Nutrition

Samedi 29 septembre 2012 6 29 /09 /Sep /2012 12:33
Dr. Jonny Bowden. If you've ever struggled with weight gain, Jonny sheds some light on why that happens and the 5 "little demons" that seem to be out of your control that are conspiring to make you fat, particularly around your belly. Enjoy! Warmest regards, Daniel G. Amen, MD Founder, and Medical Director Amen Clinics, Inc. Article: Nobody smokes cigarettes because they didn’t get the memo about lung cancer. And nobody over-eats junk food because they didn’t get the memo about sugar. No, we continue to eat foods that pack on the belly fat not because we don’t know how bad those foods are, but because we can’t resist them – and that’s by design. You see, there are powerful forces that are seemingly outside of our control that conspire to not just make us fat, but also to make us sick, tired and even depressed. I call these forces the “little demons” and they wreak havoc on our ability to control our cravings, combat urges and avoid temptation and result in expanded waistlines, failed diets and drained energy. But there is a series of simple steps you can take to send these little demons scurrying, take back control of your life and your waistline. Let me explain. Little Demon #1: Addictive Food Big Food has learned how to layer their products with just the right, scientifically determined amounts of salt, fat and sugar to produce what they call “super-palatable” food – or what you and I would simple call “addictive”. Brain studies have shown that these foods are just as addictive as drugs, alcohol and gambling are. It’s no accident that “you can’t eat just one”. For example, your brain remembers the sensation of eating a CinnaBon; next time you smell one, your neurons secrete a brain chemical called dopamine which virtually insures that you won’t stop till you eat one. So next time you feel yourself being magnetically pulled to eat a particular food, just know that there is some mad food scientist smiling somewhere, eager to line his pockets at your expense, so turn the other way and don’t give him the satisfaction! Little Demon #2: Food Labeling Tricks Manufacturers have to list ingredients used in greatest amounts listed first. So when manufacturers don’t want you to know that the main ingredient is sugar, they deceive you by using a dozen different forms of sugar so they can list each one further down. Sneaky huh? For example, all of the following are sugar in disguise: agave nectar, barley malt syrup, dehydrated cane juice, dextrose, corn syrup, brown rice syrup, raw sugar, turbinado sugar, sucrose, maltodextrin. You can avoid succumbing to food labeling tricks by, well, avoiding foods that have labels in the first place! Shop around the perimeter of your grocery story and eat fresh, whole, real foods focusing on leafy green vegetables and grass-fed, pasture-raised or organic meats. Little Demon #3: The Troll in your Brain The reward pathways in our brains are powerful motivators, and they will trick your conscious mind every single time. Whenever you hear yourself saying, “Aw, just one won’t kill me”, “I just don’t have time to cook” or “I can start my diet tomorrow”, you can be sure that’s the big fat ugly “troll” in your brain, doing the bidding of your dopamine reward system. These voices can sabotage your willpower, but there is a way to turn the table: next time you hear this voice, think of it as coming from someone – or something else, like a troll. By externalizing this voice, you’ll then realize something “else” is trying to manipulate you and you can train yourself to ignore these voices. Little Demon #4: Chronic Stress Chronic stress may begin in your brain—but it ends up packing on packing on fat, especially around your belly. When you’re stressed, one way body responds is by churning out a big dose of cortisol. Cortisol “instructs” the body to preserve fat around the middle, stimulates insulin – the primary hormone responsible for storing the food you eat as fat – and it also breaks down muscle, slowing your metabolic rate and making fat storage certain. And cortisol sends a signal to the brain to “refuel” for an emergency, usually with foods highest in fat, salt and sugar. The result? You walk around stressed and starving and you’ll eat anything in sight, particularly the stuff that makes you fat and sick. Because it’s so hard to resist temptation when you are stressed, the #1 way to combat the effects of stress you can do is to take an inventory of your life, and figure out how to minimize stress as much as possible. Also consider doing some form of active relaxation, whether meditation, yoga, deep breathing or something similar. Little Demon #5: Cheap Food Available 24x7 The previous 4 little demons wouldn’t make much of a difference if the food that makes us fat and sick weren’t available. But it is. Everywhere. And that’s little demon #5. Hunting and gathering? Fooey. Just go to the nearest drive through or pick up the phone. The easiest way to combat this toxic food environment is to remove temptation from your immediate environment so it’s NOT convenient. For example, at home, get rid of all the sugary junk food that will tempt you when your defenses are down. If an urge comes, you’ll have created a practical barrier that’s large enough to give you enough time for that urge to pass. What to Do Next… These 5 little demons conspire to make us sick and fat – but that does NOT mean we are all doomed. Simply by reading this article and becoming aware of these little demons that silently influence you to get fat, you’ve taken the first step toward building a mental defense to withstand their assault. Yours truly, Jonny Bowden, PhD, CNS aka “the Rogue Nutritionist”™
Par Chronimed - Publié dans : Nutrition
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Vendredi 28 septembre 2012 5 28 /09 /Sep /2012 05:32
