Tag Archives: diabetes

Fish oil and fat loss

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I have often said, “It takes fat to burn fat”. As I describe in my book “Toxic Fat,” increased cellular inflammation in the fat cells turns them into “fat traps” (1). This means that fat cells become increasingly compromised in their ability to release stored fat for conversion into chemical energy needed to allow you to move around and survive. As a result, you get fatter, and you are constantly tired and hungry.

One of the best ways to reduce cellular inflammation in the fat cells is by increasing your intake of omega-3 fatty acids. This was demonstrated in a recent article that indicated supplementing a calorie-restricted diet with 1.5 grams of EPA and DHA per day resulted in more than two pounds of additional weight loss compared to the control group in a eight-week period (2).

How omega-3 fatty acids help to ”burn fat faster” is most likely related to their ability to reduce cellular inflammation in the fat cells (3,4) and to increase the levels of adiponectin (5). Both mechanisms will help relax a “fat trap” that has been activated by cellular inflammation.

However, there is a cautionary note. This is because omega-3 fatty acids are very prone to oxidation once they enter the body. This is especially true relative to the enhanced oxidation of the LDL particles (6-9).

This means that to get the full benefits any fish oil supplementation, you have to increase your intake of polyphenols to protect the omega-3 fatty acids from oxidation. How much? I recommend at least 8,000 additional ORAC units for every 2.5 grams of EPA and DHA that you add to your diet. That's about 10 servings per day of fruits and vegetables, which should be no problem if you are following the Zone diet. If not, then consider taking a good polyphenol supplement.

Once you add both extra fish oil and polyphenols to a calorie-restricted diet, you will burn fat faster without any concern about increased oxidation in the body that can lead to accelerated aging.

References

  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, and Martinez JA. “Randomized trial of weight-loss diets for young adults varying in fish and fish oil content.” Int J Obes 31: 1560-1566 (2007)
  3. Huber J, Loffler M, Bilban M, Reimers M, Kadl A, Todoric J, Zeyda M, Geyeregger R, Schreiner M, Weichhart T, Leitinger N, Waldhausl W, and Stulnig TM. “Prevention of high-fat diet-induced adipose tissue remodeling in obese diabetic mice by n-3 polyunsaturated fatty acids.” Int J Obes 31: 1004-1013 (2007)
  4. Todoric J, Loffler M, Huber J, Bilban M, Reimers M, Kadl A, Zeyda M, Waldhausl W, and Stulnig TM. “Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids.” Diabetologia 49: 2109-2119 (2006)
  5. Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, and Jebb SA. “Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women.” Int J Obes 30: 1535-1544 (2006)
  6. Pedersen H, Petersen M, Major-Pedersen A, Jensen T, Nielsen NS, Lauridsen ST, and Marckmann P. “Influence of fish oil supplementation on in vivo and in vitro oxidation resistance of low-density lipoprotein in type 2 diabetes.” Eur J Clin Nutr 57: 713-720 (2003)
  7. Turini ME, Crozier GL, Donnet-Hughes A, and Richelle MA. “Short-term fish oil supplementation improved innate immunity, but increased ex vivo oxidation of LDL in man–a pilot study.” Eur J Nutr 40: 56-65 (2001)
  8. Stalenhoef AF, de Graaf J, Wittekoek ME, Bredie SJ, Demacker PN, and Kastelein JJ. “The effect of concentrated n-3 fatty acids versus gemfibrozil on plasma lipoproteins, low-density lipoprotein heterogeneity and oxidizability in patients with hypertriglyceridemia.” Atherosclerosis 153: 129-138 (2000)
  9. Finnegan YE. Minihane AM, Leigh-Firbank EC, Kew S, Meijer GW, Muggli R, Calder PC, and Williams CM. “Plant- and marine-derived n-3 polyunsaturated fatty acids have differential effects on fasting and postprandial blood lipid concentrations and on the susceptibility of LDL to oxidative modification in moderately hyperlipidemic subjects.” Am J Clin Nutr 77: 783-795 (2003)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Fetal programming: Gene transformation gone wild (Part I)

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Normally genes change very slowly through mutation. Most mutations are harmful and hence provide no survival advantage to the organism. This is why there is a less than a 2 percent difference between our genes and those of a chimpanzee, even though we became a separate species more than six million years ago. What distinguishes mankind is not the number of genes (corn has twice as many genes as humans), but the speed at which our genes can be turned on and off. This is because of the presence of gene transcription factors that can be activated or inhibited by nutrients. The effect of nutrients on gene expression is known as nutrigenomics.

