Coffee and diabetes: What’s the connection?

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.

Another good reason to eat your fruits and vegetables

Your grandmother always told you, you couldn’t leave the table until you ate all your vegetables. She was giving you the essence of reducing your chances of dying from cardiovascular disease.

The trouble with testing any dietary hypothesis (even Grandma’s advice on vegetables) is the complexity of understanding nutrition. Unlike drugs, which are based on linear thinking (one drug affects one enzyme and that treats you), nutrition is based on non-linear thinking. That means nutrition is more like a three-dimensional chess match. Whenever you change one component (i.e. amount of fat) in the diet, there will be unintended changes as something else is automatically changed as a consequence (like either an increase in dietary protein or carbohydrate to make up the difference of the reduction of dietary fat). This secondary dietary change may totally obscure what you are trying to study. This explains why so many dietary studies appear to produce such wishy-washy results. To try to get around this constant dilemma, investigators often do extremely large epidemiological studies, using people who are initially disease-free and ask how an exposure to some dietary variable affects the development of a particular disease or more importantly death from a particular disease. These are called prospective cohort studies.

As you might imagine, there are very few of these studies since they require a very large number of subjects, and if the outcome is death, then they have to be followed for a very long time. This also means that these studies are extremely expensive. In a soon-to-be-published article in the European Heart Journal is a massive prospective cohort study (with more than 300,000 subjects and based upon an average of eight years of follow-up) that suggested if you ate more fruits and vegetables, your likelihood of dying of heart disease was reduced by 22 percent (1).

How much is more fruits and vegetables? It is about eight servings per day, and it appeared to be a dose-response effect. For each serving of fruits or vegetables, the risk of death from heart disease goes down by 4 percent. Bottom line, the more fruits and vegetables you eat, the greater the reduction in cardiovascular death.

Since you have to eat, why not eat right if your goal is reducing the risk of death from heart disease. If you are eating more fruits and vegetables, then something must be removed from the diet if the calories are to remain constant. The most logical choice would be reducing grains and starches as you increase fruits and vegetables. In the process, you reduce the glycemic load of the diet and reduce production of insulin. This will not only reduce your risk of dying from heart disease, but also help you lose excess body fat (2)

Notice that I keep emphasizing the words death and dying. The prevailing “wisdom” in the cardiovascular community is that it doesn’t matter what you eat as long as you reduce cholesterol levels. And since increased fruits and vegetables consumption has little impact on cholesterol levels, we are told that if you really want to reduce the risk of dying from heart disease, it’s imperative that you must take a statin drug for the rest of your life. Unfortunately, the research data doesn’t support such optimism. For example, if subjects are studied who have no heart disease (these are called primary prevention studies), then taking statin drugs has no impact on reducing their all-cause mortality (3). In other words, any reduction in cardiovascular death was offset by increases of death from other causes. Not such a good deal if your goal is reducing death whatever the cause. Another group of researchers came to the conclusion after analyzing a number of published trials using statin drugs for the primary prevention of developing heart disease, that there was no compelling reason for their use (4). Since the vast majority of the people taking statin drugs have no established heart disease, this would mean the continued prescription of these drugs comes close to health-care fraud.

But what if you already have heart disease? What is the best way to reduce the risk of dying from it? To answer that question, you undertake secondary prevention studies using death (it’s very easy to measure) as your clinical endpoint. In secondary prevention studies, statins will reduce cardiovascular mortality by about 20 percent in people who already have established heart disease. But if you really want to reduce the likelihood of dying from existing heart disease (like by 70 percent), then you not only have to have the patients increase their intake of fruits and vegetables, but also remove much of the omega-6 fatty acids from the diet and replace them with omega-3 fats (5).

If you do both of these dietary changes (replace grains and starches with more fruits and vegetables as well as replace omega-6 fats with omega-3 fats), then you are essentially following the anti inflammatory diet. That’s how you live longer whether you have heart disease or not.

References

1. Crowe FL, Roddam AW, Key TJ, et al. “Fruit and vegetable intake and mortality form ischaemic heart disease.” Eur Heart Journal 32: doi 10.1093 (2011)

2. Sears B. “The Zone.” Regan Books. New York, NY (1995)

3. Ray KK, Seshsai SRK, Erqou S, Sever P, Jukema JW, Ford I, and Sattar NS. “Statins and all-cause morality in high-risk primary prevention.” Arch Intern Med 170: 1024-1031 (2010)

4. Taylor F, Ward K, Moore THM, Burke M, Davey-Smith G, Casas JP, and Ebrahim S. “Statins for the primary prevention of cardiovascular disease.” The Cochrane Library Issue 1 (2011)

5. de Lorgeril M, Renaud S, Mamelle N, Salen P, Martin JL, Monjaud I, Guidollet J, Touboul P, and Delaye J. “Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease.” Lancet 343: 1454-1459 (1994)

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

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.

