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.

Does living longer mean living poorly?

America has the highest health-care costs in the world. But are we really living better as a consequence of this massive cost? The January 2011 issue of the Journals of Gerontology says maybe not (1). There is no question that Americans are living longer, but our years of disease-free and functional living are declining faster. In particular, the chances of someone age 65 reaching age 85 have doubled from (from 20 percent to 40 percent), but a longer life is coming with more chronic disease and an increasing inability to function normally. In other words, the number of healthy years we can expect to have has actually decreased over the last decade.

So where are all our health-care dollars going? They appear to be keeping us alive. We are delaying death at the price of decreased quality of life as we age. As the lead author stated, “Longer life is what we want. But we’re going to have to pay for it with more treatment of diseases and accommodations for disability.” Since 40 percent of our health-care costs come after age 65, we can expect that Medicare costs will rise even faster than expected as an increasingly sicker baby-boomer population begins to enter Medicare starting this year.

But what about all the news we hear about “anti-aging” research where we can just inject “youth hormones,” like growth hormone, to reverse the aging process? It turns out that there may be trouble brewing in that area also. These hormones are growth factors. This means they turn on DNA synthesis that leads to a shortening of telomeres at the end of a DNA strand. When these telomeres become short enough, any future DNA turnover stops, and the cell dies. This has been demonstrated to occur in mice in which you can increase the levels of growth hormone. When you do so, the animals die prematurely, and there appears to be an acceleration of aging in many organs, including the brain (2).

This potential side effect of increased growth hormone is further confirmed in another recent study (3). This particular study demonstrated that giving mice inhibitors of the release of growth hormone increased their longevity. What was unique in this study was that they used specially bred mice that age prematurely. So if you want to speed up the aging process by taking growth hormone injections, you might look great in the process, but don’t count on an extended lifetime.

Of course, there is another way of looking better and living a longer, healthier life: Calorie restriction without hunger or deprivation. This is the foundation of the anti inflammatory diet. By maintaining the appropriate balance of protein to carbohydrate at every meal and snack, you are able to maintain satiety (i.e. absence of hunger). If you aren’t hungry, then you don’t eat as many calories. This automatically slows down the aging process as long as you are getting adequate protein and supplying necessary micronutrients (4). Not surprisingly, this is also how you squeeze out more quality years as you age.

References
1. Crimmins EM and Beltran-Sanchez H. “Mortality and morbidity trends: Is there a compression of morbidity?” Journals of Gerontology Series B 66B: 75-86 (2011)
2. Bartke A. “Can growth hormone accelerate aging?” Neuroendocrinology 78: 210-216 (2003)
3. Banks WA, Morely JE, Farr SA, Price TO, Ercal N, Vidaurre I, and Schally AV. “Effect of a growth hormone-releasing hormone antagonist on teleomerase activity, oxidative, stress, longevity, and aging in mice.” Proc Nat Acad Sci USA 107: 22272-22277 (2010)
4. Sears B. “The Anti-Aging Zone.” Regan Books. New York, NY (1999)

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.

Why the Atkins diet doesn’t work and never will

The goal of any diet is to help you lose excess weight and keep it off. The first part is relatively easy to achieve; the second part is incredibly difficult to maintain. Any diet that restricts calories will do the first part, but invariably the lost weight returns. This is definitely the situation for the Atkins diet. I knew Bob Atkins well, and the only answer he had as to why people regain weight on his diet was that they are addicted to carbohydrates. Frankly, I never bought into that explanation from Bob any more than I believed the reasoning of the advocates for low-fat diets saying the failure to maintain weight loss is because people are addicted to fat. To paraphrase former President Clinton, “It’s the hormones, stupid.”

In most cases what really causes weight regain is cellular inflammation induced by hormonal imbalance. This is why any diet that uses the word “low” or “high” to describe itself will induce hormonal imbalance, and therefore ultimately fail. Low-fat diets are generally high-carbohydrate diets. High levels of carbohydrates will increase the production of insulin, which is the hormone that makes you fat and keeps you fat. This increase in insulin will generate increased cellular inflammation that increases the likelihood for weight regain (1). On the other hand, the Atkins diet is a low-carbohydrate diet that is also a high-fat diet. If those fats on the Atkins diet are rich in saturated and omega-6 fats (which they usually are), then their presence will also increase cellular inflammation (1). This increase in cellular inflammation (by either type of diet) disrupts hormonal signaling patterns (especially for insulin signaling) that generate increased insulin resistance. This was shown in one of my earlier research articles that demonstrated that under carefully controlled clinical conditions, following the Atkins diet shows significant increases in cellular inflammation compared to those subjects following the Zone Diet (2). In addition, there was decreased endurance capacity of the subjects on the Atkins diet compared to those on the Zone Diet (3).