Because of mankind’s rapid gene switching abilities, gene expression can be influenced significantly by the diet. Due to the speed at which new food ingredients are being introduced into the human diet, these types of nutrigenomic interactions can create radical changes in gene expression in a very short period of time. Normally what a person eats should only affect their gene expression during their lifetime. But is it possible that these changes in genetic expression can be transferred to the next generation?

We can see how genetic engineering (i.e. cross-breeding) can rapidly change the size and shape of dogs, flowers, vegetables and fruits. The genes in each of these species don’t change, but changes in gene expression induced by crossbreeding can persist from one generation to the next, especially if they are constantly reinforced. This is known as epigenetics.

Somehow we don’t think this type of epigenetic change can happen to us, but it does as a result of fetal programming. The prenatal period in the womb is the time that a child’s genes are most susceptible to epigenetic programming. Epigenetic programming can be amplified by the ongoing dietary effects on gene transcription factors (i.e. nutrigenomics) taking place in the mother. The result is the imprinting of epigenetic changes on the genes of the developing fetus that can alter the metabolic future of the child (1).

Examples of how this type of epigenetic programming influences future metabolic effects has been demonstrated under the conditions of famine, which generate increased obesity and cardiovascular disease in the next generation (2). This is also true of children who were exposed to excess calories or elevated levels of glucose while they were developing in the womb (3,4). Likewise hypertension (i.e. pre-eclampsia) during pregnancy increases the risk of stroke as adults if the fetus is exposed to the high blood pressure in the womb (5) as well as the increased risk of adult obesity if the fetus is exposed to gestational diabetes in the mother (6).

Bottom line: The dietary and metabolic environment the fetus is exposed to in the womb can echo through the rest of his or her life. In part II of this blog, I will explore how the Perfect Nutritional Storm, described in my book “Toxic Fat” (7) has been making Americans fatter, sicker and dumber for the last three generations.

References

  1. Kussman M, Krause L, and Siffert W. “Nutrigenomics: where are we with genetic and epigenic markers for disposition and susceptibility?” Nutrition Rev 68: S38-S47 (2010)
  2. Painter RC, Roseboom TJ, and Bleker OP. “Prenatal exposure to the Dutch famine and disease in later life.” Reprod Toxicol 20: 345-352 (2005)
  3. Singhal A. “Early nutrition and long-term cardiovascular health.” Nutrition Rev 64: S44-S49 (2006)
  4. Boney CM, Verma A, Tucker R, and Bovh BR. “Metabolic syndrome in childhood: associated with birth weight, maternal obesity, and gestational diabetes mellitus.” Pediatrics 115: e290-e296 (2005)
  5. Kajantie E, Eriksson JG, Osmond C, Thornburg K, and Barker DJP. “Pre-eclampsia is associated with increased risk of stroke in the adult offspring.” Stroke 40: 1176-1180 (2009)
  6. Lawlor DA, Pichtenstein P, and Langstrom N. “Association of maternal diabetes mellitus in pregnancy with offspring adiposity into early adulthood.” Circulation 123: 258-265 (2011)
  7. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Omega-3 fatty acids and blood pressure

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Blood Pressure CuffIt was recognized many years ago that fish oil has a dose-dependent effect on lowering blood pressure (1). So how does it do it? There are a lot of different ways.

The first is the ability of the omega-3 fatty acids in fish oil to alter the levels of a group of hormones known as eicosanoids (2,3). These are the hormones that cause blood vessels to contract, thereby increasing the pressure needed to pump blood through the arteries. The omega-3 fatty acids, especially eicosapentaenoic acid (EPA), inhibit both the synthesis and release of the omega-6 fatty acid arachidonic acid (AA) that is the molecular building block necessary to produce those eicosanoids that cause constriction of blood vessels.

The second way that fish oil helps reduce blood pressure is to accelerate weight loss. When you lose excess weight, blood pressure invariably decreases. A recent trial has indicated that when you add fish oil to a calorie-restricted diet, there is greater weight loss (4). This study was followed by an additional trial that indicated when adding fish oil to a weight-reduction diet, there was a further effect on lowering blood pressure (5). So how does fish oil help you lose excess weight? The answer lies in the ability of the omega-3 fatty acids in fish oil to reduce cellular inflammation in the fat cells (6). It's that cellular inflammation that makes you fat and keeps you fat. Reducing that cellular inflammation in the fat cells is the key to weight loss.

Finally another cause of increased blood pressure is increased stress. It was shown in 2003 that high levels of fish oil reduce the rise of blood pressure induced by mental stress (7).

Of course, the best way to reduce blood pressure is to follow an anti-inflammatory diet rich in omega-3 fatty acids. That means a diet rich in fruits and vegetables with adequate levels of low-fat protein and low levels of omega-6 and saturated fats. It's also commonly known as the Zone diet.