Increased satiety: The real secret to weight loss

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

1. 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)

2. 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)

3. 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)

4. 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)

5. 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)

6. 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)

7. 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)

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.

Want to lose Weight? Eat like our Paleolithic ancestors

A recent article appeared in the British Journal of Nutrition that gives an updated estimate of what diet (i.e. Paleolithic) our ancestors may have eaten during the time from their first appearance in Africa some 200,000 years ago until they started leaving Africa 100,000 years later (1). This is important because this type of diet until 10,000 years ago (with the advent of agriculture) was the nutritional foundation through which our genes evolved. Since our diet and gene expression are intimately tied together (2), understanding the dietary forces that molded how our genes respond to diet is important. This is particularly true since nutritional science has many conflicting interactions that make the study of a single nutrient often result in conflicting data. One such example is the study of insulin responses induced by the diet without studying the impact of fatty acid composition on insulin secretion and vice versa. This is why the study of Paleolithic nutrition provides a template to ask questions to optimize our current diet. In fact, I actually I stated this on page 99 of my first book, “The Zone” (3).

So what are the newest updates on the composition of the Paleolithic diet of our African ancestors? It appears the protein content was between 25 and 29 percent, the carbohydrates were about 40 percent and the total fat was about 30-36 percent. If that sounds familiar to the 30 percent protein, 40 percent carbohydrate, and 30 percent fat ratio in the anti inflammatory diet, it should. Essentially the newest estimate of the Paleolithic diet of our human ancestors in Africa is the anti inflammatory diet.

Equally important, it was estimated that the intake of long-chain omega-3 fatty acids (EPA and DHA) was about 6 grams per day. This is similar to my recommendations in “The OmegaRx Zone,” published in 2002 (4). The dietary ratio of arachidonic acid (AA) to EPA was also estimated in this article and was found to be about 2. Since the dietary intake of these fatty acids would be reflected in the blood, then we can assume the AA/EPA ratio in Paleolithic man was about 2. This AA/EPA ratio is again strikingly similar to the recommendations in my various books about what the best AA/EPA ratio should be for optimal control of the cellular inflammation, which leads to the acceleration of chronic disease (4-6).

When you follow the Paleolithic diet (a.k.a. the anti inflammatory diet), you find almost instantaneous changes in hormonal responses (7, 8) and improved glycemic control (8,9) before there is any weight loss. And if you continue to follow it, you not only lose weight, but also burn fat faster (11-14).

Was I just taking lucky guesses on my recommendations for the anti inflammatory diet over the past 15 years? I would like to think they were not lucky guesses, but based on insight coming from my background in drug delivery technology that strives for a therapeutic zone for optimal results. The lucky part was having the perseverance to stay true to those insights. On the other hand, it is always nice to get validation even 15 years after the fact.

References
1. Kuipers RS, Luxwolda MF, Dijck-Brouwer DJA, Eaton SB, Crawford, MA, Cordain L, and Muskiet FAJ. “Estimate macronutrient and fatty acid intakes from an East African paleolithic diet.” British J Nutr 104: 1666-1687 (2010)
2. Sears B and Ricordi C. “Anti-Inflammatory nutrition as a pharmacological approach to treat obesity.” J Obesity published online September 30, 2010. doi: 10.1155/2011/431985. (2010)
3. Sears B. “The Zone.” Regan Books. New York, NY (1995)
4. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
5. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)
6. Sears B. “Toxic Fat.” Nelson Publishing. Nashville, TN (2008)
7. 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)
8. Markovic TP, Jenkins AB, Campbell LV, Furler SM, Kragen EW, and Chisholm DJ. “The determinants of glycemic responses to diet restriction and weight loss in obesity and NIDDM.” Diabetes Care 21: 687-694 (1998)
9. Lindberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjorstrom K, and Ahren B. “A Paleolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease.” Diabetologia 50: 1795-1807 (2007)
10. Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC, and Sebastian A. “Metabolic and physiologic improvements from consuming a Paleolithic, hunter-gatherer type diet.” Eur J Clin Nutr 63: 947-955 (2009)
11. Osterdahl M. Kocturk T. Koochek A, and Wandell PE. “Effects of a short-term intervention with a Paleolithic diet in healthy volunteers.” Eur J Clin Nutr 62: 682-685 (2008)
12. 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)
13. 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)
14. 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)

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.

