Easy Hearty And Healthy Chili Recipe
Fall is here, and with it the familiar chill in the air signaling winter can't be far behind. This satisfying chili is one of my favorite ways to warm up from an afternoon outdoors. It's great for tailgating too. There are a few tips to make the most of this recipe. For a quicker prep time replace the chopped peppers with one package of frozen stoplight peppers (red, yellow and green). You can use ground ostrich or ground emu in place of the turkey. Both have the flavor of beef but are much more Zone friendly. For a thinner chili use the larger can of tomatoes. If you like things on the mild side, reduce the amount of chili powder. I use a low-sodium unfermented type of soy sauce (Bragg's Liquid Aminos) in place of salt. It adds a little salt plus some additional flavor. To double or triple the recipe for a crowd, make it in a stockpot or Dutch oven with a heavy bottom suitable for sautéing the meat and vegetables. Place the optional toppings in cereal-sized bowls so that your family or guests can choose their own. Sue's Turkey Chili (Makes four 3-block servings) Ingredients: 1 large onion, chopped 2-3 cloves garlic, minced 4 teaspoons olive oil 1 1/2-2 tablespoons chili powder 1/2 teaspoon cocoa powder, adjust to your taste 1 1/2 - 2 teaspoons cumin 1 teaspoon onion powder 1 lb. ground turkey 1 large red bell pepper, chopped 1 large yellow bell pepper, chopped 1 large green bell pepper, chopped 1 can diced tomatoes in juice, either 14.5 oz., or 28 oz., do not drain the juice 1/2 can (about 3/4 cup) black beans, drained and rinsed 1/2 can (about 3/4 cup) kidney beans, drained and rinsed 1 teaspoon low-sodium soy sauce Garnish 4 rounded tablespoons shredded low-fat cheese 4 tablespoons plain yogurt Optional Additional Toppings: Diced fresh tomato, diced avocado, sliced jalapeno's, guacamole, cilantro, a few crumbled baked corn chips, chopped scallions, salsa, pico de gallo (a mixture of diced tomatoes, onions, garlic, cilantro, lime juice, salt and pepper), hot sauce Directions: In a large skillet over medium heat sauté the onion and garlic in olive oil until transparent. Stir in the chili powder, cocoa powder, cumin and onion powder, mixing well to thoroughly coat the onions. Add the turkey, stirring constantly until cooked through with no pink remaining. Add the peppers and cook 2 to 3 minutes longer, just until slightly softened. Stir in the diced tomatoes with juice, black beans, kidney beans and soy sauce. Bring to a boil; then reduce heat and simmer, covered, for 20 to 30 minutes. Ladle into bowls to serve. Top each bowl with 1 tablespoon of shredded cheese, 1 tablespoon of yogurt, and the desired optional toppings. Enjoy!
What is Cellular Inflammation?
People (including virtually all physicians) are constantly confused what cellular inflammation is. So I decided to take the opportunity to explain the concept in more detail. There are two types of inflammation. The first type is classical inflammation, which generates the inflammatory response we associate with pain such as, heat, redness, swelling, pain, and eventually loss of organ function. The other type is cellular inflammation, which is below the perception of pain. Cellular inflammation is the initiating cause of chronic disease because it disrupts hormonal signaling networks throughout the body. Definition of Cellular Inflammation The definition of cellular inflammation is increased activity of the gene transcription factor know as Nuclear Factor-kappaB (NF-κB). This is the gene transcription factor found in every cell, and it activates the inflammatory response of the innate immune system. Although the innate immune system is the most primitive part of our immune response, it has been resistant to study without recent breakthroughs in molecular biology. In fact, the 2011 Nobel Prize in Medicine was awarded for the earliest studies on the innate immune system and its implications in the development of chronic disease. There are several extracellular events through which NF-κB can be activated by distinct mechanisms. These include microbial invasion recognized by toll-like receptors (TLR), generation of reactive oxygen species (ROS), cellular generation of inflammatory eicosanoids, and interaction with inflammatory cytokines via defined cell surface receptors. We also know that several of these initiating events are modulated by dietary factors. This also means that appropriate use of the diet can either turn on or turn off the activation of NF-κB. This new knowledge is the foundation of anti-inflammatory nutrition (1-3). Understanding Cellular Inflammation Although the innate immune system