References:

  1. Morris MC, Sacks F, and Rosner B. “Does fish oil lower blood pressure? A meta-analysis of controlled trials.” Circulation 88: 523-533 (1993)
  2. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  3. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  4. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, and Martinez JA. “Randomized trial of weight-loss diets for young adults varying in fish and fish oil content.” Int J Obes 31: 1560-1566 (2007)
  5. Ramel A, Martinez JA, Kiely M, Bandarra NM, and Thorsdottir I. “Moderate consumption of fatty fish reduces diastolic blood pressure in overweight and obese European young adults during energy restriction.” Nutrition 26: 168-174 (2010)
  6. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  7. Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, and Tappy L. “Fish oil prevents the adrenal activation elicited by mental stress in healthy men.” Diabetes Metab 29: 289-295 (2003)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

New solution or simply admitting failure?

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SurgeryLast week the International Diabetes Federation (IDF) announced that gastric bypass surgery is a cost-effective treatment for type 2 diabetes. This marks the first time in modern medicine that cutting out normal tissue is now considered good medicine. It also indicates the pathetic state of medical science for the treatment of diabetes.

Make no mistake: Type 2 diabetes is now a pandemic, affecting approximately 300 million people worldwide. This is projected to increase to some 450 million people worldwide by 2030. Since diabetes is one of the most costly chronic disease conditions, it is the most likely to break the financial backbone of health-care systems in every advanced country.

The typical gastric bypass surgery costs from $15,000 to $24,000. Just for argument's sake, let's assume it is $20,000 for each surgery. Since some 26 million people in the United States have type 2 diabetes, then a mere $520 billion dollars spent on gastric bypass surgery would solve our growing epidemic. Obviously we don't have that type of money floating in the health-care system.

Furthermore, the 10-year failure rate is relatively high for this type of surgery (1). For example, 20 percent of patients who were initially obese (BMI >50 percent) could not maintain their long-term BMI below 35 percent (the definition of morbidly obese). This failure rate rises to 58 percent for those whose initial BMI was greater than 50.

The key feature as to why gastric bypass surgery works is the almost immediate suppression of hunger, mediated by improved release of hormones from the gut (i.e. PYY) that go directly to the brain to tell the patient to stop eating. Over time it would appear that this initial enhancement of PYY release is being compromised. As a result, those patients regain the lost weight.

So maybe gastric bypass is not the best long-term solution (and definitely not a cost-effective one in those patients that regain much of their lost weight) for solving the current epidemic of diabetes. So what's the alternative? One solution would be an anti-inflammatory diet that supplies adequate protein to stimulate PYY release as well as control the levels of cellular inflammation in the pancreas, the underlying reason why insufficient insulin levels are secreted in the first place (2).

Call me crazy, but this dietary approach appears far more cost-effective.

References

  1. Christou NV, Look D, and MacLean LD. “Weight gain after short- and long-limb gastric bypass in patients followed for longer than 10 years.” Ann Surg 244: 734-740 (2006)
  2. Donath MY,Boni-Schnetzler M, Ellingsgaard H, and Ehses JA. “Islet inflammation impairs the pancreatic beta-cell in type 2 diabetes.” Physiology 24: 325-331 (2009)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

What is the Mediterranean diet?

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The mediterranean dietToday we continually hear about the health benefits of following a Mediterranean diet. For example, a recent analysis of more than 50 published studies indicated that a Mediterranean diet would lead to a 30-percent reduction in metabolic syndrome (1). Since metabolic syndrome can be considered pre-diabetes, the public health implications are enormous. However, are we talking about the Spanish Mediterranean diet or the Italian, or the Moroccan, the Egyptian or the Lebanese versions? Here is the basic problem with all diets: Trying to define them correctly.

In order to compare one diet to another, each diet must ultimately be defined by its balance of the macronutrients (protein, carbohydrate and fat). This is because the macronutrient balance determines hormonal responses generated by that diet (2).

A Mediterranean diet can be considered to contain approximately 50 percent of the calories as carbohydrates, 20 percent of the calories as protein and 30 percent of the calories as fat. This is a higher protein-to-carbohydrate balance than is found in the usually recommended “healthy” diets for weight loss and cardiovascular health. As a result, this difference in the balance of the protein-to-carbohydrate ratio will generate different hormonal responses between the two types of diets, especially in terms of reducing insulin responses and controlling cellular inflammation.

