Fish oil, sterol absorption, and Zetia - Blanchet

Dr. Blanchet podcast on fish oil and sterol absorption re heart disease.

http://tuesdaytalkshow.podomatic.com/entry/2013-10-08T10_41_51-07_00


Questions -
     Are you a hyper absorber of plant sterols?
     What is optimal range of EPA/DHA intake?
     What about Zetia?

Fish Oil Triglycerides vs. Ethyl Esters: A comparative review of absorption, stability and safety concerns

Fish Oil Triglycerides vs. Ethyl Esters: A comparative review of absorption, stability and safety concerns

Media exposure, scientific findings, and word of mouth have lead to a significant increase in fish oil supplementation over the past five years. The popularity of these supplements has also lead to an increased concern over product quality. The term “pharmaceutical quality” is typically associated with fish oils that are highly refined; however, the use of this term is not regulated and can be freely used by any branded fish oil product. Most experts associate pharmaceutical quality with products that comply with a fish oil monograph developed by the Council for Responsible Nutrition (CRN). The CRN Monograph established strict limits for environmental contaminants and oxidative quality parameters. Although the CRN Monograph represents an important step forward in the standardization of high quality fish oil it does not address every issue relating to quality. In particular the monograph does not differentiate between lipid classes (molecular forms). Although a product label may say “Fish Oil”, the chances are the product is not an oil at all, rather it is an alternate lipid class called a fatty acid ethyl ester (FAEE) or just EE for short. This differs in molecular structure from authentic fish oil which has a chemical structure known as a triglyceride (TG).

What are triglycerides?

The National Academy of Sciences defines fats and oils as “complex organic molecules that are formed by combining three fatty acids with one molecule of glycerol”. Triglycerides, or triacylglycerols, are the terms used to define this molecular structure combining three fatty acids (i.e. EPA and DHA) esterified (bonded) to a glycerol backbone. TGs are the natural molecular form that make up virtually all fats and oils in both animal and plants species. The omega-3 fats present in fish are almost exclusively TGs¹. Because free fatty acids are rapidly oxidized the TG structure offers greater stability to the fatty acids and prevents breakdown and oxidation².

What are ethyl esters, and how are they produced?

Fatty acid ethyl esters are a class of lipids that are derived by reacting free fatty acids with ethanol (alcohol)³. Called trans-esterification, the process involves a reaction whereby the glycerol backbone of a TG is removed and substituted with ethanol⁴. The resulting EE allow for the fractional distillation (concentration) of the long chain fatty acids at lower temperatures. Commonly referred to as molecular distillation in the fish oil industry this step allows for the selective concentration of the EPA and DHA fatty acids to levels greater than found naturally in fish3. The resulting EPA and DHA concentrate is typically the end product that is subsequently marketed and sold as “Fish Oil concentrate”. This situation presents several issues. Because the term fat or oil refers only to TG the EPA and DHA ethyl ester concentrate is, by definition, no longer a fat or oil and is incorrectly marketed as fish oil. Because EEs rarely occur in nature this affects the way they are digested and absorbed in the body.

Are all fish oil concentrates ethyl esters?

The vast majority of fish oil concentrates sold globally; including those sold in North America are EPA and DHA EE concentrates. A small percentage of fish oil concentrates on the market are natural TGs. In the manufacturing of EE concentrates it is possible to convert the fatty acids back to TGs using food grade enzymes. This process, called glycerolysis, removes the ethanol molecule and re-esterifies the EPA and DHA fatty acids to a glycerol backbone. These are commonly referred to as re-esterfied or concentrated triglycerides (rTGs). The process of converting EE to TG is uncommon due to cost constraints adding 30-40 % to the end bulk oil cost. Therefore, the only rationale for omitting the glycerolysis step is cost cutting.

