Tag Archives: aging

Harvard explains why people regain weight with the Atkins diet

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A study from Harvard Medical School explains that even though people can lose weight on a ketogenic diet, all lost weight usually rapidly returns.

Ketogenic diets have been recommended for decades for rapid weight loss. The most famous is the Atkins diet. Ketogenic diets are based on high-protein and very low-carbohydrate intake. For the past 40 years such diets have been routinely used in America for weight loss, yet America remains in the midst of a growing epidemic of obesity. While ketogenic diets can induce initial weight loss, all lost weight usually rapidly returns, resulting in more weight (and even more fat) than when the person started the ketogenic diet.

For many years it was thought that such weight regain was due to poor dietary compliance. Now Harvard Medical School in an article in the June 27, 2012, issue of the Journal of the American Medical Association shows the reason for weight regain is more ominous than simple dietary non-compliance. In carefully controlled studies Harvard researchers demonstrated that on a ketogenic diet the levels of the hormone cortisol increase by 18%, and the levels of active thyroid hormone (T3) control metabolism decrease by 12% (1).

The effect of increased cortisol is to cause rapid fat accumulation, as any patient who has ever used prescription cortisol-like drugs knows. It also causes depression of the immune system, loss of memory, and thinning of the skin. These are also hallmarks of the acceleration of the aging process. Furthermore, the lowering of the active form of the thyroid hormone slows down the metabolism, making even seemingly small increases in calorie intake result in increased body fat accumulation. Besides setting you up to regain all the lost weight, the Atkins diet apparently also increases the rate of aging.

However, many people seem willing to continue to try such ketogenic diets in hopes of losing weight quickly. Yet highly controlled studies I published in the world’s most prestigious nutrition journal in world more than six years ago demonstrated that is simply not a true statement (2). In this study either a ketogenic diet (the Atkins diet) or a non-ketogenic diet (the Zone Diet) were compared in obese individuals. For the first six weeks all meals for both groups were prepared in a metabolic kitchen at Arizona State University (in essence treating subjects like lab rats). Both diets contained an equal number of calories.

When it came to weight loss, the subjects following the Zone Diet actually lost slightly more weight than as those on the ketogenic diet during the initial six-week period as shown in Figure 1.

Figure 1. Weight Loss (Zone Diet in open circles, Atkins diet in black squares)

Relative to fat loss on the non-ketogenic Zone Diet, their loss of body fat was again superior to the Atkins diet as shown in Figure 2. Fat loss is far more important than weight loss since all the health benefits from weight loss come from the loss of excess body fat; not from the loss of retained water or loss of muscle mass.

Figure 2. Fat Loss (Zone Diet in open circles, Atkins diet in black squares)

When the subjects continued on the respective diets for another four weeks (but now preparing meals on their own), those subjects on the non-ketogenic Zone Diet continued to lose even more weight and body fat, whereas those on the ketogenic Atkins diet did not. They had reached a plateau. The new research from Harvard Medical explains why.

One of the major problems in following a calorie-restricted diet is lack of energy. In this same study, the subjects on the Zone Diet demonstrated improved daily energy compared to those on the Atkins diet. In another publication using the same subjects, we also demonstrated that those subjects following the Zone Diet had greater performance in endurance testing compared to those following the ketogenic Atkins diet (3).

Figure 3. Energy levels (Zone Diet in open circles, Atkins diet in black squares)

For the past 40 years, ketogenic diets (like the Atkins diet) have failed to treat obesity in America. That is why one relies upon science, not hype, to determine which is the best diet to lose weight (and really body fat), keep it off, and increase energy. Continuing research from Harvard Medical School since 1999 demonstrates that the Zone Diet is the best dietary program to accomplish both goals (1,4-7). And the one thing Harvard will always tell you is that they are never wrong.

References

  1. Ebbeling CB, Swain JF, Feldman HA, Wong WA, Hachey DL, Garcia-Logo E, and Ludwig DD. “Effects of dietary composition on energy expenditure during weight loss maintenance.” JAMA 307: 267-2634 (2012)
  2. Johnston, C.S., Tjonn, S., Swan, P.D., 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. Ludwig, DS, Majzoub AJ, 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 EA, and Ludwig DS. “Dietary composition and physiologic adaptations to energy restriction.” Am J Clin Nutr 71:901–907 (2000)
  6. Pereira MA, Swain J, Goldfine AB, Rifai N, and Ludwig DS. “Effect of low-glycemic diet on resting energy expenditure and heart disease risk factors during weight loss.” JAMA. 292: 2482-2490 (2004)
  7. Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, and Ludwig DS. “Effects of a low–glycemic load vs. low-fat diet in obese young adults”. JAMA 297: 2092-2102 (2007)

What are the real differences between EPA and DHA?

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The first casualty of marketing is usually the truth. The reality is that the two key omega-3 fatty acids (EPA and DHA) do a lot of different things, and as a result the benefits of EPA and DHA are often very different. That’s why you need them both. But as to why, let me go into more detail.

Benefits of EPA

The ultimate goal of using omega-3 fatty acids is the reduction of cellular inflammation. Since eicosanoids derived from arachidonic acid (AA), an omega-6 fatty acid, are the primary mediators of cellular inflammation, EPA is the most important of the omega-3 fatty acids to reduce cellular inflammation for a number of reasons. First, EPA is an inhibitor of the enzyme delta-5-desaturase (D5D) that produces AA (1). The more EPA you have in the diet, the less AA you produce. This essentially chokes off the supply of AA necessary for the production of pro-inflammatory eicosanoids (prostaglandins, thromboxanes, leukotrienes, etc.)