This is important since it is excess insulin that makes you fat and keeps you fat, and it's cellular inflammation that makes you sick. Since insulin levels are determined by the protein-to-carbohydrate ratio, would more protein and less carbohydrate generate an even better response? Of course it would. That is why the Zone diet contains 40 percent of the calories as carbohydrates, 30 percent of the calories as protein, and 30 percent of the calories as fat. This improved protein-to-carbohydrate balance means lower insulin levels and less cellular inflammation.

Why stop there? Let's just continue reducing the carbohydrates. Now you get low-carbohydrate diets, like the Atkins diet. Unlike the Zone diet, carbohydrates are no longer the primary macronutrient in a true low-carbohydrate diet. Now the primary macronutrient is fat. Using these low-carbohydrate diets creates some real problems by generating an abnormal metabolic state known as ketosis. This occurs when you don't have enough carbohydrates (fewer than 20 percent of total calories) in the diet to metabolize fat completely to carbon dioxide and water. When that happens, your blood vessels lose their elastic nature, (3) increasing the risk of a heart attack (4). This is probably a consequence of lowering insulin too much as well as increasing inflammatory mediators (3). If you are trying to lose weight, increasing the likelihood of a heart attack is not a good idea. So it seems you need some carbohydrates, but not too few if your goal is to lose weight safely.

That's why people (as well as physicians and diet editors) get confused when they read articles in the New England Journal of Medicine talking about low-carbohydrate diets for weight loss when such diets actually contain 40 percent carbohydrates (5). To be correct, they should use the term “the Zone diet” instead of a “low-carbohydrate diet” to be correct. Despite the poor dietary description used in this article, the “low-carbohydrate” (aka the Zone) diet generated greater weight loss after two years, a greater reduction in the total cholesterol-to-HDL cholesterol (a marker of future cardiovascular risk), a greater decrease in triglycerides and a greater decrease in inflammatory markers when compared to a Mediterranean diet or the always-recommended low-fat diet (5). That's why you do controlled clinical trials instead of guessing what the best might be.

So if you want to lose weight and reduce your future heart disease risk, it seems prudent to follow the Zone diet and make most of your carbohydrates colorful ones (i.e., fruits and vegetables) and add olive oil and nuts for fat instead of using vegetable oils and saturated fats just as I recommended more than 15 years ago (2). Just call it the Mediterranean Zone diet. Now everyone is not only happy, but also they are finally using the proper diet terminology.

References

  1. Kastorini C-M, Milionis HJ, Esposito K, Giuglian D, Goudevnos JA, and Panagiotakos DB. “The effect of Mediterranean diet on metabolic syndrome and its components.” J Am Coll Cardiol 57: 1299-1313 (2011)
  2. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  3. Buscemi S, Verga S, Tranchina MR, Cottone S, and Cerasola G. “Effects of hypocaloric very-low-carbohydrate diet vs. Mediterranean diet on endothelial function in obese women.” Eur J Clin Invest 39: 339-347 (2009)
  4. Yeboah J, Crouse JR, Hsu FC, Burke GL, and Herrington DM. “Brachial flow-mediated dilation predicts incident cardiovascular events in older adults.” J Am Coll Cardio 51: 997-1002 (2008)
  5. Shai I, Schwarzfuchs D, Henkin Y, Shahaar DR, Witkow S, Greenberg I, Golan R, Fraser D, boltin A, Vardi H, Tangi-Roxental O, Zuk-Ramot R, Sarusi B, Fricner D, Schwartz Z, Sheiner E, Marko R, Katorza E, Thiery J, Fielder GM, Bluher M, Stumvoll M and Stamper MJ. “Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet.” N Engl J Med 359: 229-241 (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Blame weight gain on the brain

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Many people claim they are addicted to food. That may not be too far from the truth.

Over millions of years of evolution, our brains have adapted to provide us a reward for successfully ingesting food. The hormone dopamine appears to be the key link in this reward process. But to complete the circuit, dopamine has to interact with its receptor. It has been known for many years that the ability of dopamine to combine with one of its receptors (the D2 dopamine receptor) is compromised in obese individuals compared to normal-weight individuals (1). This led to the hypothesis that obese individuals overeat as a way to compensate for the reduction in the dopamine reward circuits just as individuals with addictive behaviors (drugs, alcohol, gambling, etc.) do when their dopamine levels are low. It is also known that food restriction up-regulates the number of D2 receptors (2). This likely completes the reward circuit.

This effect of increasing D2 receptors is confirmed in obese patients who have undergone gastric bypass surgery that results in calorie restriction (3). This may explain why gastric bypass surgery is currently the only proven long-term solution of obesity. More recent studies with functional magnetic resonance imaging (fMRI) have indicated that unlike women with a stable weight where the mere visual image of palatable food increases the reward activity in the brain, that response is highly reduced in women who have gained weight in the past six months (4). This suggests that the dopamine reward circuits are compromised in women with recent weight gain, thus prompting a further increased risk for overeating in those individuals to increase dopamine output.