Absorption and metabolism of natural triglycerides vs. ethyl esters

Dietary fish oil (triglycerides) is digested in the small intestine by the emulsifying action of bile salts and the hydrolytic activity of pancreatic lipase^1,5. The hydrolysis of a TG molecule produces two free fatty acids (FFA) and a monoglyceride (one fatty acid combined to glycerol)^1,5. These metabolic products are then absorbed by intestinal enterocytes and reassembled again as TGs^1,5. Carrier molecules called chylomicrons then transport the TGs into the lymphatic channel and finally into the blood⁶. The digestion of EEs is slightly different due to the lack of a glycerol backbone¹. In the small intestine it is again the pancreatic lipase that hydrolyzes the fatty acids from the ethanol backbone, however; the fatty acid-ethanol bond is up to 50 times more resistant to pancreatic lipase as compared to hydrolysis of TGs^7,8. The EEs that get hydrolyzed produce FFA plus ethanol. The FFA’s are taken up by the enterocytes and must be reconverted to TGs to be transported in the blood¹. The TG form of fish oil contains its own monoglyceride substrate; whereas EE fish oils, coupled to ethanol, do not. EE must therefore obtain a glycerol substrate from another source. Without a glycerol or monoglyceride substrate TG re-synthesis is delayed, suggesting that transport to the blood is more efficient in natural TG fish oils in comparison to EEs. Furthermore, this delay of TG re-synthesis in EE fish oils could cause an increase in free fatty acids and subsequent oxidation of those free fatty acids.

Bioavailability of triglycerides vs. ethyl ester fish oils

Numerous studies have assessed the absorption and bioavailability of EE fish oils. Most studies have measured the amount of EPA and DHA in blood plasma after ingestion of fatty acids as either TG or EE. Although a few studies have found that the absorption rate is similar between the two types of oils, the overall evidence suggests that TG fish oils are better absorbed in comparison to EE. Natural TG fish oil results in 50 % more plasma EPA and DHA after absorption in comparison to EE oils¹¹, TG forms of EPA and DHA were shown to be 48 % and 36 % better absorbed than EE forms¹², EPA incorporation into plasma lipids was found to be considerably smaller and took longer when administered as an EE¹³, plasma lipid concentrations of EPA and DHA were significantly higher with daily portions of salmon in comparison to 3 capsules of EE fish oil¹⁴ and in the rat, DHA TG supplementation led to higher plasma and erythrocyte DHA content than did DHA EE¹⁵ and a higher lymphatic recovery of EPA and DHA¹⁶.

One of the causative factors for the poor bioavailability of EE is a much greater resistance to digestive enzymes. As previously mentioned, during the digestive process, pancreatic lipase enzymes hydrolyse (cleave) the oils to liberate the fatty acids and EEs are much more resistant to this enzymatic process than the natural TG form⁷. A recent study assessed the specificity of five lipases towards EPA and DHA in TG and EE forms. All of the investigated lipases discriminated against both EPA and DHA more in EE than in the natural TG oils. In other words, both EPA and DHA were more easily hydrolysed from a TG than from an EE. EPA and DHA hydrolysis would be further compromised in individuals who suffer from a digestive disorder, such as pancreatic insufficiency. EEs should be avoided in such populations as they would likely cause malabsorption of EPA and DHA. Review of the existing literature provides evidence which, suggests that omega-3 fatty acids in the natural form of TGs are more efficiently digested and significantly better incorporated into plasma lipids in comparison to EE forms. Recently, two clinical trials have settled the debate of which fish oil form is more bio-available in humans; the ethyl ester (EE) versus the triglyceride (TG) form. The Dyerberg et al., 2010 study was done to demonstrate the differences in absorption levels of plasma EPA+DHA following consumption of various fish oil forms including EE and TG. They noticed that with about the same grand total of EPA+DHA administered to the EE and TG group compared to the placebo group, the EE form was given the lowest assimilation as a measure of bioavailability⁹. The mechanism of action was simple, in that, pancreatic lipase breaks down EE to a lesser extent than TG⁹. Since, the omega 3 fatty acid plasma profile can significantly be elevated with the consumption of TG versus EE fish oil; then clearly TG fish oil can be more effective. In another more recent study done by Neubronner et al., 2010 a similar comparison was made utilizing a different study design. A unique method of bio-availability was used (Omega 3 index) this method looks at the omega 3 FA (EPA+DHA) incorporated into the RBC membranes¹⁰. In comparison to the plasma levels measured in the Dyerberg et al., study, this method is even more specific because it can measure EPA+DHA at the level of the tissues¹⁰. Therefore, the outcome of this study showed a statistically significant incorporation of EPA+DHA in the RBC membranes via TG over EE by over 25 percent¹⁰. Therefore, in both of the above studies the overall bioavailability of omega 3 fatty acids with equal EPA+DHA in the form of TG showed to be more effective.