is exceptionally complex, it can be illustrated in a relatively simple diagram as shown below in Figure 1. Figure 1. Simplified View of the Innate Immune System Essential fatty acids are the most powerful modulators of NF-κB. In particular, the omega-6 fatty acid arachidonic acid (AA) activates NF-κB, whereas the omega-3 fatty acid eicosapentaenoic acid (EPA) does not (4). Recent work suggests that a subgroup of eicosanoids known as leukotrienes that are derived from AA may play a significant factor in NF-κB activation (5,6) Extracellular inflammatory cytokines can also activate NF-κB by their interaction with specific receptors on the cell surface. The primary cytokine that activates NF-κB is tumor necrosis factor (TNF) (7). Toll-like receptors (TLR) are another starting point for the activation of NF-κB. In particular, TLR-4 is sensitive to dietary saturated fatty acids (8). The binding of saturated fatty acids to TLR-4 can be inhibited by omega-3 fatty acids such as EPA. Finally ROS either induced by ionizing radiation or by excess free radical formation are additional activators of NF-κB (9). Anti-inflammatory Nutrition To Inhibit Cellular Inflammation Anti-inflammatory nutrition is based on the ability of certain nutrients to reduce the activation of NF-κB. The most effective way to lower the activation of NF-κB is to reduce the levels of AA in the target cell membrane thus reducing the formation of leukotrienes that can activate NF-κB. Having the patient follow an anti-inflammatory diet, such as the Zone Diet coupled with the simultaneous lowering omega-6 fatty acid intake are the primary dietary strategies to accomplish this goal (1-3). Another effective dietary approach (and often easier for the patient to comply with) is the dietary supplementation with adequate levels of high-dose fish oil rich in omega-3 fatty acids, such as EPA and DHA. These omega-3 fatty acids taken at high enough levels will lower AA levels and increase EPA levels. This change of the AA/EPA ratio in the cell membrane will reduce the likelihood of the formation of inflammatory leukotrienes that can activate NF-κB. This is because leukotrienes derived from AA are pro-inflammatory, whereas those from EPA are non-inflammatory. The increased intake of omega-3 fatty acids is also a dietary approach that can activate the anti-inflammatory gene transcription factor PPAR-γ (10-12), decrease the formation of ROS (13) and decrease the binding of saturated fatty acids to TLR-4 (14). This illustrates the multi-functional roles that omega-3 fatty acids have in controlling cellular inflammation. A third dietary approach is the adequate intake of dietary polyphenols. These are compounds that give fruits and vegetables their color. At high levels they are powerful anti-oxidants to reduce the generation of ROS (15). They can also inhibit the activation of NF-κB (16). Finally, the least effective dietary strategy (but still useful) is the reduction of dietary saturated fat intake. This is because saturated fatty acids will cause the activation of the TLR-4 receptor in the cell membrane (8,14). Obviously, the greater the number of these dietary strategies implemented by the patient, the greater the overall effect on reducing cellular inflammation. Clinical Measurement of Cellular Inflammation Since cellular inflammation is confined to the cell itself, there are few blood markers that can be used to directly measure the levels of systemic cellular inflammation in a cell. However, the AA/EPA ratio in the blood appears to be a precise and reproducible marker of the levels of the same ratio of these essential fatty acids in the cell membrane. As described above, the leukotrienes derived from AA are powerful modulators of NF-κB. Thus a reduction in the AA/EPA ratio in the target cell membrane will lead to a reduced activation of NF-κB by decreased formation of inflammatory leukotrienes. The cell membrane is constantly being supplied by AA and EPA from the blood. Therefore the AA/EPA ratio in the blood becomes an excellent marker of the same ratio in the cell membrane (17). Currently the best and most reproducible marker of cellular inflammation is the AA/EPA ratio in the blood as it represents an upstream control point for the control of NF-κB activation. The most commonly used diagnostic marker of inflammation is C-reactive protein (CRP). Unlike the AA/EPA ratio, CRP is a very distant downstream marker of past NF-κB activation. This is because one of inflammatory mediators expressed in the target cell is IL-6. It must eventually reach a high enough level in the blood to eventually interact with the liver or the fat cells to