So does this mean that the obese patient with a disrupted dopamine reward system has no hope of overcoming these powerful neurological deficits? Not necessarily. There are a number of dietary interventions to increase the levels of dopamine and its receptors. The first is calorie restriction, which is only possible if you aren’t hungry. The usual culprit that triggers constant hunger is a disruption of hormonal communication of hunger and satiety signals in the brain. It has been shown that following a strict Zone diet can quickly restore the desired balance that leads to greater satiety (5-7). The probable mechanism is the reduction of cellular inflammation by an anti-inflammatory diet (8-10).

Another dietary intervention is high-dose fish oil that has been demonstrated to both increase dopamine and dopamine receptors in animals (11,12). This would explain why high-dose fish oil has been found useful in the treatment of ADHD, a condition characterized by low dopamine levels (13). Finally, high-dose fish oil can reduce the synthesis of endocannabinoids in the brain that are powerful stimulators of hunger (14).

I often say that if you are fat, it may not be your fault. The blame can be placed on your genes and recent changes in the human food supply that are changing their expression, especially in the dopamine reward system. However, once you know what causes the problem, you have the potential to correct it. If you are apparently addicted to food, the answer may very well lie in an anti-inflammatory diet coupled with high-dose fish oil.

References

  1. Wang GJ, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, Netusil N, and Fowler JS. “Brain dopamine and obesity.” Lancet 357: 354-357 (2001)
  2. Thanos PK, Michaelides M, Piyis YK, Wang GJ, and Volkow ND. “Food restriction markedly increases dopamine D2 receptor (D2R) in a rat model of obesity as assessed with in-vivo muPET imaging and in-vitro autoradiography.” Synapse 62: 50-61 (2008)
  3. Steele KE, Prokopowicz GP, Schweitzer MA, Magunsuon TH, Lidor AO, Kuwabawa H, Kumar A, Brasic J, and Wong DF. “Alterations of central dopamine receptors before and after gastric bypass surgery.” Obes Surg 20: 369-374 (2010)
  4. Stice E, Yokum S, Blum K, and Bohon C. “Weight gain is associated with reduced striatal response to palatable food.” J Neurosci 30 :13105-13109 (2010)
  5. 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)
  6. Agus MS, Swain JF, Larson CL, Eckert EA, and Ludwig DS. “Dietary composition and physiologic adaptations to energy restriction.” Am J Clin Nutr 71: 901-7 (2000)
  7. Jonsson T, Granfeldt Y, Erlanson-Albertsson C, Ahren B, and Lindeberg S. “A paleolithic diet is more satiating per calorie than a mediterranean-like diet in individuals with ischemic heart disease.” Nutr Metab 7:85 (2010)
  8. Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS. “Effects of a low glycemic-load diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA 292: 2482-2490 (2004)
  9. Pittas AG, Roberts SB, Das SK, Gilhooly CH, Saltzman E, Golden J, Stark PC, and Greenberg AS. “The effects of the dietary glycemic load on type 2 diabetes risk factors during weight loss.” Obesity 14: 2200-2209 (2006)
  10. 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)
  11. Chalon S, Delion-Vancassel S, Belzung C, Guilloteau D, Leguisquet AM, Besnard JC, and Durand G. “Dietary fish oil affects monoaminergic neurotransmission and behavior in rats.“ J Nutr 128: 2512-2519 (1998)
  12. Chalon S. “Omega-3 fatty acids and monoamine neurotransmission. Prostaglandins Leukot Essent Fatty Acids 75: 259-269 (2006)
  13. Sorgi PJ, Hallowell EM, Hutchins HL, and Sears B. “Effects of an open-label pilot study with high-dose EPA/DHA concentrates on plasma phospholipids and behavior in children with attention deficit hyperactivity disorder.” Nutr J 6: 16 (2007)
  14. Watanabe S, Doshi M, and Hamazaki T. “n-3 Polyunsaturated fatty acid (PUFA) deficiency elevates and n-3 PUFA enrichment reduces brain 2-arachidonylglycerol level in mice.” Prostaglandin Leukot Essent Fatty Acids 69:51–59 (2003)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

When is a diet not a diet?

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One of the major problems in nutrition is the lack of rigor in describing diets. The first problem is that the root of the word diet comes from the ancient Greek phrase “way of life”. A diet is not a short-term plan to fit into a swimsuit, but rather it is a way of life to reach a lifetime goal, like a longer and better life. If your goal is less grand like simply to lose weight, then to lose that weight and keep it off, you had better maintain that diet for the rest of your life. From that perspective, a diet like the Grapefruit diet doesn’t make much sense.

