Breast cancer and inflammation

Breast cancer is probably the greatest fear women have, even though they are 10 times more likely to die from heart disease. Yet both diseases are driven by cellular inflammation.

Cellular inflammation occurs when the most primitive part of your immune system (the innate immune system) is activated. The key player in the innate immune system is a gene transcription protein known as nuclear factor-kappaB (NF-κB). Once activated, NF-κB moves into the cell’s nucleus and causes the expression of a wide variety of pro-inflammatory mediators that accelerate the growth of the tumor. A recent publication in Cancer Research has demonstrated that complete inhibition of the NF-κB in the breast tissue prevents the development of breast cancer in animal models (1).

Of course, there is one slight problem with this approach. If you inhibit NF-κB too much, you make yourself a sitting target for microbial invasion. So the question is what activates the NF-κB in the first place? The answer is the diet, and specifically how the diet increases the levels of arachidonic acid, as I described in my most recent book, “Toxic Fat” (2). As the levels of arachidonic acid increase in the cell, there is an increased formation of inflammatory compounds (i.e. leukotrienes) that activate NF-κB (3).

So what might the best approach be for reducing the risk of breast cancer? The obvious answer is to decrease the levels of arachidonic acid in the breast tissue. The best way would be to follow a strict anti inflammatory diet to reduce the formation of arachidonic acid in the first place (4).

Unfortunately, most women (and men) are not willing to take that step. That being the case, then what other dietary approach can be used? I would suggest that supplementing the diet with high-purity omega-3 fatty acid concentrates rich in EPA and DHA is the one approach that everyone can follow. This is especially true since it takes only 15 seconds a day. The benefits of this approach was recently demonstrated in another article published last year in the American Journal of Clinical Nutrition that demonstrated supplementation with purified omega-3 concentrates can dramatically increase the levels of omega-3 fatty acids in the breast tissue of women who have a high-risk potential of developing breast cancer (5).

Of course, if you not only take high-purity omega-3 fatty acid concentrates, but also follow the anti inflammatory diet, then you will have done every possible dietary intervention to reduce the activation of NF-κB in the target tissue for breast cancer (not to mention also reducing the risk for heart disease). Of course, there are some side effects to this dietary approach: You become thinner, smarter and happier in the process.

References

  1. Liu M, Sakamaki T, Casimiro MC, Willmarth NE, Quong AA, Ju X, Ojeifo J, Jiao X, Yeow WS, Katiyar S, Shirley LA, Joyce D, Lisanti MP, Albanese C, and Pestell RG. “The canonical NF-kappaB pathway governs mammary tumorigenesis in transgenic mice and tumor stem cell expansion.” Cancer Res 24: 10464-10473 (2010)
  2. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN. (2008)
  3. Sanchez-Galan E, Gomez-Hernandez A, Vidal C, Martin-Ventura JL, Blanco-Colio LM, Munoz-Garcia B. Ortega L, Egido J, and Tunon J. “Leukotriene B4 enhances the activity of nuclear factor-kappaB pathway through BLT1 and BLT2 receptors in atherosclerosis.” Cardiovasc Res 81: 216-225 (2009)
  4. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  5. Yee LD, Lester JL, Cole RM, Richardson JR, Hsu JC, Li Y, Lehman A, Belury MA, and Clinton SK. “Omega-3 fatty acid supplements in women at high risk of breast cancer have dose-dependent effects on breast adipose tissue fatty acid composition.” Am J Clin Nutr 91:1185–1194 (2010)

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.

Good thing I listened to Dr. Sears

By Mary Dinehart-Perry

Having recently delivered a baby, I was surprised to see the latest article published in the Journal of The American Medical Association that fish oil supplementation rich in DHA has no impact on postpartum depression or cognitive and language development in early childhood.

The study looked at approximately 2,400 Australian women who began supplementation at around 21 weeks gestation through to the birth of their children (1). Individuals were randomized into one of two groups, one getting a fish oil supplement exceptionally rich in DHA (800mg DHA and 100mg EPA) and the other vegetable oil. It has been know for years that fish oils containing both EPA and DHA have dramatic benefits for fetal outcome. However, since there is little EPA in the brain, it was assumed in the past that it was only DHA that contributed to all of these benefits. However, recent studies have demonstrated that EPA rapidly gets into the brain and is rapidly oxidized, but DHA is not (2).