produce CRP. This makes CRP a more long-lived marker in the blood stream compared to the primary inflammatory gene products (IL-1, IL-6, TNF, and COX-2) released after the activation of NF-κB. As a consequence, CRP is easier to measure than the most immediate inflammatory products generated by NF-κB activation. However, easier doesn’t necessarily translate into better. In fact, an increase AA/EPA ratio in the target cell membrane often precedes any increase of C-reactive protein by several years. An elevated AA/EPA ratio indicates that NF-κB is at the tipping point and the cell is primed for increased genetic expression of a wide variety of inflammatory mediators. The measurement of CRP indicates that NF-κB has been activated for a considerable period of time and that cellular inflammation is now causing systemic damage. In Summary I believe the future of medicine lies in the control of cellular inflammation. This is most effectively accomplished by the constant application of anti-inflammatory nutrition. The success of such dietary interventions can be measured clinically by the reduction of the AA/EPA ratio in the blood. {{cta('4f5c5df9-024e-4218-ab5e-8490f8243f6f')}} References: Sears B. The Anti-Inflammation Zone. Regan Books. New York, NY (2005). Sears B. Toxic Fat. Thomas Nelson. Nashville, TN (2008). Sears B and Riccordi C. “Anti-inflammatory nutrition as a pharmacological approach to treat obesity.” J Obesity doi:10.1155/2011/431985 (2011). Camandola S, Leonarduzzi G,Musso T, Varesio L, Carini R, Scavazza A, Chiarpotto E, Baeuerle PA, and Poli G. “Nuclear factor kB is activated by arachidonic acid but not by eicosapentaenoic acid.” Biochem Biophys Res Commun 229:643-647 (1996). Sears DD, Miles PD, Chapman J, Ofrecio JM, Almazan F, Thapar D, and Miller YI. “12/15-lipoxygenase is required for the early onset of high fat diet-induced adipose tissue inflammation and insulin resistance in mice.” PLoS One 4:e7250 (2009). Chakrabarti SK, Cole BK, Wen Y, Keller SR, and Nadler JL. “12/15-lipoxygenase products induce inflammation and impair insulin signaling in 3T3-L1 adipocytes.” Obesity 17:1657-1663 (2009). Min JK, Kim YM, Kim SW, Kwon MC, Kong YY, Hwang IK, Won MH, Rho J, and Kwon YG. “TNF-related activation-induced cytokine enhances leukocyte adhesiveness: induction of ICAM-1 and VCAM-1 via TNF receptor-associated factor and protein kinase C-dependent NF-kappaB activation in endothelial cells.” J Immunol 175: 531-540 (2005). Kim JJ and Sears DD. “TLR4 and Insulin Resistance.” Gastroenterol Res Pract doi:10./2010/212563 (2010). Bubici C, Papa S, Dean K, and Franzoso G. “Mutual cross-talk between reactive oxygen species and nuclear factor-kappa B: molecular basis and biological significance.” Oncogene 25: 6731-6748 (2006). Li H, Ruan XZ, Powis SH, Fernando R, Mon WY, Wheeler DC, Moorhead JF, and Varghese Z. “EPA and DHA reduce LPS-induced inflammation responses in HK-2 cells: Evidence for a PPAR-gamma-dependent mechanism.” Kidney Int 67: 867-874 (2005). Kawashima A, Harada T, Imada K, Yano T, and Mizuguchi K. “Eicosapentaenoic acid inhibits interleukin-6 production in interleukin-1beta-stimulated C6 glioma cells through peroxisome proliferator-activated receptor-gamma.” Prostaglandins LeukotEssent Fatty Acids 79: 59-65 (2008). Chambrier C, Bastard JP, Rieusset J, Chevillotte E, Bonnefont-Rousselot D, Therond P, Hainque B, Riou JP, Laville M, and Vidal H. “Eicosapentaenoic acid induces mRNA expression of peroxisome proliferator-activated receptor gamma.” Obes Res 10: 518-525 (2002). Mas E, Woodman RJ, Burke V, Puddey IB, Beilin LJ, Durand T, and Mori TA. “The omega-3 fatty acids EPA and DHA decrease plasma F(2)-isoprostanes.” Free Radic Res 44: 983-990 (2010). Lee JY, Plakidas A, Lee WH, Heikkinen A, Chanmugam P, Bray G, and Hwang DH. “Differential modulation of Toll-like receptors by fatty acids: preferential inhibition by n-3 polyunsaturated fatty acids.” J Lipid Res 44: 479-486 (2003). Crispo JA, Ansell DR, Piche M, Eibl JK, Khaper N, Ross GM, and Tai TC. “Protective effects of polyphenolic compounds on oxidative stress-induced cytotoxicity in PC12 cells.” Can J Physiol Pharmacol 88: 429-438 (2010). Romier B, Van De Walle J, During A, Larondelle Y, and Schneider YJ. “Modulation of signaling nuclear factor-kappaB activation pathway by polyphenols in human intestinal Caco-2 cells.” Br J Nutr 100: 542-551 (2008). Yee LD, Lester JL, Cole RM, Richardson JR, Hsu JC, Li Y, Lehman A, Belury MA, and Clinton SK. “Omega-3 fatty acid supplements in women at high risk of breast cancer have dose-dependent effects on breast adipose tissue fatty acid composition.” Am J Clin Nutr 91: 1185-1194 (2010).