Ethyl ester fish oils are less stable, and readily oxidize

Omega-3 fatty acids in the form of EEs are much less stable than those in the natural TG form and readily oxidize. The oxidation kinetics of DHA as an EE or as a TG was assessed by measuring the concentration of oxygen found in the head space of a reaction vessel with both TG and EE forms¹⁷. The EE form of DHA was more reactive, and quickly oxidized, demonstrating that EEs are far less stable and can more readily produce harmful oxidation products¹⁷. Furthermore, the stability of phospholipid, triglyceride and EEs containing DHA has been assessed¹⁸. After a ten-week oxidation period, the EE DHA oil decayed 33 % more rapidly¹⁸.

Ethyl ester fish oil safety

During the digestive process, EEs are converted back to TGs by intestinal enterocytes1 which, results in the release of ethanol. Although the amount of ethanol released in a typical dose of fish oil is small, those with sensitivities to alcohol or those who are alcoholics should refrain from the consumption of EEs. Young children may also be more vulnerable to the toxic effects of ethanol even in small quantities. The exact amount of ethanol released from the EE fish oil is dependent on the exact profile of the fatty acids. For a typical 60 % omega-3 EE concentrate the amount of ethanol would be approximately 15 % by weight (see Figure 1). Additional concern exists regarding whether a small portion of EE is absorbed directly into the body¹⁹. Unlike TGs, the presence of EEs in the body has been found to potentiate cytotoxicity¹⁹. Several in vitro studies using purified lysosomes²⁰, purified mitochondria¹⁹ or intact Hep G2 cells²² have provided evidence for toxicity of EEs. Studies in animals have shown that ethanol released into the liver and pancreas can result in severe organ damage²³. Post mortem organ analysis has demonstrated that EEs are toxic mediators of ethanol induced cellular injury²⁴, and have been shown to induce pancreatic injuries when infused in vivo into rats²⁵. It is possible that efficient EE digestion in the GI tract could prevent toxicity³, but until further studies carefully examine EE oxidation, the potential for direct uptake of EEs, or EE absorption into the circulation via the stomach, EEs should be consumed with caution.

How can I determine if my fish oil is a natural triglyceride or an ethyl ester?

There is a simple, inexpensive and rapid method to determine if a fish oil supplement is in the TG or EE form by using polystyrene (Styrofoam) cups.

Method

Measure and place 20 ml of fish oil in a polystyrene cup. Place the cup on a plate to avoid any mess. Observe the cup after 10 minutes. If the fish oil has leaked significantly through the cup it contains EE. Due to their chemical composition, EE will actually eat straight through the polystyrene cup. This effect will become evident after just a few minutes; however, significant leakage is seen after 10 minutes. Natural TG fish oils placed in the same cup will not show leakage after 10 minutes. Natural TG fish oils may show leakage through the cup in very small amounts after 2-3 hours.

Conclusion

Fish oil supplements in the natural TG form offer numerous advantages when compared to those in the EE form: oils in a TG form are completely safe to consume, are naturally occurring, provide increased absorption, and are much more stable. Therefore, since TG fish oil can be more effectively absorbed then it can be potentially better at reaching therapeutic ranges in comparison to EE fish oil. While EEs are a source of omega-3 fatty acids, research shows that they are not as beneficial as TGs and additional research is required to fully assess potential toxicity. While some countries (e.g. Australia) have gone as far as banning the sale of EEs, other countries such as the US, Canada, and the UK allow the sale of the EE form and furthermore do not require any additionally labeling. These supplements are therefore often incorrectly labeled as “Fish Oil” and pose a risk to those who must avoid ingestion of alcohol.