The second problem is the lack of precision in defining a diet. My definition of a diet is based on the macronutrient balance that ultimately determines hormonal responses. From this perspective, there are really only four diets based on the glycemic load, assuming that each diet contains the same number of calories.

Diet Common Name
Very low glycemic-load diet Ketogenic (i.e. Atkins diet)
Low glycemic-load diet Non-ketogenic (i.e. Zone Diet)
High glycemic-load diet American Heart (or Diabetes or Cancer, etc.) Association diet
Very high glycemic-load diet Strict vegetarian (i.e. Ornish diet)

Assuming these diets have an equal number of calories, you can then rank them in terms of the total amount of calories coming from protein, carbohydrates and fat as shown below:

Diet Macronutrient Composition
Very low glycemic-load diet 30% P, 10% C, and 60% F
Low glycemic-load diet 30% P, 40% C, and 30% F
High glycemic-load diet 15% P, 55% C, and 30% F
Very high glycemic-load diet 10% P, 80% C, and 10% F

You can see that depending on the macronutrient composition of the diet you choose to follow, it will generate very different hormonal responses. A ketogenic diet will induce increased cortisol levels that make you fat and keep you fat. High-glycemic diets induce excess insulin levels that make you fat and keep you fat. It’s only a low-glycemic diet that has been shown to burn fat faster (1) as well as maintain weight loss most effectively (2).

That’s why unless you define a diet carefully in terms of macronutrient balance, you can’t ever undertake any meaningful nutritional research to validate whether or not it achieves its stated goal. This is why most diet studies produce such conflicting results.

The wild card is which food ingredients you choose for a particular diet. This is where much of the confusion emerges as people throw around arbitrary terms like a Paleolithic diet or a Mediterranean diet. What the heck is a Mediterranean diet? Is it the diet from Morocco, Lebanon, Italy, or Spain? What you can do, however, is to review the food ingredients found in these diets.

For example, Paleolithic food ingredients would consist only of fruits, vegetables, nuts, grass-fed beef, eggs, and fish. A pretty limited group of foods to choose from, but it was all that was available to man 10,000 years ago. Mediterranean food ingredients include all of those in the Paleolithic group but now adding whole grains, alcohol, legumes, and dairy products. These were the dietary choices available about 2,000 years ago — a more diverse number of food choices for a particular diet, but now with a greater potential for generating inflammatory responses. Finally, there are the “Do-You-Feel-Lucky” food ingredients. This includes very recent additions to the human diet, such as sugar, refined carbohydrates and vegetable oils. These are food ingredients that make processed foods possible. However, they carry with them the greatest potential to increase cellular inflammation. Remember, it is increased cellular inflammation that makes you fat, sick, and dumb.

So if you want to be correct about the use of the word diet, then you should use the right terms. It could be an anti inflammatory diet using only Paleolithic food ingredients (i.e. a Paleo Zone Diet), or an anti inflammatory diet using only Mediterranean food ingredients (i.e. a Mediterranean Zone Diet), or even an anti inflammatory diet using the “Do-You-Feel-Lucky” food ingredients. This designation includes the most recent additions (sugar, refined carbohydrates, and vegetable oils) that have the greatest impact on inducing cellular inflammation, regardless of the macronutrient balance. Ultimately important are the hormonal responses of the macronutrient balance of the diet (especially after avoiding the worst offenders in the “Do-You-Feel-Lucky” group). The more restrictive your choices for food ingredients for any diet, the better the hormonal outcome for that particular diet. In particular, the primary clinical outcome for the anti inflammatory diet is the life-long management of cellular inflammation. And for that clinical parameter, the clinical research has found the anti inflammatory diet to be the clear winner regardless of the food ingredients selected (3-5).

References

  1. Layman DK, Evans EM, Erickson D, Seyler J, Weber J,; Bagshaw D, Griel A, Psota T, and Kris-Etherton P. “A moderate-protein diet produces sustained weight loss and long-term changes in body composition and blood lipids in obese adults.” J Nutr 139: 514-521 (2009)
  2. 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)
  3. Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS. “Effects of a low glycemic-load diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA 292: 2482-2490 (2004)
  4. 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)
  5. Pittas AG, Roberts SB, Das SK, Gilhooly CH, Saltzman E, Golden J, Stark PC, and Greenberg AS. “The effects of the dietary glycemic load on type 2 diabetes risk factors during weight loss.” Obesity 14: 2200-2209 (2006)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

The new “eat less” USDA Food Pyramid

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For the first time in recent history the new USDA dietary guidelines finally reflect the realization that America has an obesity epidemic.