How Polyphenols Make Probiotics Work Better
Today we hear a lot about probiotics, especially when popular yogurts are fortified with them. So what are they? The term probiotics is simply a synthesized word for live microorganisms (bacteria or yeast) that may have some health benefits. In the lower part of your gut, you have a virtual zoo of microorganisms. Some are beneficial; others are very harmful. In fact, it is estimated that you have 10 times as many microorganisms in the gut than the entire number of cells that constitute your body. Of the hundreds of different microorganisms in the gut, two usually stand out as probiotic stars: Lactobacillus and bifidobacterium. It appears that selected strains of these particular microorganisms have anti-inflammatory properties, which inhibit the activity of nuclear factor-κB (NF-κB), the genetic “master switch” that turns on inflammation (1,2). Certain yeasts secrete a soluble factor that also inhibits NF-κB (3), and this may be the same mechanism that those “friendly” bacteria use to reduce inflammation. But here's the problem with probiotics — you have to get enough of the live organisms into the gut to provide any benefits. It's easy to fortify them into some yogurt product that is kept at low temperature, but getting those bacteria to pass through the digestive system and reach the lower part of the large intestine is another story. It is estimated that 99.999 percent of the live probiotics are digested in the process. So how can you enhance the biological action of those extremely few probiotics that actually make it alive to the lower intestine? The answer is polyphenols. Like probiotics, polyphenols also inhibit NF-κB (4,5). In fact, polyphenols are the primary agents that protect plants from microbial attack. Unlike probiotics, polyphenols are more robust in their ability to reach the lower intestine. But like probiotics you have to take enough polyphenols to have a therapeutic effect in the gut. You will probably need at least 8,000 ORAC units per day to maintain adequate levels of polyphenols in the gut. That is approximately 10 servings of fruits and vegetables per day. But if you want to significantly reduce the existing inflammatory burden in the gut and the rest of body, you have to consume a lot more polyphenols. Supplementation with highly purified polyphenols becomes your only realistic alternative. And here is where I think the real benefits of dietary polyphenols may reside. By reducing the inflammatory load in the gut, you can automatically reduce the anti-inflammatory load in the rest of the entire body. So before you take that next serving of probiotic-fortified yogurt, make sure you are taking adequate levels of polyphenols to make sure those probiotics actually deliver their marketing promises. References: Hegazy SK and El-Bedewy MM. “Effect of probiotics on pro-inflammatory cytokines and NF-kappaB activation in ulcerative colitis.” World J Gastroenterol 16: 4145-4151 (2010). Bai AP, Ouyang Q, Xiao XR, and Li SF. “Probiotics modulate inflammatory cytokine secretion from inflamed mucosa in active ulcerative colitis.” Int J Clin Pract 60: 284-288 (2006). Sougioultzis S, Simeonidis S, Bhaskar KR, Chen X, Anton PM, Keates S, Pothoulakis C, and Kelly CP. “Saccharomyces boulardii produces a soluble anti-inflammatory factor that inhibits NF-kappaB-mediated IL-8 gene expression. Biochem Biophys Res Commun 343: 69-76 (2006). Romier B, Van De Walle J, During A, Larondelle Y, and Schneider YJ. “Modulation of signaling nuclear factor-kappaB activation pathway by polyphenols in human intestinal Caco-2 cells.” Br J Nutr 100: 542-551 (2008). Jung M, Triebel S, Anke T,Richling E, and Erkel G. “Influence of apple polyphenols on inflammatory gene expression.” Mol Nutr Food Res 53: 1263-1280 (2009).