DHA is not an inhibitor of this enzyme because it can’t fit into the active catalytic site of the enzyme due to its larger spatial size. As an additional insurance policy, EPA also competes with AA for the enzyme phospholipase A2 necessary to release AA from the membrane phospholipids (where it is stored). Inhibition of this enzyme is the mechanism of action used by corticosteroids. If you have adequate levels of EPA to compete with AA (i.e. a low AA/EPA ratio), you can realize many of the benefits of corticosteroids but without their side effects. That’s because if you don’t release AA from the cell membrane, you can’t make inflammatory eicosanoids. Because of its increased spatial dimensions, DHA is not a good competitor of phospholipase A2 relative to EPA. On the other hand, EPA and AA are very similar spatially so they are in constant competition for the phospholipase A2 enzyme, just as both fatty acids are in constant competition for the delta-5 desaturase enzyme. This is why measuring the AA/EPA ratio is such a powerful predictor of the state of cellular inflammation in your body.

The various enzymes (COX and LOX) that make inflammatory eicosanoids can accommodate both AA and EPA, but again due to the greater spatial size of DHA, these enzymes will have difficulty-converting DHA into eicosanoids. This makes DHA a poor substrate for these key inflammatory enzymes. Thus DHA again has little effect on cellular inflammation, whereas EPA can have a powerful impact.

Finally, it is often assumed since there are not high levels of EPA in the brain, that it is not important for neurological function. Actually, it is key for reducing neuro-inflammation by competing against AA for access to the same enzymes needed to produce inflammatory eicosanoids. However, once EPA enters into the brain, it is rapidly oxidized (2,3). This is not the case with DHA (4). The only way to control cellular inflammation in the brain is to maintain high levels of EPA in the blood. This is why all the work on depression, ADHD, brain trauma, etc., has demonstrated that EPA is superior to DHA (5).

Benefits of DHA

At this point, you might think that DHA is useless. Just the opposite, because DHA can do a lot of different things than EPA and some of them even better.

First is in the area of omega-6 fatty acid metabolism. Whereas EPA is the inhibitor of the enzyme (D5D) that directly produces AA, DHA is an inhibitor of another key enzyme, delta-6-desaturase (D6D), that produces the first metabolite from linoleic acid known as gamma linolenic acid or GLA (6). However, this is not exactly an advantage. Even though reduction of GLA will eventually decrease AA production, it also has the more immediate effect of reducing the production of the next metabolite known as dihomo gamma linolenic acid or DGLA. This can be a disaster as a great number of powerful anti-inflammatory eicosanoids are derived from DGLA. This is why if you use high-dose DHA, it is essential to add back trace amounts of GLA to maintain sufficient levels of DGLA to continue to make anti-inflammatory eicosanoids.

In my opinion, the key benefit of DHA lies in its unique spatial characteristics. As mentioned earlier, the extra double bonds and length of DHA compared to EPA means it takes up a lot more space in the membrane. Although this increase in spatial volume makes DHA a poor substrate for phospholipase A2 as well as the COX and LOX enzymes, it does a great job of making membranes (especially those in the brain) a lot more fluid as the DHA sweeps out a much greater volume in the membrane than EPA. This increase in membrane fluidity is critical for synaptic vesicles and the retina of the eye because it allows receptors to rotate more effectively, thus increasing the transmission of signals from the surface of the membrane to the interior of the nerve cells. This is why DHA is a critical component of these parts of the nerves (7). On the other hand, the myelin membrane is essentially an insulator so that relatively little DHA is found in that part of the membrane.

This constant sweeping motion of DHA also causes the breakup of lipid rafts in membranes (8). Disruption of these islands of relatively solid lipids makes it more difficult for cancer cells to continue to survive and more difficult for inflammatory cytokines to initiate the signaling responses to turn on inflammatory genes (9). In addition, these greater spatial characteristics of DHA increase the size of LDL particles to a greater extent compared to EPA. As a result DHA helps reduce the entry of these enlarged LDL particles into the muscle cells that line the artery, thus reducing the likelihood of developing atherosclerotic lesions (10). Thus the increased spatial territory swept out by DHA is good news for making certain areas of membranes more fluid or lipoprotein particles larger, even though it reduces the benefits of DHA in competing with AA for key enzymes important in the development of cellular inflammation.

Common Effects for Both EPA and DHA

Not surprisingly, there are some areas in which both EPA and DHA appear to be equally beneficial. For example, both are equally effective in reducing triglyceride levels (10). This is probably due to the relatively equivalent activation of the gene transcription factor (PPAR alpha) that causes the enhanced synthesis of the enzymes that oxidize fats in lipoprotein particles. There is also apparently equal activation of the anti-inflammatory gene transcription factor PPAR-gamma (11). Both seem to be equally effective in making powerful anti-inflammatory eicosanoids known as resolvins (12). Finally, although both have no effect on total cholesterol levels, DHA can increase the size of LDL particle to a greater extent than EPA can (10).

Summary

EPA and DHA do different things, so you need them both. If your goal is reducing cellular inflammation, then you probably need more EPA than DHA. How much more? Probably twice the levels, but you always cover your bets with omega-3 fatty acids by using both at the same time.