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.

References

1. 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)
2. 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)
3. 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)
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. 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)
6. 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.

Aspirin…not just for heart disease

As I pointed in my first book, “The Zone,” more than 15 years ago, aspirin remains a wonder drug because of its ability to reduce inflammation (1). The medical community now uses aspirin for the prevention of strokes and heart attacks, but a recent study may extend its anti-inflammatory benefits to cancer survivors.

A study pre-published online from The Lancet examined various clinical trials comparing the long-term mortality of those individuals who used aspirin or didn’t (2). This meta-analysis study indicated that relatively low-dose aspirin (about 75 mg or a baby aspirin a day) reduced cancer deaths in various long-term cancer survivors by about 20 percent. So should all of us be taking a baby aspirin daily? Possibly, but aspirin does have side effects, especially in terms of bleeding.

But one thing you can do with total safety is to boost your intake of fruits and vegetables. It turns out that fruits and vegetables contain salicylates, the group of compounds that represents the major active ingredient in aspirin. In addition, fruits and vegetables also contain other anti-inflammatory polyphenols (the chemicals that give plants their color). Since plants don’t have access to the local pharmacy to protect themselves from microbial invasion, they have to synthesize their own “drugs”. By consuming fruits and vegetables, we are constantly visiting our “food” pharmacy. Their defense mechanisms now become our nutritional allies in silencing inflammatory gene expression that is turned on when certain food components (such as omega-6 and saturated fats) fool the most primitive part of the immune system (the innate immune system) to think it is under microbial attack.

Most of the inflammation that drives cardiovascular disease and cancer starts with this type of cellular inflammation induced by our diet (3). It’s taken new breakthroughs in molecular biology to finally understand that what’s good for the plant is also going to be great for us if we want to live a longer and better life.

References
1. Sears B. “The Zone.” Regan Books. New York, NY (1995)
2. Rothwell PM, Fowkes FG, Belch JF, Ogawa H, Warlow CP, and Meade TW. “Effects of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomized trials.” Lancet, Early Online Publication, 7 December (2010)
3. 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.

Does eating fat make you fat?

The 1990s brought with it an era of people fearing fat. After all, “if no fat touches my lips, then no fat reaches my hips”. Harvard took charge of this debate and declared war against fat, especially saturated fat. Manufacturers created everything from fat-free yogurt to cookies. Overall, fat intake did decrease nationwide during this time, but the waist lines of the U.S. population continued to expand. Despite recent reports about the Mediterranean diet and the benefits of monounsaturated fats, the low-fat craze still has many hardwired to think that eating higher-fat foods will make them fat. Although calorically speaking, fat is more energy dense than carbohydrates and protein, a recent study may help to ease people’s preconceived notions on the role of fat and weight gain.

There have been inconsistent findings in the literature on whether the type of fat consumed influences weight change. Even studies in which poly and monounsaturated fats have been substituted for saturated fat to lower cardiovascular disease were equally wishy-washy (1). In fact, a recent study published in the American Journal of Clinical Nutrition questions whether dietary fat played a role in future weight gain (2). Of the more than 89,000 men and women studied, overall fat consumption ranged from 31.5 percent to 36.5 percent. No matter the total fat intake or the type of fat consumed, there was no effect on weight gain over the long term in either men or women. Maybe fat doesn’t make you fat.

This only proves you can always tell a Harvard man, you just can’t tell him very much.

1) Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 2010 Jan 20.

2) Forouhi NG, Sharp SJ, Du H, van der A DL, Halkjaer J, Schulze MB, Tjønneland A, Overvad K, Jakobsen MU, Boeing H, Buijsse B, Palli D, Masala G, Feskens EJ, Sørensen TI, Wareham NJ. Dietary fat intake and subsequent weight change in adults: results from the European Prospective Investigation into Cancer and Nutrition cohorts. Am J Clin Nutr. 2009 Dec;90(6):1632-41.

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.