The differences are probably due to the fact that the  anti inflammatory diet is a diet that is moderate in protein, carbohydrate and fat. It’s this type of dietary moderation of macronutrients that generates hormonal balance.Now new data from Yale Medical School indicates that a ketogenic (i.e. Atkins) diet may even have worse health implications than simply weight regain (4). In this study, it was demonstrated that although indicators of insulin resistance in the blood may be decreased on a ketogenic diet, insulin resistance in the liver was dramatically increased. Since the liver is the central processing organ for controlling metabolism, this would suggest that long-term use of the Atkins diet would cause metabolic problems leading to accumulation of excess fat. Adding even more fuel to this hormonal fire is another study that demonstrated that a ketogenic diet leads to increased production of cortisol (another hormone that makes you fat and keeps you fat) in the fat cells (5). Any increase in cortisol increases insulin resistance in that particular organ.

So it appears that ketogenic diets (like the Atkins diet) may initially reduce insulin levels in the blood, but increase insulin resistance in organs, such as the liver and the adipose tissue. The bottom line: Any initial weight loss with the Atkins diet is a false hope since it causes insulin resistance in various organs that ultimately cause the regain of any lost weight as excess fat. That’s a very bad prescription.

References:
1. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
2. 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)
3. 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)

4. Jornayvaz FR, Jurczak MJ, Lee HY, Birkenfeld AL, Frederick DW, Zhang D, Zhang XM, Samuel VT, and Shulman GI. “A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain.” Am J Physiol Endocrinol Metab 299: E808-815 (2010)
5. Stimson RH, Johnstone AM, Homer NZ, Wake DJ, Morton NM, Andrew R, Lobley GE, and Walker BR. “Dietary macronutrient content alters cortisol metabolism independently of body weight changes in obese men.” J Clin Endocrinol Metab 92: 4480-4484 (2007)

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 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)
2. 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)
3. 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)

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.

A cash cow based on bad science

There has been no more profitable class of drugs than the cholesterol-lowering statins. Their success is based on a very simple premise: High cholesterol levels mean certain cardiovascular death. While there has always been questioning of the cholesterol story at the fringes of academic research (1), now the cries are rising within the highest reaches of the academic research community that something is just not right.

Since no one wants to die, you would think that measurement of mortality would be the primary clinical end-point for any clinical trial of a statin drug. There is no question that for people who have already had a heart attack, taking a statin prolongs their life by reducing all-cause mortality. But what about the people who have never had a heart attack but have high cholesterol levels? There the answer is much more open.

One recent article has studied all the published studies with some 65,000 patients who had high cholesterol but no evidence of heart disease to see the effect that statin drugs have on their mortality (2). The answer was virtually none. In fact, in all the statin trials published since 2005, there has been a striking lack of benefits in populations that simply had high cholesterol levels but no evidence of any cardiovascular disease (3). This is true except for one trial that was funded by a drug company that makes a new powerful, statin and run by the individual who has the patent for measuring C-reactive protein as a marker for cardiovascular risk (3).

Here was a new premise: People who had normal levels of cholesterol and no heart disease but high levels of C-reactive protein also need even more powerful statins. The fact that C-reactive protein is an unreliable marker in cardiovascular patients because it changes so quickly was conveniently ignored (4). Nonetheless a successful trial would generate more sales for the drug company and more testing of C-reactive protein for everyone going to see a physician.

So when a careful analysis of this “highly-successful” trial was published this year, it was found that there were no benefits in reducing cardiovascular mortality between the active and placebo groups (3). As the cholesterol story appears to have a growing number of flaws in it, I predict it will become more commonplace to have drug companies and medical researchers continue to use sleight-of-hand statistical dodges to make it appear their “wonder” drugs are actually doing wonderful things, like reducing death from heart disease in those who have no evidence of heart disease.

Maybe it’s time to return to a better working hypothesis of what really drives heart disease—inflammation and to use anti-inflammatory diets to prevent the occurrence of cardiovascular disease (5,6).

References

1. Ravnshov U. The Cholesterol Myths. New Trends Publishing. Warsaw, IN (2002)
2. Ray KK, Seshasai SRK, Erqou, S, Sever P, Jukema JW, Ford I, and Sattar N. “Statins and all-cause mortality in high-risk primary prevention.” Arch Intern Med 170: 1-024-1031 (2010)
3. De Lorgeril M, Salen P, Abramson J, Dodin S, Hamazaki T, Kotucki W, Okuyama H, Pavy B, and Rabaeus M. “Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITER controversy.” Arch Intern Med 170 1032-1036 (2010)
4. Bogaty P, Brophy JM, Boyer L, Simard S, Joseph L, Bertrand F, and Dagenais GR. “Fluctuating inflammatory markers in patients with stable ischemic heart disease. Arch Intern Med 165: 221-226 (2005)

5. Sears B. “The Zone.” Regan Books. New York, NY (1995)
6. Sears B. “The Anti-Inflammation Zone.” Regan Books. New York, NY (2005)

Nothing contained in this blog is intend 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.