References

  1. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  2. Chen CT, Liu Z, Ouellet M, Calon F, and Bazinet RP. “Rapid beta-oxidation of eicosapentaenoic acid in mouse brain: an in situ study.” Prostaglandins Leukot Essent Fatty Acids 80:157-163 (2009)
  3. Chen CT, Liu Z, and Bazinet RP. “Rapid de-esterification and loss of eicosapentaenoic acid from rat brain phospholipids: an intracerebroventricular study. J Neurochem 116:363-373 (2011)
  4. Umhau JC, Zhou W, Carson RE, Rapoport SI, Polozova A, Demar J, Hussein N, Bhattacharjee AK, Ma K, Esposito G, Majchrzak S, Herscovitch P, Eckelman WC, Kurdziel KA, and Salem N. “Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography.” J Lipid Res 50:1259-1268 (2009)
  5. Martins JG. “EPA but not DHA appears to be responsible for the efficacy of omega-3 long chain polyunsaturated fatty acid supplementation in depression: evidence from a meta-analysis of randomized controlled trials.” J Am Coll Nutr 28:525-542 (2009)
  6. Sato M, Adan Y, Shibata K, Shoji Y, Sato H, and Imaizumi K. “Cloning of rat delta 6-desaturase and its regulation by dietary eicosapentaenoic or docosahexaenoic acid.” World Rev Nutr Diet 88:196-199 (2001)
  7. Stillwell W and Wassall SR. “Docosahexaenoic acid: membrane properties of a unique fatty acid. Chem Phys Lipids 126:1-27 (2003)
  8. Chapkin RS, McMurray DN, Davidson LA, Patil BS, Fan YY, and Lupton JR. “Bioactive dietary long-chain fatty acids: emerging mechanisms of action.” Br J Nutr 100:1152-1157 (2008)
  9. Li Q, Wang M, Tan L, Wang C, Ma J, Li N, Li Y, Xu G, and Li J. “Docosahexaenoic acid changes lipid composition and interleukin-2 receptor signaling in membrane rafts.” J Lipid Res 46:1904-1913 (2005)
  10. Mori TA, Burke V, Puddey IB, Watts GF, O’Neal DN, Best JD, and Beilin LJ. “Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men.” Am J Clin Nutr 71:1085-1094 (2000)
  11. Li H, Ruan XZ, Powis SH, Fernando R, Mon WY, Wheeler DC, Moorhead JF, and Varghese Z. “EPA and DHA reduce LPS-induced inflammation responses in HK-2 cells: evidence for a PPAR-gamma-dependent mechanism.” Kidney Int 67:867-874 (2005)
  12. Serhan CN, Hong S, Gronert K, Colgan SP, Devchand PR, Mirick G, and Moussignac RL. “Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals.” J Exp Med 1996:1025-1037

Hard times are ahead

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Last month was a red-letter month for the future of mankind as the world population passed 7 billion. Unfortunately, this fact dovetails with recent research that indicates it is likely that one-half of all Americans will be diabetic by 2050 (1).

The combination of these two trends does not bode well for the future. To begin with, how are we going to feed all these people? Most of the arable land on the planet is already under cultivation. Furthermore, urbanization is destroying prime cropland at a rapid pace.

Added to these facts is that the diversity of most of the world’s calories is rapidly decreasing. Currently the five top sources of calories in the world are corn, soybeans, wheat, rice and potatoes (as well as its kissin’ cousin cassava, which is incredibly poor in protein and nutrients). The first two crops (corn and soy) are rich sources of omega-6 fatty acids. In addition, corn, wheat, and rice provide extremely high-glycemic carbohydrates that can be easily refined to last forever and make thus a wide variety of processed foods. (Potatoes and cassava tend to decompose rapidly and can’t be easily refined, except perhaps as potato chips). As a consequence, omega-6 fatty acids and refined carbohydrates are now the cheapest form of calories in the world. In fact, it is estimated that they are 400 times less expensive per calorie than fresh fruits and vegetables.

So how can you feed this growing population of more than 7 billion people? The answer is easy—produce even more refined carbohydrates and omega-6 fatty acids.

Unfortunately, feeding the growing population of the world with cheap omega-6 fatty acids and refined carbohydrates is exactly the best way to increase cellular inflammation and drive the development of diabetes (2). It is estimated that by 2050 diabetes will be the primary non-infectious disease on the planet. This is equally bad news as it is also the most expensive chronic disease to treat on a long-term basis.

Today, more than 26 percent of all Americans older than 65 has diabetes. If the estimates of increased diabetes are correct (1), then it is likely that the number of Americans older than 65 in 2050 with diabetes may be greater than 50 percent. The current level of diabetes is the primary reason why our health-care expenses are spiraling out of control. If you double number of older Americans with diabetes by 2050, there is no way the current health-care system, as we know it can possibly survive. Add to the fact that once you have diabetes, you are 2-4 times more likely to develop heart disease and Alzheimer’s. It is not a very pleasant picture of the future of health care in America.

What can you do about it? On a global basis, not much unless you would like to see an apocalyptic event that reduces the population from 7 billion to a more manageable 1-2 billion individuals. Of course, this is highly unlikely. However, on the individual basis there is a lot you can do to protect yourself in the future. Simply take control of your future by focusing on managing cellular inflammation for a lifetime by following an anti-inflammatory diet. This may be your only real health security in times of increasing demands on the planet’s resources to produce food. There is no question that we have other troubles brewing like climate change, decreasing water supplies, and decreasing cheap energy, all of which will also impact the cost of food, driving more individuals toward inexpensive sources of calories no matter what the health consequences. But the rise of diabetes will occur first.

Old folks like myself will probably be OK, but the future generations will take the brunt of trouble brewing ahead.