Lack of awareness has led to the mistaken belief that DHA is the only omega-3 fatty acid attributed to optimal brain functioning. Needless to say, companies that market DHA-rich products work very hard to continue to foster this misconception. This explains why the clinical trials that have used only DHA to treat depression or other conditions such as ADHD have been found it to be wanting. This is because DHA is a structural omega-3 fatty acid, not an anti-inflammatory one like EPA.

As long as adequate EPA is constantly in the blood, there will be enough EPA in the brain to address any neurological problems for both the mother and the fetus. That’s why this published study with only 100 mg of EPA was providing essentially a placebo level of this critical omega-3 fatty acid (3).

Although I myself am only a data point of one, I took the same dosage of DHA described above (800mg) during my pregnancy, however, it was coupled with 1600mg EPA. I can’t help but think that it may have been the combination of EPA/DHA that helped me avoid postpartum depression.

Mary Dinehart-Perry is clinical trials director of Zone Labs.

  • Makrides M., Gibson RA, McPhee AJ, Yelland L, Quinlivan J, Ryan P and the DOMInO Investigative Team. Effect of DHA Supplementation During Pregnancy on Maternal Depression and Neurodevelopment of Young Children: A Randomized Controlled Trial. JAMA 2010; 304:1675-1683.
  • Chen CT, Liu Z, Ouellet M, Calon F, RichardP, and Bazinet RP. Rapid beta-oxidation of eicosapentaenoic acid in mouse brain. Prostaglandins, Leukotrienes and Essential Fatty Acids 2009; 80: 157–163
  • Wojcicki JM, Heyman MB. Maternal omega-3 fatty acid supplementation and risk for perinatal maternal depression. J Matern Fetal Neonatal Med. 2010 Oct 7. [Epub ahead of print]
  • Hill AM, Buckley JD, Murphy KJ, and Howe PRC. Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors. Am J Clin Nutr 2007;85:1267–1274.

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.

Study: High-dose, high purity omega-3 oil lowers breast-cancer risk

Breast cancer accounts for more than 25 percent of all female cancers. Breast cancer is also strongly linked to obesity. This means as our obesity crisis accelerates, we can expect breast cancer rates to follow. The reason that breast cancer and obesity are linked is due to cellular inflammation caused by the diet.

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.

For losing weight, exercise is good; diet is better

Here’s standard quote: “Losing weight can improve health and reduce many of the risk factors related to diabetes and heart disease.” Unfortunately, that’s not true. The correct statement is “losing excess body fat can improve health and reduce many of the risk factors related to diabetes and heart disease.”

It may seem like a minor difference, but it makes a world of difference. Weight loss could be due to water loss or cannibalization of lean body mass (muscles and organs), neither of which will lead to any health benefits.

If you want to reduce excess body fat, you have to lower insulin levels. How do you control that on a consistent basis? Remember the 80/20 rule. That means 80 percent of your insulin control will come from following a strict anti inflammatory diet, and 20 percent will come from increased physical activity.

This means the best exercise program can be undone by the wrong diet. Physical exercise has many important benefits, such as reducing the likelihood of diabetes and heart disease, improving sense of self-worth and hanging out with like-minded individuals.

Unfortunately, initial weight loss is not one of those benefits since research has demonstrated that exercise increases one’s appetite. This is why following a strict anti inflammatory diet is imperative if you are trying to lose weight by increasing your exercise. Another helpful hint is to increase your high purity omega-3 oil intake, as it has been demonstrated that fat loss is significantly increased when high purity omega-3 oil is used in combination with exercise.

On the other hand, after you reach your weight goals, the balance of diet and exercise to maintain your weight shifts to a 50/50 balance. Now exercise becomes an ideal way to maintain your weight as long as you continue to control insulin through the anti inflammatory diet.

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.

High purity omega-3 oil doesn’t work if you don’t take enough

On Aug. 29, the New England Journal of Medicine published an electronic article stating that giving supplements of EPA and DHA to people with a prior heart attack had no benefits on preventing future cardiovascular events (1). Of course, this article states the reason is that current drugs the patients are receiving are so good that adding extra high purity omega-3 oil is worthless, which of course made the national press. It sounded pretty fishy to me. First of all, this study was actually much smaller than the previously published studies (2,3) that had demonstrated striking benefits of omega-3 fatty acids on cardiovascular outcomes. The GISSI study demonstrated a 20-percent reduction in heart attacks and a 45 percent reduction in sudden cardiac death (2). The even larger JELIS study demonstrated a 20 percent reduction in cardiovascular events, and all the patients were taking statins.

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.