Five years ago, its dietary guidelines were best characterized as “eat more; exercise more”. After all, their constituency is not the American public but American agribusiness. Due to the constant fear of incurring the wrath of powerful food lobbies, the USDA dietary recommendations were virtually useless in preventing the spread of obesity and diabetes in America.

Now the Guidelines are somewhat helpful as they suggest that fruits and vegetables should occupy one-half your plate. Although that volume is not equal to the two-thirds of the plate that I have advocated for more than 15 years, at least it is a start. Unfortunately, the “eat-less” message is more deeply buried within the Guidelines.

This is because the “eat-less” message is a difficult one to digest for American agribusiness, whose revenue growth is based on “eat more”. Today agribusiness produces more than 4,000 calories per day for every American. For Americans to eat less, every sector of agribusiness (except the fruit and vegetable sector) has to make less money. In reality these new guidelines don't come out and actually say eat less of anything.

When the secretary of agriculture was asked if the guidelines might suggest something like eating less meat, his response was like asking President Clinton his definition of sex — it depends. (Well, that remark will drive comments for sure!). Obviously, he didn't want to offend the meat lobby.

The one segment of the agribusiness sector the USDA was willing to throw under the bus was the salt lobby due to the strong USDA message to eat less salt. Of course, the Salt Institute responded, “Obesity, not salt, is the main culprit in rising blood pressure rates”. The obvious implication is salt has no calories; therefore, the blame should be on those sectors of agribusiness that sell products that contain calories. Unfortunately, it is the responsibility of the USDA to promote those specific sectors.

If you are encouraged to increase the consumption of fruits and vegetables, eat more seafood (just forget about contamination), and replace dairy with soy protein, then what do you have to reduce in order to eat fewer calories? The usual suspects would be saturated fats, (which Harvard now tells us aren't so bad for heart disease), and sugar. Unfortunately, those recommendations are buried deep within the report. Without those ingredients it is difficult to make the tasty, cheap processed foods that drive the profits of agribusiness. This sounds very similar to our current budget crisis: No one wants to raise taxes, and no one wants to lower spending, although everyone wants to reduce the deficit.

Finally, the new guidelines contain the message that there is “no optimal proportion of macronutrients that can facilitate weight loss or assist in maintaining weight loss”. Maybe they should read the DIOGENES study published in the New England Journal of Medicine that came to an opposite conclusion (1). Of course, why let published nutritional science stand in the way of intuitive eating. I guess we will have to wait another five years for the next update of the USDA Guidelines.

References

  1. 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)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Coffee and diabetes: What’s the connection?

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One of the great controversies in nutrition is the role of coffee and human health. On the one hand, coffee is the primary source of polyphenols in the American diet because of the lack of consumption of fruits and vegetables. On the other hand, coffee is rich in caffeine, an alkaloid that acts as a stimulant on the central nervous system and is known to be an addictive agent (1). In fact, Roland Griffiths, professor of Behavioral Biology at the John Hopkins School of Medicine (and my old college roommate), says, “Caffeine is the world’s most widely used mood-altering drug.” So the question remains is caffeine good for you?

No one knows for sure, but one interesting point has been made that it appears the more coffee you drink, the lower your risk for developing diabetes (2). In fact, if you drink more than four cups of coffee per day, you decrease your risk of diabetes by 50 percent. This new research demonstrates that coffee increases the levels of sex hormone-binding globlin (SHBG) in the blood. As I pointed out in my book “The Anti-Aging Zone,” SHBG plays an important role in sequestering the levels of estrogen and testosterone in the blood so that levels of these unbound sex hormones that can interact with their receptors are tightly regulated (3). Usually as insulin resistance increases, the levels of SHBG decrease in the blood (4). This can lead to an over-stimulation of the receptors by the unbound sex hormones resulting in increased risk for breast and prostate cancer development.

What in the coffee actually causes the increase in SHBG is unknown, but what is known is that once you decaffeinate the coffee, all its benefits on the elevation of SHBG levels and any reduction in risk for diabetes disappear.

It is highly unlikely that caffeine by itself is beneficial for reducing type 2 diabetes, since there were no benefits related to drinking tea or to total daily caffeine intake (2). Perhaps some other compound that was also extracted with the caffeine may play a role in the reduction of type 2 diabetes.

