitors are effective in reducing renal damage in hypertensive animal models. For example, ACE inhibition prevents the development of glomerulosclerosis after subtotal nephrectomy in the remnant kidney rat model. The ACE inhibitor enalapril attenuates atherosclerosis and vascular inflammation induced by angiotensin II infusion in apolipoprotein E-deficient mice.73 ACE inhibition also inhibits development of nephrosclerosis in young spontaneous hypertensive rats treated with N-nitro-L-arginine methyl ester (l-NAME). The increase in kinin levels by ACE inhibition provides an additional renoprotective effect in LNAME spontaneous hypertensive...

Modified LDL Antibodies and LDLContaining Immunocomplexes

As suggested by recent reports showing that common carotid and femoral IMT are directly related to the levels of IgG oxLDL antibodies and inversely related to the levels of IgM oxLDL antibodies (196). Also of interest is the fact that the levels of IgG oxLDL and MDA-LDL antibodies are associated with the metabolic syndrome and smoking (197).

Abnormalities in the fibrinolytic system

Another well-recognized contributor to augmented activity of PAI-1 in diabetes is the adipocyte. PAI-1 may be released directly from an increased mass of adipose tissue, particularly visceral fat, and that may account, in part, for the association between obesity and impaired fibrinolysis (293-295). However, abnormal concentrations of cytokines such as TGF-P and TNF-a, may also contribute to augment PAI-1 expression in adipocytes (296). Other cytokines including IL-1 and -6 have also been implicated as agonists for PAI-1 synthesis (297). Another factor likely to influence PAI-1 expression in diabetes is the renin-angiotensin system (RAS) because PAI-1 synthesis is augmented

Effect of Insulin Resistance Treatment on Polycystic Ovary Syndrome Weight Loss

Data on HRT in postmenopausal women with diabetes are scarce but are of major importance, because these women are characterized by hyperandrogenicity, insulin resistance, and dyslipidemia and are at a higher risk for developing CHD. Evidence from the available data suggest that short-term unopposed oral estradiol has a beneficial effect on glucose homeostasis, lipid profile, and other components of the metabolic syndrome, which may be compatible with a reduced risk of CHD. The addition of a progestogen may attenuate some of these favourable effects. On the other hand, HRT consisting of continuous combined transdermal 17 -estradiol and oral norethisterone, reduces plasma triglycerides and cholesterol concentrations, factor VII activity and von Willebrand factor antigen levels without concomitant changes in adiposity and glycemic control. These effects, allied with favorable effects on CRP and potential beneficial effects on vascular reactivity, suggest that this regimen may hold...


Over the last 15 years, it has become established that insulin is a vascular hormone. Insulin's vascular actions extend beyond its effect to increase skeletal muscle blood flow and glucose uptake. Current data suggest that insulin modulates vascular tone, and vascular smooth muscle cell proliferation and migration via the release of NO and other yet unidentified mechanisms. Thus, insulin's effects on the vascular system may be important to prevent or delay the progression of CVD. The metabolic syndrome affects the vascular system at multiple levels. Resistance to the vascular actions of insulin may explain, at least in part, the abnormalities associated with the metabolic syndrome. The altered state of the vascular system in the metabolic syndrome may contribute to the higher rates of hypertension and macrovascular disease. Future research assessing the interaction between insulin's effect on the vasculature and newly discovered adipocytokines and other vasoactive hormones will better...


Recent findings have shown that small, dense LDLs, and excess triglyceride-rich remnants, which are highly atherogenic, are increased in the insulin-resistant states (105). Hyperinsulinemia and central obesity, which are commonly accompanied by insulin resistance and type 2 diabetes can lead to an overproduction of very low-density lipoproteins (VLDLs) (106). VLDL particles contain a number of apolipoproteins and triglycerides. Increased free fatty acid and glucose levels can increase VLDL output from the liver, and elevated triglyceride levels can inhibit apoB degradation, resulting in increased secretion of VLDL. Lipoprotein lipase (LPL) activity in decreased in diabetic patients because insulin is a major regulator of LPL activity. Because LPL is necessary for the breakdown of chylomicrons and triglycerides and results in decreased clearance of VLDL, decreases in LPL activity are one of the causes for the increase in VLDLs. A decrease in LDL levels results in more glyceride-rich...

Praderwilli Syndrome

Excessive or rapid weight gain on weight-for-length chart (excessive is defined as crossing two centile channels) after 12 months but before 6 years of age central obesity in the absence of intervention. 3. Excessive eating (hyperphagia, obsession with food) with central obesity if uncontrolled. 2. Excessive eating (hyperphagia, obsession with food) with central obesity if uncontrolled.