References

  1. Boyle JP , Thompson TJ, Gregg EW, Barker LE, and Williamson DF. “Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence.” Population Health Metrics 8:29 (2010)
  2. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)

Meditation: Push-ups for the brain?

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Meditation has always been considered a “fringe” area of medicine. Although it has been around for thousands of years, it was never considered “high-tech”.

However, the development of new imaging technologies has finally given researchers the ability to ask some interesting questions about meditation and its effect on brain structure and cognitive performance.

When comparing brain wave patterns using old technologies like an EEG, it has been demonstrated that experienced meditators have higher levels of alpha waves (indicative of a relaxed brain) and lower levels of beta waves (indicative of focusing on intentional tasks or anxiety) during mediation (1). More recent imaging technology like the SPECT scan indicates that experienced meditators have improved cerebral blood flow (2). MRI technology has shown that experienced meditators have a greater density of grey matter in the brain (3), improved neural connections (4), and lower sensitivity to induced pain (5) when compared to matched control groups.

One of the problems with these types of studies has always been subject recruitment. The studies described above are simply various examples of case-control epidemiological studies. This type of study is often done in cancer epidemiology and is used to compare someone with cancer to a control without cancer to see if any differences are apparent (like if smoking is associated with lung cancer). The problem is that experienced meditators may already have different brain structures or improved neural networks and corresponding improved attention spans that attracted them to meditation in the first place. This is like comparing professional athletes to their fans watching them on TV and then looking for differences in fitness between the two groups.

Aware of these shortcomings, more recent, better controlled, shorter-term studies have taken either non-meditators or experienced meditators and put them into an intensive meditation program to be compared to equally matched subjects waiting to enter the same a program. Using a more tightly controlled group of subjects, it has been found that meditation does indeed have benefits in reducing sensitivity to pain (6), improving ability to modulate alpha waves that help reduce distractions (7), increasing brain grey matter (8), and increasing telomerase activity (9). The increased telomerase activity is usually associated with increased lifespan because when telomeres on the DNA become too short, the cell dies.

There are a lot of health benefits that stem from sitting in a comfortable chair thinking of nothing for at least 20 minutes a day. In fact, it is so easy that most people never get around to doing it.

So if you don’t have time to take at least 20 minutes a day to meditate, then consider taking high-dose fish oil. In as little as 35 days, you will see it also generates significant increases in the intensity of alpha waves, increased attention span, and improved mood (10) just like experienced meditators, who have spent years trying to reach the same goals. And if you maintain high levels of omega-3 fatty acids in your blood for a longer period of time, it appears that you get decreased telomere shortening that should help you live longer (11). And if you are worried about time, taking adequate levels of fish oil to get these benefits only takes 15 seconds a day.

Of course, if you were really smart, you would do both every day.

References

  1. Lagopoulos J, Xu J, Rasmussen I, Vik A, Malhi GS, Eliassen CF, Arntsen IE, Saether JG, Hollup S, Holen A, Davanger S, and Ellingsen O. “Increased theta and alpha EEG activity during nondirective meditation.” J Alt Complementary Medicine 15: 1187-1192 (2009)
  2. Newberg A, Alavi A, Baime M, Pourdehnad M, Santanna J, and d’Aquili E. “The measurement of regional cerebral blood flow during the complex cognitive task of meditation: a preliminary SPECT study.” Psychiatry Res 106: 113-122 (2001)
  3. Toga AW, Lepore N., Gaser C. The underlying anatomical correlates of long-term meditation: larger hippocampal and frontal volumes of gray matter. Neuroimage 45: 672-678 (2009)
  5. Luders E, Clark K, Narr KL, Toga AW. “Enhanced brain connectivity in long-term meditation practitioners [In Process Citation] Neuroimage 57: 1308-1316 (2011)
  7. Grant JA, Courtemanche J, Duerden EG, Duncan GH, and Rainville P. “Cortical thickness and pain sensitivity in zen meditators.” Emotion 10: 43-53 (2010)
  8. Zeidan F, Martucci KT, Kraft RA, Gordon NS, McHaffie JG, and Coghill RC. “Brain mechanisms supporting the modulation of pain by mindfulness meditation.” J Neuroscience 31: 5540-5548 (2011)
  9. Kerr CE, Jones SR, Wan Q, Pritchett DL, Wasserman RH, Wexler A, Villanueva JJ, Shaw JR, Lazar SW, Kaptchuk TJ, Littenberg R, Hamalainen MS, and Moore CI. “Effects of mindfulness meditation training on anticipatory alpha modulation in primary somatosensory cortex.” Brain Research Bulletin 85: 96-103 (2011)
  10. Holzel BK, Carmody J, Vangel M, Congleton C, Yerramsetti SM, Gard T, and Lazar SW. “Mindfulness practice leads to increases in regional brain gray matter density.” Psychiatry Research 191: 36-43 (2011)
  11. Jacobs TL, Epel ES, Lin J, Blackburn EH, Wolkowitz OM, Bridwell DA, Zanesco AP, Aichele SR, Sahdra BK, Maclean KA, King BG, Shaver PR, Rosenberg EL, Ferrer E,; Wallace BA, and Saron CD. “Intensive meditation training, immune cell telomerase activity, and psychological mediators.” Psychoneuroendocrinology 36: 664-681 (2011)
  12. Fontani G, Corradeschi F, Felici A, Alfatti F, Migliorini S, and Lodi L. “Cognitive and physiological effects of omega-3 polyunsaturated fatty acid supplementation in healthy subjects.” Eur J Clin Invest 35: 691-
  13. Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, and Whooley MA. “Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease.” JAMA 303: 250-257 (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.