The Real Secret To Weight Loss: Increased Satiety
Satiety is defined as lack of hunger. If you aren’t hungry, then cutting back calories is easy. Unfortunately, Americans seem to be hungrier than ever. This is not caused by a lack of willpower but due to hormonal imbalances in the hypothalamus that tell the brain to either seek more food or spend time on more productive activities. So the real question is not what is the best diet for weight loss, but what is the best diet for satiety? The anti inflammatory diet has been clinically shown to burn fat faster than standard, recommended diets (1-3) as well as decreasing hunger compared to standard, recommended diets (4,5). But then whoever said that standard, recommended diets (like the USDA Food Pyramid) are good? A better comparison might be the anti inflammatory diet versus a Mediterranean diet. I have often said that the anti inflammatory diet should be considered as the evolution of the Mediterranean diet because of its enhanced hormonal control. So where is the data for my contention? The first randomized controlled research appeared in 2007 using patients with existing heart disease (6). In this study, while both groups lost weight, it was only the group on a Paleolithic diet that had any benefits in glucose reduction. So what’s a Paleolithic diet? In this study it was one that supplied 40 percent of the calories as low-glycemic-load carbohydrates, 28 percent of the calories as low-fat protein, and 28 percent from fat (the remaining calories came from alcohol, which didn’t exist in Paleolithic times). That sounds exactly like the anti inflammatory diet to me, so I will simply call it that. On the other hand, the Mediterranean diet was lower in protein (20 percent) and higher in carbohydrates (50 percent) as well as containing far more cereals and dairy products than the anti inflammatory diet. The interesting thing that came out of this initial study was that patients on the anti inflammatory diet were apparently eating fewer calories, but with greater satiety. So they repeated the study again with another set of cardiovascular patients, except they measured leptin levels this time. The results were exactly the same (7), that is the anti inflammatory diet was more satiating per calorie, and there was also a greater reduction in leptin levels. This makes perfect sense since improved glycemic control seen in the first comparison study (6) would have been a consequence of reducing insulin resistance. The decrease in the leptin levels in the second study (7) would have been a consequence of the reduction of leptin resistance. The most likely cause of this hormone resistance would be the anti-inflammatory benefits of the anti inflammatory diet because it decreases cellular inflammation. It’s cellular inflammation that disrupts hormonal signaling efficiency and causes hormone resistance. So here we have two randomized controlled studies (6,7) that indicate the superiority of the anti inflammatory diet compared to Mediterranean diet relative to reducing hormone resistance as well providing greater satiety with fewer calories, just as demonstrated in earlier studies when the anti inflammatory diet was compared to standard recommended diets (4,5). It is increased satiety that is ultimately how you lose weight and keep it off. The anti inflammatory diet appears the easiest way to reach that goal. References: Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, and Christou DD. “A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women.” J Nutr 133: 411-417 (2003). Lasker DA, Evans EM, and Layman DK, “Moderate-carbohydrate, moderate-protein weight-loss diet reduces cardiovascular disease risk compared to high-carbohydrate, low-protein diet in obese adults. A randomized clinical trial.” Nutrition and Metabolism 5: 30 (2008). Fontani G, Corradeschi F, Felici A, Alfatti F, Bugarini R, Fiaschi AI, Cerretani D, Montorfano G, Rizzo AM and Berra B. “Blood profiles, body fat and mood state in healthy subjects on different diets supplemented with omega-3 polyunsaturated fatty acids.” Eur J Clin Invest 35: 499-507 (2005). Ludwig DS, Majzoub JA, Al-Zahrani A, Dallal GE, Blanco I, and Roberts SB. “High glycemic-index foods, overeating, and obesity.” Pediatrics 103:e26 (1999). Agus MSD, Swain JF, Larson CL, Eckert E, and Ludwig DS. “Dietary composition and physiological adaptations to energy restriction.” Am J Clin Nutr 71: 901-907 (2000). Lindberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjostrom K and Ahren B. “A Paleolithic diet improves glucose tolerance more than a Mediterrean-like diet in individuals with ischaemic heart disease.” Diabetologia 50: 1795-1807 (2007). Jonsson T, Granfeldt Y, Erlanson-Albertsson, Ahren B, and Lindeber S. “A Paleolithic diet is more satiating per calorie than a Mediterrean-like diet in individuals with ischemic heart disease.” Nutrition & Metabolism 7:85 (2010).