Table 1

Studies comparing the absorption of triglyceride and ethyl ester Fish Oils Cod Liver Oil
Hansen JB, Olsen JO, Wilsgard L, Lyngmo V, Svensson B. Comparative effects of prolonged intake of highly purified fish oils as ethyl ester or triglyceride on lipids, haemostasis and platelet function in normolipaemic men. Eur J Clin Nutr,47, 497-507.	31 normolipaemic non-obese men (21-47 yrs) were given 4 g highly purified omega-3 ethyl ester fatty acids, 4 g corn oil as a placebo, or 12 g n-3 triglycerides for 7 weeks. The daily intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) was 2.2 and 1.4 for TG, and 2.2 and 1.2 for EE. Blood samples were collected at week 1, 3 and 7. Comparison of time course incorporation of n-3 fatty acids in plasma phospholipids by repeated measures of variance did not show any difference between the TG and EE n-3 sources. Repeated measure ANOVA did however reveal a significant difference between TG and EE with respect to the incorporation of EPA into plasma cholesterol esters. Argument is made that higher amounts of omega-3 fatty acid lead to decreased differences between absorptions. Although higher doses of omega-3 fatty are not always realistic.
Beckermann B, Beneke M, Seitz I. 1990. Comparative bioavailability of eicosapentaenoic acid and docosahexaenoic acid from triglycerides, free fatty acids and ethyl esters in volunteers. Arzneimittelforschung, 40(6):700-4.	The bioavailability of EPA and DHA from triglycerides, free fatty acids and ethyl esters was investigated in 8 female volunteers in a randomized triple cross-over trial with baseline control. EPA/DHA was administered in capsules in form of triglycerides, free fatty acids and ethyl esters. The resulting EPA/DHA plasma levels were determined and evaluated. The mean relative bioavailability of EPA/DHA compared to triglycerides was 186/136 % from free fatty acids and 40/48 % from ethyl esters. Maximal plasma levels were about 50 % higher with free fatty acids and about 50 % lower with ethyl esters as compared to triglycerides. The tolerability of the free fatty acids was much worse than that of triglycerides and ethyl esters. The main side effect was eructation.
Krokan HE, Bjerve KS, Mork E. 1993. The enteral bioavailability of eicosapentaenoic acid and docosahexaenoic acid is as good from ethyl esters as from glyceryl esters in spite of lower hydrolytic rates by pancreatic lipase in vitro. Biochim Biophys Acta,1168, 59-67.	Enteral absorption by healthy male volunteers of EPA and DHA from an ethyl ester andnatural triglyceride fish oil was found to be similar after intake of equivalent doses, however; hydrolysis of natural triglyceride fish oil was more efficient. In spite of the similar serum levels of EPA and DHA obtained in vivo, in vitro hydrolysis by porcine pancreatic lipase of the ethyl ester was 3-fold slower than hydrolysis of a the triglyceride. Under similar conditions release of AA from triglyceride and ethyl ester was essentially similar and approx. 1.5-fold faster than release of EPA and DHA from ethyl esters. There are therefore differences in the rate of hydrolysis of ethyl ester and triglycerides fish oils.
el Boustani S, Colette C, Monnier L, Descomps B, Crastes de Paulet A, Mendy F. (1987). Enteral absorption in man of eicosapentaenoic acid in different chemical forms. Lipids, 10, 711-4.	After administering the equivalent of 1 g of EPA in four different chemical forms, the kinetics of EPA incorporation into plasma triglycerides were compared by gas liquid chromatography on a capillary column following separation of the lipid fraction by thin layer chromatography. EPA incorporation into plasma triglycerides was markedly smaller and later when EPA was administered as an ethyl ester rather than as EPA free fatty acid, EPA arginine salt or 1,3-dioctanoyl-2-eicosapentaenoyl glycerol. Our results and the data in the literature are compatible with the hypothesis that the glycerol form of EPA is absorbed with minimum hydrolysis and escapes random distribution between the other positions of the glycerol molecule during the absorption process.
Lawson LD, Hughes BG. (1988). Human absorption of fish oil fatty acids as triacylglycerols, free acids, or ethyl esters. Biochem Biophys Res Commun, 52, 328-35.	As triacylglycerols, eicosapentaenoic acid (1.00 g) and docosahexaenoic acid (0.67g) were absorbed only 68 % and 57 % as well as the free acids. The ethyl esters were absorbed only 20 % and 21 % as well as the free acids. The incomplete absorption of eicosapentaenoic and docosahexaenoic acids from fish oil triacylglycerols correlates well with known in vitro pancreatic lipase activity.
Visioli F, Rise P, Barassi MC, Marangoni F, Galli C. (2003). Dietary intake of fish vs. formulations leads to higher plasma concentrations of n-3 fatty acids. Lipids, 38, 415-8.	For six weeks, volunteers were given 100 g/d of salmon, or 1 or 3 capsules of ethyl ester fish oil/d. Marked increments in plasma EPA and DHA concentrations (microgram/mg total lipid) and percentages of total fatty acids were recorded at the end of treatment with either omega-3 capsules or salmon. Increments in plasma EPA and DHA concentration after salmon intake were significantly higher than after administration of capsules. The same increments would be obtained with at least two and nine-fold higher doses of EPA and DHA, respectively, if administered with capsules rather than salmon. We provide experimental evidence that natural omega-3 fatty acids from fish are more effectively incorporated into plasma lipids than when administered as capsules.