So what really happens when you decaffeinate coffee? First, you soak the beans in water to remove the caffeine and flavors as well as the polyphenols. Then you treat the water with organic solvents (methylene chloride or ethyl acetate) to remove the caffeine (as well as many of the polyphenols and much of the flavor). Then (assuming you have removed all of the organic solvent), you add back the treated water extract to the beans to hopefully reabsorb some of the flavors back into them. Obviously, not all the flavors or polyphenols return since the resulting taste is far less robust than the original coffee bean.

So it seems to me that exploring what else has been extracted in addition to the caffeine may lead to new dietary treatments for diabetes. Whether that will be done is highly unlikely. Instead of waiting for such experiments, you might as well follow the best treatment for preventing diabetes, which is following the anti inflammatory diet for a lifetime. That is how you control cellular inflammation, which is the driving force for development of type 2 diabetes (5,6).

References

1. Juliano LM and Griffiths RR. “A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features.” Psychopharmacology 176: 1-29 (2004)

2. Goto A, Song Y, Chen BH, Manson JE, Buring JE, and Liu S. “Coffee and caffeine consumption in relation to sex hormone-binding globulin and risk of type 2 diabetes in postmenopausal women.” Diabetes 60: 269-275 (2011)

3. Sears B. “The Anti-Aging Zone.” Regan Books. New York, NY (1999)

4. Akin F, Bastemir M, and Alkis E. “Effect of insulin sensitivity on SHBG levels in premenopausal versus postmenopausal obese women.” Adv Ther 24: 1210-1220 (2007)

5. Sears B. “Anti-inflammatory diets for obesity and diabetes.” J Coll Amer Nutr 28: 482S-491S (2009)

6. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Try the team approach to nutrition

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One of the problems with nutrition is that it is too complex for simple thinking. Unlike drugs, which are designed to inhibit a particular target enzyme, nutrients often work in combinations like a team operating at the genetic level. When you try to apply drug-like thinking (i.e. one compound has to do all the work) to nutrient research, then the results are often underwhelming. Nowhere is this clearer than when we look at how nutrients interact to control body weight.

Weight gain can be best understood as a defect in both metabolism (the conversion of dietary energy into chemical energy) and storage (the stockpiling of excess dietary intake). This involves a four-way conversation between the brain, the gut, the liver and the adipose tissue. The only way these various organs can communicate with each other is via hormones. The gut sends signals to the brain when to stop eating. If the brain receives those signals loud and clear, your desire for food decreases (i.e. satiety). Finally, the food that has been ingested is either converted by the liver into suitable metabolites that can either be used for generating chemical energy (i.e. ATP) or stored (primarily in the fat cells) for future use. When it all works together, it runs smoothly. When it doesn’t work well, you end up gaining more body fat accelerating the pathway toward chronic disease.

One of the key hormones in this complex communication process is adiponectin. Apidonectin is an anti-inflammatory hormone made by the fat cells that is essential for reducing insulin resistance and preventing lipotoxicity (1). In other words, it is at the center of this complex hormonal communication system to help keep body weight in check and slow the development of chronic disease. Great, but how do you increase adiponectin?

First, there is no drug that can do it, but there are nutrients that can. One approach is to consume more omega-3 fatty acids (1). High levels of omega-3 fatty acids activate a genetic transcription factor that causes the increased production of adiponectin. But it takes a lot of high purity omega-3 oil to turn on that gene transcription factor. Now there appears to be another way: Taking polyphenols (2). The polyphenols don’t increase the activity of the genetic transcription factor, but they do facilitate the assembly of adiponectin into its most active form. Of course, if you don’t have enough omega-3 fatty acids in the diet, you can’t produce the necessary adiponectin building blocks to be assembled. When you combine the two (high purity omega-3 oil and polyphenols), then you don’t need to use as much of either one for the desired end result (3).

That’s how nutrition really works. You have to use a team nutrient approach to alter genetic expression. A lot more complicated than giving a single drug, but of course without the inherent side effects.

References

  1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  2. Neschen S, Morino K, Rossbacher JC, Pongratz RL, Cline GW, Sono S, Gillum M, and Shulman GI. “Fish oil regulates adiponectin secretion by a peroxisome proliferator-activated receptor-gamma-dependent mechanism in mice.” Diabetes 55: 924-928 (2006)
  3. Wang Q, Liu M, Liu X, Dong LQ, Glickman RD, Slage TJ, Zhou Z, and Liu F. “Up-regulation of adiponectin by resveratrol.” J Biol Chem 286: 60-66 (2011)
  4. Shirai N and Suzuki H. “Effects of simultaneous intakes of fish oil and green tea extracts on plasma, glucose, insulin, C-peptide, and adiponectin and on liver lipid concentrations in mice fed low- and high-fat diets.” Ann Nutr Metab 52: 241-249 (2008)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.