How to eliminate 50 percent of all coronary events

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The European Society of Cardiology estimates a 50 percent reduction of coronary events if you can stabilize soft, vulnerable plaques (1). We are often led to believe that plaques you can see on an angiogram are “killer” plaques. It’s true that if they are large enough to obstruct blood flow, they will decrease oxygen transfer to the heart muscle cells making them more tired with less effort.

This is the definition of stable angina. It simply means it takes less effort to over-exert the heart muscles before they fatigue. However, you need approximately a 90 percent total obstruction of the blood vessel to develop stable angina. These plaques account for most of the plaques you might find in an angiogram. This is why if you take an angiogram, you are often immediately wheeled into the operating room to have a stent put into the artery with the belief you are only seconds away from an immediate heart attack and death.

However, the same angiogram can’t see a few plaques (because they are so small), known as the soft, vulnerable ones. When soft, vulnerable plaques rupture (like a pimple), then you have the death and disability (i.e., damaged heart tissue) that truly characterize heart disease. Technically, this is called an acute coronary event, and it has very little to do with the stable plaques that can cause angina. It is this small number of “rogue” soft, vulnerable plaques that are the true killers in heart disease (2,3).

The ultimate cause of plaque rupture is cellular inflammation inside the plaque. Cellular inflammation degrades the fibrous external coating of the plaque. Usually inside these soft, vulnerable plaques are also a lot of macrophages engorged with lipids. This is called the “necrotic core”. When the plaque bursts, these lipid pools are released into the bloodstream causing platelet aggregation and the rapid blockage of the artery resulting in a complete restriction of blood flow (as opposed to a limited restriction of blood flow with a typical stable plaque that will never rupture). It is estimated that about 75 percent of all coronary events are caused by ruptures of the soft, vulnerable plaques (2).

As I mentioned above, the really scary part of this story is that there is no type of imaging technology that can detect dangerous soft, vulnerable plaques. In essence, you don’t know if you have them or not. This is why the prediction of impeding cardiovascular events remains a guessing game. Even more interesting is that these soft, vulnerable plaques seem to form rather quickly (in about 10 years) as opposed to growing slowly over a lifetime (4). Moreover, the rate of growth of these soft, vulnerable plaques is strongly correlated with increasing insulin levels in the blood (4).

So what does this mean for people who don’t want to die from a sudden rupture of soft, vulnerable plaques that can’t be detected? The first thing is to reduce the inflammation within the plaque. Surprisingly, there is only one clinical study that has ever been published that addressed this question, and it used fish oil (5). This study indicated that if you give patients relatively high doses of fish oil, you could see a definite remodeling of the soft, vulnerable plaques in about 40 days compared to subjects taking a placebo composed of safflower oil. The plaques in the subjects taking the fish oil became less inflamed, had higher levels of omega-3 fatty acids, fewer macrophages and more well-formed fibrous caps compared to those taking the placebo. So taking a therapeutic level of fish oil for a lifetime seems to be a good way to reduce the rupture of these plaques.

Another way to potentially reduce their formation in the first place is lower insulin levels. The reason insulin levels are elevated is because organs, such as the adipose tissue, the liver and the muscles, are also inflamed (6). The best way to reduce that systemic inflammation is to follow the anti-inflammatory diet and take therapeutic levels of fish oil for a lifetime. Your success is best measured by the AA/EPA ratio in the blood. Call me crazy, but I think that’s what I have been recommending for the past 16 years (7).

References

  1. Yia-Herttulala S, Bentzon JF, Daemen M, Falk E, Garcia-Garcia HM, Merrmann J, Hoefer IM, Juekma JW, Krams R, Kwak BR, Marx N, Maruszeqica M, Newby A, Pasterkamp G, Serruys PWJC, Waltenberger J, Weber C, and Tokgozoglu L. “Stabilization of atherosclerotic plaques.” Thomobosis and Haemostasis 106: 1-19 (2011)
  2. Schaar JA, Muller JE, Falk E, Virmani R, Fuster V, Serruys PW, Colombo A, Stefanadis C, Ward Casscells S, Moreno PR, Maseri A, and van der Steen AF. “Terminology for high-risk and vulnerable coronary artery plaques. Report of a meeting on the vulnerable plaque.” Eur Heart J 25: 1077-1082 (2004)
  3. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, Ford E, Furie K, Go A, Greenlund K, Haase N, Hailpern S, Ho M, Howard V, Kissela B, Kittner S, Lackland D, Lisabeth L, Marelli A, McDermott M, Meigs J, Mozaffarian D, Nichol G, O’Donnell C, Roger V, Rosamond W, Sacco R, Sorlie P, Stafford R, Steinberger J, Thom T, Wasserthiel-Smoller S, Wong N, Wylie-Rosett J, and Hong Y. “Heart disease and stroke statistics–2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.” Circulation 119:480-486 (2009)
  4. Hagg S, Salehpour M, Noori P, Lundstrom J, Possnert G, Takolander R, Konrad P, Rosfors S, Ruusalepp A, Skogsberg J, Tegner J, and Bjorkegren J. “Carotid plaque age is a feature of plaque stability inversely related to levels of plasma insulin.” PLoS One 6: e1824 (2011)
  5. Thies F, Garry JM, Yaqoob P, Rerkasem K, Williams J, Shearman CP, Gallagher PJ, Calder PC, and Grimble RF. “Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomized controlled trial.” Lancet 2003 361: 477-485 (2003)
  6. Sears, B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  7. Sears B. “The Zone.” Regan Books. New York, NY (1995)

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 key to a healthy gut

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Most people think all you need for a healthy gut is to consume bacterial-fortified yogurt products. In reality, the balance of bacteria in your gut may hold a key toward managing systemic inflammation in our bodies.