Valenzuela A, Valenzuela V, San hueza, J, Nieto S. (2005). Effect of supplementation with docosahexaenoic acid ethyl ester and sn-2 docosahexaenyl monoacylglyceride on plasma and erythrocyte fatty acids in rats. Ann Nutr Metab. 49, 49-53.	Female rats received a 40 day supplementation of either DHA ethyl ester or DHAmonoglycerate. Plasma and erythrocyte fatty acid composition were assessed by gas chromatography at day 0 and 40 of supplementation. DHA ethyl ester increased plasma and erythrocyte DHA by 15 and 11.9 %, respectively, with no modification of arachidonic acid (AA) con tent. DHA-monoglycerate supplementation increased plasma and erythrocyte DHA by 24 and 23.8 %, respectively, and reduced AA by 5.5 and 3 %, respectively. Although this data is done with animals, the authors conclude that in the rat, DHAmonoglycerate supplementation allows a higher plasma and erythrocyte DHA content than DHA-ethyl ester.
Ikeda I, Sasaki E, Yasunami H, Nomiyama S, Nakayama M, Sugano M, Imaizumi K, Yazawa K. (1995). Digestion and lymphatic transport of eicosapentaenoic and docosahexaenoic acids given in the form of triacylglycerol, free acid and ethyl ester in rats. Biochim Biophys Acta; 1259: 297-304.	Lymphatic transport of EPA and DHA with trieicosapentaenoyl glycerol (TriEPA) and tridocosahexaenoyl glycerol (TriDHA) was compared with the transport of ethyl ester and free acid in rats cannulated with thoracic duct. Trioleoylglycerol (TO) served as a control. Lymphatic recovery of EPA and DHA in rats given TriEPA and TriDHA was significantly higher at the first 3 h after the administration compared to those given as free acid or ethyl ester. The 24-h recovery was comparable between triacylglycerol (TAG) and free acid, while it was significantly lower in ethyl ester. The hydrolysis rate of ethyl esters was extremely low even in 6 h incubation with lipase. Although this data is done with animals, the authors conclude that there is less lymphatic recover of EPA and DHA when they are in ethyl ester form.
Nordoy A, Barstad L, Connor WE, Hatcher L. 1991. Absorption of the n-3 eicosapentaenoic and docosahexaenoic acids as ethyl esters and triglycerides by humans. Am J Clin Nutr. 53:1185-90.	Five normolipemic subjects received three test meals. 1) 40g n-3 triglycerides, 2) 28 g n-3 ethyl ester plus 12 g olive oil, 3) 28 g n-3 ethyl ester and 4) 40g olive oil. When equivalent amounts of fat were given, the increase in chylomicrons and plasma triglycerides was similar; n-3 fatty acid contents were also similar after n-3 fatty acid intake as ethyl esters or triglycerides. Ethyl esters alone were well absorbed and produced similar n-3 fatty acid responses in plasma triglycerides and chylomicrons. At 24 h after the n-3 fatty acid containing meals, the fatty acid plasma concentration of these acids was similar. This study suggests that n-3 fatty acids given as ethyl esters or triglycerides were equally well absorbed. However, the doses of fish oil given were unrealistically high thus one should be hesitant to draw conclusions from such data.
J Dyerberg , P Madsen , JM Moller ,I Aardestrup ,EB Schmidt. Bioavailability of marine n-3 fatty acid formations. Prostaglandins Leutkot. Essent. Fatty Acids 83 (2010),137-141.	Seventy- two volunteers were split into 6 groups 4 of which were double blinded and 2 of which were the EE and rTG groups. Each group was given approximately the same amount of fish oil 3.1-3.6 grams and then compared to a corn oil fed placebo group. Base line plasma cholesterol esters (CE), phospholipids (PL) and triglycerides (TG) were measured as the mean increase as a grand total of the EPA+DHA present and then taken again at the end of the two week period9. They noticed that with about the same grand total of EPA+DHA administered to the EE and rTG group compared to the placebo group, the EE form was given the lowest assimilation as a measure of bioavailability. Once adjusted for the results were 76% and 134% for the EE and rTG groups respectively.
J Neubronner , JP Schuchardt, G Kressel, M Merkel, C von Schacky and A Hahn. Enhanced increase of omega-3 index in response to long term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters. Eur. J. of Clin. Nutr.(2010),1-8.	The study randomized 150 subjects in one of three groups; two fish oil groups versus placebo. The two fish oil groups (EE and rTAG) had the exact amount of combined EPA+DHA per capsule and the total dose per day was 1.68grams. The two fish oil groups were compared to a corn oil placebo group and the duration of the study was 6 months. A unique method of bio-availability was used (Omega 3 index) this method looks at the omega 3 FA (EPA+DHA) incorporated into the RBC membranes. Therefore, the outcome of this study showed a statistically significant incorporation of EPA+DHA in the RBC membranes via re-esterified triacylglycerides (rTAG) over ethyl esters (EE) by more than a 25 percent.