Simple dietary changes ease diabetes risk

Since 1980 the number of individuals with diabetes in the United States has nearly tripled to an astonishing 17 million (1), leading physicians, researchers and pharmaceutical companies on the hunt for the most effective treatment options. A recent publication in Diabetes Care studied approximately 400 non-diabetic individuals at high cardiovascular risk and randomized them to one of three diets: Low-fat, Mediterranean with nuts, and Mediterranean with olive oil (2). Individuals were educated on the various diets but did not have to follow a certain calorie allotment or physical activity plan. After four years, the number of individuals with diabetes was 10.1 percent in the Mediterranean with olive oil group, 11 percent in the Mediterranean with nuts group and 17.9 percent in the low-fat group. Collectively when compared to the low-fat group, those following a Mediterranean diet were 52 percent less likely to develop diabetes. These results show the significant impact that simple dietary changes can have on diabetes risk reduction without having to dramatically change caloric intake or activity levels.

1. Diabetes Data and Trends. Available at: http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm. Accessed: 10/14/2010

2. Salas-Salvadó J, Bulló M, Babio N, Martínez-González MA, Ibarrola-Jurado N, Basora J, Estruch R, Covas MI, Corella D, Arós F, Ruiz-Gutiérrez V, Ros E; For the PREDIMED Study investigators. Reduction in the Incidence of Type 2-Diabetes with the Mediterranean Diet: Results of the PREDIMED-Reus Nutrition Intervention Randomized Trial. Diabetes Care. 2010 Oct 13. [Epub ahead of print]

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.

Eat your breakfast

You’ve probably heard it a billion times. “Don’t skip breakfast!” But most Americans, adults and children, are not heeding this advice. There are a bunch of reasons why you should eat breakfast within one hour of waking. And it’s even better if the meal is Zone balanced – the correct amount of lean protein, low-glycemic carbohydrates and a dash of monounsaturated fat.

After sleeping a full night, your blood sugar level is low, and you are in a catabolic state. This means that body has been using up stored energy in the liver as well as beginning to cannibalize your muscle for energy. If you skip breakfast, your blood sugar stays low and cannibalization of your muscle will continue. This is a stress situation, and the body releases more cortisol as a response. This creates insulin resistance that increases insulin levels further, driving down blood sugar even more. No wonder by mid-morning you are incredibly hungry.

The whole basis of the anti inflammatory diet is to keep your insulin in a zone, not too high and not too low. This will stabilize blood sugar and prevent continuing muscle degradation for energy. Eating a Zone breakfast can help keep your insulin stabilized, provide the necessary protein to start rebuilding muscle mass and increase the levels of glycogen in the liver. This is called anabolism. It is this continued balance of catabolism and anabolism that we call metabolism. As long as the two phases of metabolism are balanced, so are your weight and your mood. This is why breakfast is so critically important for your alertness, productivity, increased cognition and memory, satiety, and weight control because it starts your day out on a high note as opposed to digging a deeper hormonal hole that you try to crawl out during the rest of the day. A balanced Zone breakfast is also the easiest way to keep your sugar cravings under control during the day. In other words, you will not need the constant trips to the vending machine or your secret stash of candy to artificially maintain blood sugar levels.

Still not convinced? Then give your kids breakfast. Research shows a link between regular breakfast consumption and improvement in academic performance and psychosocial functioning as well as cognition among children. Eating a breakfast every day will be the best way to protect any child against becoming overweight. Make that a Zone breakfast balanced in protein, low glycemic-load carbohyrates, and monounsaturated fat, and you have the ideal pediatric weight-loss program as obese children are less hungry at their next meal as demonstrated at Harvard Medical School more than a decade ago.2 This finding at Harvard was also confirmed by a research study in the Journal of the American Dietetic Association on breakfast consumption among children that found the prevalence of obesity to be higher in those who regularly skipped breakfast.3 Evidence also suggests that breakfast consumption may improve cognitive function related to memory, test grades, and school attendance.4 Want the smartest and leanness kid in the school? It’s easy — feed them a Zone breakfast every day. While you are at it, make each of their meals a Zone meal and give them plenty of EPA and DHA at the same time.

[1] Affenito S. “Breakfast: A Missed Opportunity.” Journal of the American Dietetic Association 107:565-69 (2007)

2 Ludwig DS et al, “High glycemic index foods, overeating, and obesity.” Pediatrics 103: e26 (1999)

3 Deshmukh-Taskar P et al. “The relationship of breakfast skipping and type of breakfast consumption with nutrient intake and weight status in children and adolescents: The National Health and Nutrition Examination Survey 1999-2006.” Journal of American Dietetic Association 110:869-78 (2010)

4 Rampersaud G et al. “Breakfast habits, nutritional status, body weight, and academic performance in children and adolescents.” Journal of American Dietetic Association 105: 843-60 (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.