Gut bacteria to control obesity K. S. Jayaraman Indian scientists studying gut bacteria in lean and fat people report that the research may open up a "novel and natural way" of combating obesity1. © Macmillan South Africa The scientists, who studied the differences between the dominant gut microbiota of lean and obese Indians, discovered that certain bacterial groups are prominent in the obese in comparison to the lean. Since a large fraction of microbes inhabiting gut cannot be grown in the laboratory, they used methods based on the direct detection of their genetic material, DNA. These methods focus on a specific gene, called 16S rRNA gene present in all living organisms except viruses. They report, for the first time, an analysis and comparison of gut microbiota by sequencing 16S rRNA gene libraries. The study revealed that methane producing 'archaea' — a group of single-celled microorganisms genetically distinct from bacteria and often living in extreme environmental conditions — was one of the predominant organisms in the gut of obese people. The other major organisms in the obese were 'bacteroides', a genus of gram-negative, anaerobic, rod-shaped bacteria. Both are known to produce small chain fatty acids (SCFA) — specifically propionate and acetate. Acetate is known to increase adipose (fat) tissue in experimental animals. "The predominance of bacteroides and archea results in elevated glucose and SCFA supply resulting in obesity," Yogesh Shouche, the lead investigator at the National Centre for Cell Science in Pune told Nature India. "The phenomenon is reversed in lean individuals who have comparatively lower bacteroides and archaea." The researchers have identified a representative microbial diversity in Indians and demonstrated the prominence of certain bacterial groups in obese people. These studies are important in many ways, Shouche explains. "If one confirms the association of specific groups of microbes with leanness, then it opens up the possibility of having a novel, natural means of controlling obesity. Cultivating such microbes in the lab are especially important for this." Shouche admits that in order to establish a direct role of any bacteria in the pathogenesis or treatment of obesity, a much more in-depth study is required. "However, our work is a stepping stone in appreciation of obesity associated gut microbiota among Indians." A follow-up study2 threw a surprise when the researchers attempted the isolation of gut microflora. They noticed that more than 25% of the cultivated anaerobes — organisms that do not require oxygen for their growth — seemed to be new to science. This, Shouche said,"suggests that gut microflora in Indian population is under explored and is a good source for finding novel bacterial species." References Patil, D. P. et al. Molecular analysis of gut microbiota in obesity among Indian individuals. J. Biosci. 37, 647-657 (2012) | Article | PubMed | Marathe, N. et al. Changes in human gut flora with age: An Indian familial study. Biomed. Central (in press)
Par Chronimed - Publié dans : Nutrition
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Mardi 25 septembre 2012 2 25 /09 /Sep /2012 13:22
The inflammatory consequences of psychologic stress: relationship to insulin resistance, obesity, atherosclerosis and diabetes mellitus, type II. Authors Black PH. Journal Med Hypotheses. 2006;67(4):879-91. Epub 2006 Jun 15. Affiliation Department of Microbiology, Boston University School of Medicine, 715 Albany Street, Room L-501, Boston, MA 02118, United States. pblack@bu.edu Abstract Inflammation is frequently present in the visceral fat and vasculature in certain patients with cardiovascular disease (CVD) and/or adult onset Diabetes Mellitus Type II (NIDDM). An hypothesis is presented which argues that repeated acute or chronic psychologically stressful states may cause this inflammatory process. The mediators are the major stress hormones norepinephrine (NE) and epinephrine (E) and cortisol together with components of the renin-angiotensin system (RAS), the proinflammatory cytokines (PIC), as well as free fatty acids (ffa), the latter as a result of lipolysis of neutral fat. NE/E commence this process by activation of NF(kappa)B in macrophages, visceral fat, and endothelial cells which induces the production of toll-like receptors which, when engaged, produce a cascade of inflammatory reactions comprising the acute phase response (APR) of the innate immune system (IIS). The inflammatory process is most marked in the visceral fat depot as well as the vasculature, and is involved in the metabolic events which culminate in the insulin resistance/metabolic syndromes (IRS/MS), the components of which precede and comprise the major risk factors for CVD and NIDDM. The visceral fat has both the proclivity and capacity to undergo inflammation. It contains a rich blood and nerve supply as well as proinflammatory molecules such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), leptin, and resistin, the adipocytokines, and acute phase proteins (APP) which are activated from adipocytes and/or macrophages by sympathetic signaling. The inflammation is linked to fat accumulation. Cortisol, IL-6, angiotensin II (angio II), the enzyme 11(beta) hydroxysteroid dehydrogenase-1 and positive energy balance, the latter due to increased appetite induced by the major stress hormones, are factors which promote fat accumulation and are linked to obesity. There is also the capacity of the host to limit fat expansion. Sympathetic signaling induces TNF which stimulates the production of IL-6 and leptin from adipocytes; these molecules promote lipolysis and ffa fluxes from adipocytes. Moreover, catecholamines and certain PIC inhibit lipoprotein lipase, a fat synthesizing enzyme. The brain also participates in the regulation of fat cell mass; it is informed of fat depot mass by molecules such as leptin and ffa. Leptin stimulates corticotrophin releasing hormone in the brain which stimulates the SNS and HPA axes, i.e. the stress response. Also, ffa through portal signaling from the liver evoke a similar stress response which, like the response to psychologic stress, evokes an innate immune response (IIR), tending to limit fat expansion, which culminates in inflammatory cascades, the IRS-MS, obesity and disease if prolonged. Thus, the brain also has the capacity to limit fat expansion. A competition apparently exists between fat expansion and fat loss. In "western" cultures, with excessive food ingestion, obesity frequently results. The linkage of inflammation to fat metabolism is apparent since weight loss diminishes the concentration of inflammatory mediators. The linkage of stress to inflammation is all the more apparent since the efferent pathways from the brain in response to fat signals, which results in inflammation to decrease and limit fat cell mass, is the same as the response to psychologic stress, which strengthens the hypothesis presented herein.