The Secret Of Blueberries: It’s The Dephinidins
We continually hear about the benefits of fruits and vegetables for better health. There are a number of them. One is obviously their lower glycemic load that reduces insulin secretion. Another is their polyphenol content that gives fruits and vegetables their colors. Although virtually no research was conducted on polyphenols before 1995, since that time there has been a explosion of animal studies that have indicated their remarkable benefits as anti-oxidants and anti-inflammatory agents. Upon deeper inspection, there is one group of polyphenols that seems to generate the most consistent health benefits. These are the delphinidins. Delphinidins are a subgroup of a family of polyphenols known as anthocyanidins. To make the story about delphinidins more intriguing, they are primarily found in blueberries. More specifically, the primary sources of delphinidins are the American blueberry, the Russian blueberry (i.e. bilberry), and the Patagonian blueberry (i.e. maqui berry). This is why the published clinical studies in humans seem to consistently involve blueberries. And the clinical data is impressive. Whether it is about reducing oxidized cholesterol or improving insulin resistance in patients with metabolic syndrome (1,2) or improving memory in patients with early dementia (3), the human data on the use of blueberries simply jumps out at you. Since the active ingredient in each of these varieties of blueberries appears to be the delphinidins, then it is reasonable that the higher the levels of this particular polyphenol, the better the potential results. The Russian blueberry contains six times more delphinidins than American blueberries, and the Patagonia blueberry contains 14 times more delphinidins than the American blueberry. This probably reflects the harsher growing climates that other forms of blueberries are exposed to when compared to the American blueberry, which has become overly domesticated (making it richer in fructose and lower in delphinidins). However, as with all natural products you have to take a therapeutic dose to get a therapeutic effect. You could measure this therapeutic threshold in terms of their anti-oxidative potential (measured in ORAC units) or the actual amounts of delphinidins themselves. It appears that for a blueberry extract to be effective requires that it provides at least 16,000 ORAC units per day. To put this in perspective, this level of ORAC units is equivalent to eating greater than 20-30 servings of vegetables on a daily basis. But if the delphinidins are so important for the benefits of blueberries, isn’t it possible that the smaller amounts of the maqui berry might be even more beneficial because of its higher delphinidin concentration? That’s why we have several ongoing clinical trials to explore that potential. I will keep you informed as the results start coming in. Yet in the meantime, keep eating lots of those colorful carbohydrates just like your grandmother told you to eat. References: 1. Stull AJ, Cash KC, Johnson WD, Champagne CM, and Cefalu WT. “Bioactives in blueberries improve insulin sensitivity in obese, insulin-resistant men and women.” J Nutr 140: 1764-1768 (2010). Basu A, Du M, Leyva MJ, Sanchez K, Betts NM, Wu M, Aston CE, and Lyons TJ. “Blueberries decrease cardiovascular risk factors in obese men and women with metabolic syndrome.” J Nutr 140: 1582 1588 (2010). Krikorian R, Shidler MD, Nash TA, Kalt W, Vinqivst-Tymchuk R, Shukitt-Hale R, and Joseph JA. “Blueberry supplementation improves memory in older adults.” J Agric Food Chem 58: 3996-4000 (2010).