Additionally, differences in insulin sensitivity between women and men may also explain the higher rates of NO production release in women. Indeed, previous reports have indicated that women display higher insulin sensitivity than men of similar age and body mass index (113) suggesting that sex modulates the association between body fat distribution (central vs peripheral) and insulin sensitivity. Therefore, the enhanced endot-helial function observed in women may be secondary to the higher insulin sensitivity in women than men. Type 2 diabetes with associated central obesity and insulin resistance may obviate this sex advantage in women.

With diabetes

Healthy postmenopausal women undergo changes in lipoprotein and carbohydrate metabolism and in the pattern of body fat distribution similar to those of patients with diabetes. In fact, a picture resembling the metabolic syndrome emerges with the menopause (12). Replacement therapy with estrogen can improve the adverse impact of meno Postmenopausal women with diabetes are at risk of dyslipidemia, central obesity, hypertension, and accelerated atherosclerosis, all of which can contribute to an increased risk of CVD (127). Thus, postmenopausal women with diabetes could benefit from a reduced risk of CVD with the use of HRT. However, whether HRT confers cardiovascular protection in postmenopausal women with diabetes is currently unknown and remains an issue for further clinical research. An attempt is made in this section to shed some light in this issue based on current evidence. This is preceded by a brief review of the effects of estrogen on risk factors for diabetes and the metabolic...


In 1998, Giora Feuerstein joined DuPont Pharmaceuticals as the head of the Cardiovascular Disease Department leading thrombosis, cardiovascular, and metabolic syndrome programs. Razaxaban, a lead FXa inhibitor was advanced to phase II development prior to acquisition of the DPC by BMS. In 2003 Giora Feuerstein joined Merck Co, Inc, West Point as the Executive Director, cardiovascular diseases where he established a new department leading efforts in hypertension (renin inhibitors), metabolic syndrome and cardiac arrhythmias. In addition, Giora Feuerstein was appointed as member of strategic forums in cardiovascular drug development and chaired licensing and business development committees.

Renal Dysfunction

In addition to a role in producing the products stored in, and voided from, the bladder, the renal system is a key system in the regulation of blood pressure via its role in regulating blood volume. Diseases of the kidney encompass renal dysfunction and end-stage renal disease (ESRD), the result of the metabolic syndrome, diabetes, obesity, and hypertension (see 6.25 Renal Dysfunction in Hypertension and Obesity). Treatments to deal with these issues initiate with lifestyle changes, diet, and exercise, are progressively followed with drug regimens to treat the diabetes, obesity, and hypertension, kidney dialysis to restore normal function, and kidney transplant.


The worldwide prevalence of ED has been estimated at over 152 million males with projections for 2025 being in excess of 320 million. In older males, ED may have a physical cause, such as disease, injury, drug side effects, injury to nerves, arteries, smooth muscles, and fibrous tissues, or impaired blood flow in the penis. Other common causes of organic ED include the metabolic syndrome, diabetes, kidney disease, chronic alcoholism, multiple sclerosis, atherosclerosis, vascular disease, and neurologically related causes.9 The incidence of ED increases with age with approximately 5 of 40-year-old males and 15-25 of 65-year-old males experiencing aspects of ED. Surgery, including radical prostatectomy and bladder cancer surgery, can injure nerves and arteries near the penis, causing ED. Antihypertensives, antihistamines, antidepressants, and hypnotics can produce ED as a side effect. Psychological factors including stress, anxiety, guilt, depression, low self-esteem, and fear of sexual...

Cyp2c Cyp2j

Stimulation of the RAS increases sodium and water reabsorption through direct actions on renal tubular transport function 44.44 This effect is mainly due to the stimulation of AT-1 receptor by AT-II. Activation of angiotensin receptors by AT-II also stimulates synthesis of aldosterone in the zona glomerulosa of the adrenal gland. Aldosterone binds mineralocorticoid receptors expressed in the kidney and other organs leading to more salt and water retention. Aldosterone is involved in the development of obesity-induced hypertension. Plasma aldosterone levels are elevated in hypertensive patients with visceral obesity,45 and blocking mineralocorticoid receptors with the specific antagonist, eplerenone, inhibits development of high blood pressure in dogs fed a high-fat diet.46


However, although it is clear that administration of exogenous insulin do not lead to an increase in macrovascular disease, hyperinsulinemia syndromes like the insulin resistance syndrome, particularly when associated with central obesity, are definitively associated with accelerated development of macrovascular disease. Although the insulin resistance syndrome, characterized by glucose intolerance and hyperinsulinemia, is associated with several cardiovascular risk factors including dyslipidemia, hypertension, and dysfibrinolysis, the increased risk for macrovascular disease cannot be fully explained by the hypertension and dyslipidemia. It is likely that endothelial dysfunction, an important player in determining increased risk for macrovascular disease is involved.

Lose The Belly Fat

Lose The Belly Fat

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