First of all, there are a lot of bacteria in our guts. The human body contains about 100 trillion cells, but the number of bacteria in the gut is 10 times greater in number. Furthermore, these bacteria are not just taking up space; they are actually providing numerous useful functions that make them a symbiotic “organ” to our own body. In particular, they can ferment carbohydrates to provide additional energy, make various vitamins, break down toxins we might ingest, and help prevent the growth of pathogenic bacteria.

Although there are literally millions of different bacteria in the world, only about 500 species actually reside in our guts. We also know that these gut bacteria can be further divided into three distinct bacterial ecosystems (1). Just like there are four unique blood groups that can classify every human, we also have three distinct bacterial systems. Once one of these systems becomes established in the gut, it begins to alter the gut environment that only certain species of other bacteria can follow and safely begin their symbiotic relationship with us.

So how does each ecosystem of bacteria keep out the bad apples (like Salmonella)? First of all, the bacteria in each distinct ecosystem have to alert our own immune cells in the intestine that they are friends, not foes. Apparently they have learned how to suppress the immune system in our own cells so they can co-exist in our gut (2). However, I believe even though these ecosystems of bacteria can be recognized as friends and not foes, they still need unique nutrients to help them act as the first line of defense against millions of other harmful bacteria.

Those nutrients are polyphenols. In the plant world, these polyphenols act as antibiotics against microbial attack. There is evidence that the “good” bacteria in our gut can use them as a means to help ward off invading bacteria that threaten our own unique bacterial fingerprint. Of course, the only way we can continue to help our unique bacterial partners in our gut is to continue to eat lots of fruits and vegetables that are rich in polyphenols. That’s why your grandmother told you to eat an apple a day to keep the doctor away.

References

  1. Arumugam M, Raes J, Pelletier E, et al. “Enterotypes of the human gut microbiome.” Nature DOI: 10.1038/nature09944 (2011)
  2. Round JL, Lee SM, Li Jennifer, Tran G, Bana J, Chatila TA and Mazmanian SK. “The toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota.” Science DOI:10.1126/scienc.1206095 (2011)
  3. Moreno S, Scheyer T, Romano CS, and Vojnov AA. “Antioxidant and antimicrobial activities of rosemary extracts linked to their polyphenol composition.” Free Radic Res 40: 223-231 (2006)

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

What are we really entitled to?

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For the past year the future of the American economy has centered on the word “entitlement,” especially in terms of health care. But no one is quite certain about what the word means. Social Security is not really an entitlement because it is a forced savings program that promises you the money you put into an old-age fund will be given back to you when you need it, some time in your 60s. The fact that the government has been using that account as a piggy bank to fund itself without raising taxes and leaving behind government I.O.U.s in place of the funds is another matter. But you are definitely entitled to at least get back the money you put into it.

Medicare is a completely different matter. In this case, you put very little money into a fund (which is also heavily borrowed from by the government), and you expect to get a lot more back. In my view, you are entitled to get back the money you paid into Medicare, and anything more should be considered a gift from a rich uncle (Sam), who is no longer very rich.

In an attempt to resolve this problem, Congressman Paul Ryan came up with a plan that went nowhere but had at least some intellectual merit: You pay into the medical fund for old age, and you get back what you paid in (and a little more) at age 67. The most notable feature of this plan was getting an annual voucher for about $6,000 based on 2012 dollars to be applied for private health insurance premiums after age 67.

At the current Medicare tax rate, the only way to pay in more than $6,000 into proposed trust fund on an annual basis is if you make more than $200,000 per year. Since there aren’t too many Americans making that type of salary, it’s your rich uncle who must make up the difference. Even if you were making $200,000 per year for 40 years and only planned to live another 15 years after retirement, it is still a pretty good deal, as it is forced savings for health-care insurance in the future. Any overpayment on your part will only help those who are not lucky enough to make $200,000 a year for 40 years. Unfortunately, this proposal was politically dead on arrival

The real problem with any health-care entitlement program was pointed out in a well-reasoned article in the May 19th issue of The New Republic — you can’t cure chronic disease, you can only manage it (1). In addition, new research analyses of the current state of Americans in old age indicates that we aren’t doing a very good job of managing chronic diseases (2). Although Americans are living longer, the length of life with chronic disease and loss of functional mobility (i.e. independent living) have rapidly increased since 1998. We are living longer because the elderly are essentially on life support generated by increasingly more expensive drugs that only marginally extend the lives of the very sick. We are not going to cure heart disease, cancer, stroke, and definitely not Alzheimer’s. The best we can do is to help manage their outcomes. Unfortunately, these are also diseases of the elderly, and the cost of increasing each year of life after 65 has risen from about $50,000 in the 1970s to nearly $150,000 in the 1990s. This could possibly be justified if the rich uncle were still rich.

The solution according to the authors of the New Republic article is redirecting the money that we can spend to maximize expenditures on public health care (prevention and elongation of independent living) as opposed to “curing” elderly with chronic disease that usually results in the decreased quality of life (1). The primary beneficiaries of this shift in medical thinking should be children followed by working adults, with the lowest health-care priority going to those over age 80. It sounds harsh, but that is exactly how socialized medicine works in Europe.