Weight Loss or Fat Loss? It Makes A Difference
With the New Year comes the guaranteed resolution for most people to lose weight. Invariably that resolution is usually abandoned some time in February. Part of the reason is that we really don’t know what we are talking about when it comes to weight loss. Weight loss is composed of three separate components: water loss, muscle loss, and fat loss. If you restrict calories, you are going to lose weight. What that weight loss might consist of (water, muscle, or fat) is a very different question. There are no health benefits to water loss (i.e. dehydration) or muscle loss (i.e. protein deprivation), but there is something magical about fat loss. If you can lose excess body fat, then you are virtually guaranteed to lower blood sugar levels, blood lipid levels, and blood pressure. Not surprisingly, drugs used to reduce blood sugar, blood lipids and blood pressure are the biggest sellers in the country. Considering the continuing outcry to reverse our obesity epidemic, no one seems to bother to measure fat loss in any clinical trials. This is why you see a lot of research studies published stating it doesn’t matter what diet you follow because if you restrict calories, you will lose weight. I agree with that statement. But if you want better health (not to mention looking better in a swimsuit), then you want to make sure that you are losing fat at the fastest possible rate while conserving muscle mass at the same time. The published clinical studies that have looked at fat loss make it very clear that the anti inflammatory diet is the best dietary strategy to burn fat faster (1-3). If the moderate-carbohydrate anti inflammatory diet is good, then shouldn’t an even lower-carbohydrate diet like the Atkins diet be better? Not so fast. The published studies comparing the anti inflammatory diet to the Atkins diet make it clear that there are no benefits to consuming a lower-carbohydrate diet that generates ketosis, but there are plenty of negative consequences, such as increased cellular inflammation and decreased capacity for exercise (4,5). But losing weight is relatively easy compared to keeping it off. That’s why the recent DIOGENES study is so important (6). This study makes it very clear that if you want to keep lost weight off, then your best choice is maintaining a diet that has at least 25 percent of the calories coming from protein, and about 40 percent of the calories coming from low-glycemic carbohydrates. That’s the anti inflammatory diet. So if your New Year’s resolution is to lose weight (and really lose fat) and keep it off, then the anti inflammatory diet should be your only choice.{{cta('daffa570-1055-4766-af51-e09d66a17e47')}} References: Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, and Christou DD. “A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women.” J Nutr 133: 411-417 (2003). Lasker DA, Evans EM, and Layman DK, “Moderate-carbohydrate, moderate-protein weight-loss diet reduces cardiovascular disease risk compared to high-carbohydrate, low-protein diet in obese adults. A randomized clinical trial.” Nutrition and Metabolism 5: 30 (2008). Fontani G, Corradeschi F, Felici A, Alfatti F, Bugarini R, Fiaschi AI, Cerretani D, Montorfano G, Rizzo AM and Berra B. “Blood profiles, body fat and mood state in healthy subjects on different diets supplemented with omega-3 polyunsaturated fatty acids.” Eur J Clin Invest 35: 499-507 (2005). Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, and Sears B. “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.” Am J Clin Nutr 83: 1055-1061 (2006). White AM, Johnston CS, Swan PD, Tjonn SL, and Sears B. “Blood ketones are directly related to fatigue and perceived effort during exercise in overweight adults adhering to low-carbohydrate diets for weight loss: a pilot study.” J Am Diet Assoc 107:1792-1796 (2007). Larsen TM, Dalskov SM, van Baak M, Jebb SA, Papadaki A, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunesova M, Pihlsgard M, Stender S, Holst C, Saris WH, and Astrup A. “Diets with high or low protein content and glycemic index for weight-loss maintenance.” N Engl J Med 363: 2102-2113 (2010).
The Water and Weight Loss Connection
Throughout my career, a common question that arises is whether water consumption before or during a meal really helps with weight loss. A common responses to this question is that people often confuse hunger for hydration, but a recent study may provide an answer to this question that is based on science. A randomized clinical trial published in the February edition of Obesity examined how water intake might affect weight loss in overweight and obese individuals age 55-75 (1). One group received a low-calorie diet with an emphasis on increased water consumption (water group: 16 fluid ounces of water prior to each of the three daily meals), and the other received a low-calorie diet alone (non-water group). Neither group was aware of the true intention of the study prior to participating. There were no differences between the two groups at the start of the trial with regards to age, anthropometrics, blood chemistry or physical activity. Measurements were taken at baseline and at the end of 12 weeks. At the end of the trial both groups had lost a significant amount of weight, but those who had been instructed to consume 16 fluid ounces of water prior to each meal had a 44 percent greater weight loss than the non-water group. This equated to an approximate four-pound difference between the two groups. The mechanism through which water may be impacting weight is not fully understood, but it may be in part that it reduces energy intake at each meal and increases feelings of fullness. {{cta('cd305230-6e34-42f6-9e2c-c2beda556f50')}} Reference: Dennis EA, Dengo AL, Comber DL, Flack KD, Savla J, Davy KP, Davy BM. Water consumption increases weight loss during a hypocaloric diet intervention in middle-aged and older adults. Obesity (Silver Spring). 2010 Feb;18(2):300-7.
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