Par Chronimed - Publié dans : Nutrition
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Mardi 25 septembre 2012 2 25 /09 /Sep /2012 13:22
AuthorsDuncan BB, et al. Show all Journal Sao Paulo Med J. 2001 May 3;119(3):122-7. Affiliation Social Medicine Department, School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. bbduncan@orion.ufrgs.br Abstract CONTEXT: The metabolic syndrome is characterized by a clustering, in free-living populations, of cardiovascular and diabetes risk factors generally linked to insulin resistance, obesity and central obesity. Consonant with the well-established inflammatory pathogenesis of atherosclerotic disease, the metabolic syndrome is now being investigated in relation to its inflammatory nature. OBJECTIVE: We present cross-sectional findings demonstrating that markers of inflammation correlate with components of the metabolic syndrome, and prospective findings of the ARIC Study indicating that markers of inflammation and endothelial dysfunction predict the development of diabetes mellitus and weight gain in adults. We present biological evidence to suggest that chronic activation of the innate immune system may underlie the metabolic syndrome, characterizing the common soil for the causality of type 2 diabetes mellitus and cardiovascular disease. CONCLUSIONS: Better understanding of the role of the innate immune system in these diseases may lead to important advances in the prediction and management of diabetes and cardiovascular disease.
Par Chronimed - Publié dans : Nutrition
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Mardi 25 septembre 2012 2 25 /09 /Sep /2012 13:20
The role of inflammatory cytokines in diabetes and its complications. Authors King GL. Journal J Periodontol. 2008 Aug;79(8 Suppl):1527-34. Affiliation Section on Vascular Cell Biology, Joslin Diabetes Center and Clinic, One Joslin Place, Boston, MA 02215, USA. george.king@joslin.harvard.edu Abstract The prevalence of diabetes worldwide is increasing rapidly in association with the increase in obesity. Complications are a major fear of patients with diabetes. Complications of diabetes affect many tissues and organs, causing retinopathy, nephropathy, neuropathy, cardiovascular diseases, peripheral vascular diseases, stroke, and periodontal pathologies. Immunologic abnormalities are associated with type 1 and type 2 diabetes and diabetic complications. T cell abnormalities are believed to be the major cause of autoimmune disease in type 1 diabetes, leading to the destruction of pancreatic islets. In type 2 diabetes, inflammation and activation of monocytes are postulated to be important for enhancing insulin resistance and may contribute to the loss of insulin secretory function by islet cells. Many factors can enhance insulin resistance, including genetics, a sedentary lifestyle, obesity, and other conditions, such as chronic inflammation or infection. Increases in inflammation, such as activation of monocytes and increased levels of inflammatory markers, e.g., C-reactive protein, plasminogen activator inhibitor-1, and other cytokines, were reported in insulin-resistant states without diabetes. One possible mechanism is that abnormal levels of metabolites, such as lipids, fatty acids, and various cytokines from the adipose tissue, activate monocytes and increase the secretion of inflammatory cytokines, enhancing insulin resistance. According to this model, obesity activates monocytes and enhances insulin resistance, increasing the risk for type 2 diabetes. Abnormalities in innate immunity might also participate in the development of diabetic complications. In general, hyperglycemia is the main initiator of diabetic retinopathy, nephropathy, and neuropathy, and it participates in the development of diabetic cardiovascular diseases. Although the precise role of inflammation in the development of diabetic microvascular diseases is still unclear, it is likely that inflammation induced by diabetes and insulin resistance can accelerate atherosclerosis in patients with diabetes. Also, it was shown that conditions with an inflammatory basis, such as obesity and type 2 diabetes, can contribute to periodontal disease, suggesting that periodontal abnormalities may be partly influenced by inflammatory changes. Further research is required to confirm the role of inflammation and the onset of diabetes, microvascular diseases, and periodontal pathologies.
Par Chronimed - Publié dans : Nutrition
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