So what do you do to protect yourself in the future, especially if you are nearing 65? My suggestion is to start aggressively reducing cellular inflammation by following an anti-inflammatory diet and lifestyle. That’s the only thing you are really entitled to and that will also be the only thing your “rich” uncle can realistically pay for in the future.

References

  1. Callahan D and Nuland S. “The quagmire: how American medicine is destroying itself.” The New Republic. May 19, 2011
  2. Crimmins EM and Beltran-Sanchez H. “Mortality and morbidity trends: is there compression of morbidity?” J Gerontol B Physchol Soc Sci 66: 75-86 (2011)

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 new wrinkle in the cholesterol story

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One of the great marketing successes of the pharmaceutical industry has been the linkage between LDL cholesterol levels and heart disease. In essence, the message, “if your LDL cholesterol is high, you are going to die,” is powerful. Unfortunately, the data state otherwise.

It was known in the mid 1990s that oxidized LDL was the primary suspect in the development of atherosclerotic lesions; not natural, non-oxidized LDL. But it was also at this time that the first statin studies began to appear, and that gave the pharmaceutical industry a patented drug to “prevent” heart disease (2). It was such a good story to tell and an even better one to sell. Unfortunately, as I pointed out in an earlier blog, it has never held up well against unbiased scrutiny, especially in patients with high cholesterol levels but without any heart disease.

Part of the reason lies in the data. Shown below is the correlation of LDL cholesterol to heart disease

You can see from this data that there is a higher percentage of cardiovascular disease patients with high LDL cholesterol levels compared with very low levels, but not that much. This explains why about half the people who die from heart disease have normal LDL cholesterol levels (less than 130 mg/dl). It also means that high LDL cholesterol is not a very good predictor of heart disease.

On the other hand, a very different picture emerges if you look at the levels of oxidized LDL levels as shown below.

Even without a background in statistics you can see a very striking relationship in the prediction of heart disease with increasing levels of oxidized LDL levels.

So why don’t physicians use oxidized LDL levels as an indicator of heart disease risk? First, the test is much more difficult to do than a simple cholesterol test. Second, it ruins a great story that is easy to communicate to the patient. Third, the best way of reducing oxidized LDL levels is natural anti-oxidants, such as polyphenols, that have no patent protection (3,4). Reducing LDL cholesterol is simple. Just take a statin drug for the rest of your life. Reducing oxidized LDL cholesterol requires having plenty of antioxidants in your diet with polyphenols the most powerful.

Now there is another new entry into the LDL story. This is “super-sticky” LDL. In an online pre-publication, it was demonstrated that this new type of LDL particle may be even worse than oxidized cholesterol in promoting the development of heart disease (5). This “super-sticky” LDL comes from the formation of advanced glycosylation end products (AGEs). I described this formation of protein-carbohydrate linkages as an integral part of the aging process in my book, “The Anti-Aging Zone,” published more than a decade ago (6).

The best way to reduce the production of “super-sticky” LDL is to reduce blood sugar levels. This helps explain why individuals with diabetes are two to three times more likely to develop heart disease. The best way to reduce elevated blood sugar is the Zone diet. That’s why the latest dietary recommendations for the treatment of diabetes by the Joslin Diabetes Research Center at Harvard Medical School are essentially identical to the Zone diet.

Heart disease remains the number-one cause of death in America. Unfortunately, it is more complex than “taking a statin a day to keep death away”.

References

  1. Maor I and Aviram M. “Oxidized low-density lipoprotein leads to macrophage accumulation of unesterified cholesterol as a result of lysosomal trapping of the lipoprotein hydrolyzed cholesterol ester.” J Lipid Res 35: 803-819 (1994)
  2. Simvastatin Study Group. “Randomized trial of cholesterol lowering in 4,444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S).” Lancet 344: 1383-1389 (1994)
  3. Shafiee M, Carbonneau MA, Urban N, Descomps B, and Leger CL. “Grape and grape seed extract capacities at protecting LDL against oxidation generated by Cu2+, AAPH or SIN-1 and at decreasing superoxide THP-1 cell production.” Free Radic Res 37: 573-584 (2003) (ISSN: 1071-5762)
  4. Chen CY, Yi L, Jin X, Mi MT, Zhang T, Ling WH, and Yu B. “Delphinidin attenuates stress injury induced by oxidized low-density lipoprotein in human umbilical vein endothelial cells.” Chem Biol Interact 183: 105-112 (2010)
  5. Rabbani N, Godfrey L, Xue M, Shaheen F, Geoffrion M, Milne R, and Thornalley PJ. “Glycation of LDL by methylglyoxal increases arterial atherogenicity.” Diabetes 60 doi:10.2337/db09-1455 (2011)
  6. Sears B. “The Anti-Aging Zone.” Regan Press. 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.

The fallacy of using DHA alone for brain trauma

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I am constantly amazed by the lack of understanding by neurologists of basic essential fatty acid biochemistry in the treatment of brain trauma and concussions. They often blindly believe that the only omega-3 fatty acid that has any impact in the treatment of concussions is DHA alone. Their blind faith is based on the observation that you find a lot of DHA in the brain and little EPA. This obviously means that EPA must not be important for brain function. This is similar to stating the world is flat because it appears that way to the naked eye.

I have mentioned many times in my books that EPA and DHA have different functions, and that’s why you need both of these essential omega-3 fatty acids (1-4). This is especially true for the brain. EPA produces most of the anti-inflammatory properties of omega-3 fatty acids since it’s structurally similar to arachidonic acid (AA) as they both contain 20 carbon atoms with approximately the same spatial configuration. As a result, EPA can inhibit the enzymes that would otherwise produce pro-inflammatory eicosanoids from AA. It is AA that generates the inflammation caused by brain trauma. DHA, on the other hand, is primarily a structural component of neural tissue. They do different jobs, and that’s why you need both in combination.

So why isn’t there as much EPA in the brain compared to DHA? The reason is simple. EPA enters the brain just as quickly as DHA, but it is rapidly oxidized, whereas DHA is sent off to long-term storage in neural tissue (5-7). The lifetime of DHA in the human brain is measured in years, whereas the lifetime of the EPA is measured in days. So obviously when you kill an animal and look at the brain, you are not going to find very much EPA.

What complicates the issue is that if you only treat a concussion with DHA, some of the DHA will be converted to EPA. This gives the appearance that DHA is working to reduce inflammation. Since brain trauma and concussions generate inflammation in the brain, doesn’t it make more sense to provide as much EPA as possible to reduce the inflammation as opposed to supplementing only with DHA and hoping some fraction of it will be converted to EPA?

To answer that question, it is useful to look at two recent studies that used the same protocol to study inflammation induced by a concussion injury (8,9). The same total amount of omega-3 fatty acids was used to treat the animals after the concussion injury. One experiment used a 2:1 ratio of EPA to DHA, and the other experiment used only DHA. If the DHA was so important, then the animals treated with the DHA alone should have demonstrated three times the reduction of neuro-inflammation compared to the group that received omega-3 fatty acids containing only one-third as much DHA.

In fact, just the opposite was the case. The 2:1 EPA/DHA group demonstrated greater benefits compared to the DHA-alone group in reducing neuro-inflammation induced by a concussion. Why? EPA is a far more powerful anti-inflammatory agent than DHA. This is why in both studies the AA/EPA ratio was used as the marker of inflammation induced by the concussion injury. Since the AA/EPA ratio was decreased in both studies, this meant that some of the pure DHA was converted to EPA providing at least some anti-inflammatory actions. Thus giving 100 percent DHA is not exactly the most efficient way to decrease neuro-inflammation induced by a concussion injury. This is further emphasized by a recent study that indicated that 1 gram of DHA per day for an 18-month period had no impact in the cognitive improvement of Alzheimer’s patients (10), even though Alzheimer’s is known to be a neuro-inflammatory disease (11).

Does this mean that DHA is not important for brain repair? Of course not. This is because you need both EPA and DHA for optimal repair of brain damage after a concussion. You need the EPA to reduce the neuro-inflammation, and you need the DHA to help rebuild new neurons. But to give DHA alone without additional EPA to maximally reduce neuro-inflammation caused by concussions simply makes no sense.

References

  1. Sears B. “The Zone.” Regan Books. New York, NY (1995)
  2. Sears B. “The OmegaRx Zone.” Regan Books. New York, NY (2002)
  3. Sears B. “The Anti-inflammation Zone.” Regan Books. New York, NY (2005)
  4. Sears B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  5. Chen CT, Liu Z, and Bazinet RP. “Rapid de-esterification and loss of eicosapentaenoic acid from rat brain phospholipids: an intracerebroventricular study.” J Neurochem 116: 363-373 (2011)
  6. Chen CT, Liu Z, Ouellet M, Calon F, and Bazinet RP. “Rapid beta-oxidation of eicosapentaenoic acid in mouse brain: an in situ study. “Prostaglandins Leukot Essent Fatty Acids 80: 157-163 (2009)
  7. Umhau JC, Zhou W, Carson RE, Rapoport SI, Polozova A, Demar J, Hussein N, Bhattacharjee AK, Ma K, Esposito G, Majchrzak S, Herscovitch P, Eckelman WC, Kurdziel KA, and Salem N. “Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography.” J Lipid Res 50: 1259-1268 (2009)
  8. Mills JD, Bailes JE, Sedney CL, Hutchins H, and Sears B. “Omega-3 fatty acid supplementation and reduction of traumatic axonal injury in a rodent head injury model.” J Neurosurg 114: 77-84 (2011)
  9. Bailes JE and Mills JD. “Docosahexaenoic acid reduces traumatic axonal injury in a rodent head injury model.” J Neurotrauma 27: 1617-1624 (2010)
  10. Quinn JF, Raman R, Thomas RG, Yurko-Mauro K, Nelson EB, Van Dyck C, Galvin JE, Emond J, Jack CR, Weiner M, Shinto L, and Aisen PS. “Docosahexaenoic acid supplementation and cognitive decline in Alzheimer disease: a randomized trial.” JAMA 304: 1903-1911 (2010)
  11. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, Cooper NR, Eikelenboom P, Emmerling M, Fiebich BL, Finch CE, Frautschy S, Griffin WS, Hampel H, Hull M, Landreth G, Lue L, Mrak R, Mackenzie IR,McGeer PL, O’Banion MK, Pachter J, Pasinetti G, Plata-Salaman C, Rogers J, Rydel R, Shen Y, Streit W, Strohmeyer R, Tooyoma I, Van Muiswinkel FL,Veerhuis R, Walker D, Webster S, Wegrzyniak B, Wenk G, and Wyss-Coray T. “Inflammation and Alzheimer’s disease.” Neurobiol Aging 21: 383-421 (2000)

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.

Fish oil and fat loss

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

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

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

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

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

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

References

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

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