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Read thecomplete article here.

DHA: the crucial omega-3 - Davis

DHA: the crucial omega-3  

Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:


□ indicates baseline SBP; ▪, postintervention SBP; ○, baseline DBP; •, postintervention DBP; ⋄, baseline HR; and ♦, postintervention HR.

In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.

While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:

DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)

So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam’s Club Triple-Strength, Costco, Nature Made, Nature’s Bounty, as well as prescription Lovaza. (That’s right: prescription fish oil, from this and several other perspectives, is an inferior product.)

What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:

Ascenta NutraSea
CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.

Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.

Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.

By Dr. William Davis
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Read the complete article here.

Omega-3/Fish Oil.... Good Bad? - Blanchet

Omega-3/Fish Oil.... Good Bad?

Listen to my doctor discuss over interpretation of a single bad study.

Several articles in the news lately, pretty much said that taking fish oil, or omega 3's, did nothing to help prevent heart disease. Should you toss your supply? Hear what Dr. Blanchet has to say about omega 3’s and their role in our health. Find out the facts about the studies that were done which prompted the media concern.


http://tuesdaytalkshow.podomatic.com/entry/2012-10-18T14_26_49-07_00

Does Fish oil fail to deliver on its promise? Listen to an expert.

Fish Oil - Good for you or not?

Several articles in the news lately, pretty much said that taking fish oil, or omega 3's, did nothing to help prevent heart disease. Should you toss your supply? Hear what Dr. Blanchet has to say about omega 3’s and their role in our health. Find out the facts about the studies that were done which prompted the media concern.

Dr. Blanchet is my doctor and has helped me slow my coronary artery plaque to 5% per year. So do I take fish oil? You bet!

I am one of his patients over 65 years old and with a calcified plaque score of greater then 1000.

Listen to a pod cast by he and Lindsay talking about Omega-3 fatty acids here.
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See other info about Dr. Blanchet here.

New JAMA Study Bakes Fish Oils- Don’t Believe It! - Cohen

New JAMA Study Bakes Fish Oils- Don’t Believe It!

 

 

Dear Pharmacist,

 

I just heard about the new study that says fish oil supplements don’t prevent heart attacks, and may not help us. Should I keep taking fish oils? –S.S., Chicago

Answer: Yes, if they’re high-quality. The “study” wasn’t a study at all, it was a meta-analysis, which means researchers examine results from a bunch of trials and draw their own conclusions based on the collective data. The meta-analysis you refer to appeared in the September 2012 issue of JAMA and included 68,000 participants in 20 different studies that covered a time frame 24 years. I have some problems with their opinion that fish oils are fairly worthless. The research I know of suggests strong benefits to the heart and arteries when you take high-quality fish oils. These are my problems with the JAMA article:

1. The researchers only reviewed 20 studies, but there are thousands that suggest cardiovascular protection by fish oils, particularly the EPA and DHA components. You’re not going getting the full picture from 20 studies.
2. How much fish oil was used? Most people were taking 1,000mg per day, but you need about 2,000 mg per day (total daily dose of EPA and DHA) to truly impact coronary heart disease. We come up therapeutically short! What about the ratio of EPA to DHA; ideally, I’d like it to be 3:2; for example, 600mg of EPA to 400mg DHA is a 3:2 ratio.

3. The looked at chronically ill people who had serious conditions, like they had already suffered a heart attack and stroke, not folks taking it for prevention. Fish oils are not intended to prevent heart attack or stroke. Plus, it’s super hard to prevent more health catastrophes, once you’ve had one. Feeling skewed?

4. What about the medications these folks were taking? The participants were taking all sorts of blood pressure pills and diuretics, most of which just so happen to be drug muggers of magnesium! Do you realize that serious uncorrected magnesium deficiency can cause a heart attack, no matter how much fish oil you take! To me, this is a huge gap in their premature conclusion.
5. What about Gamma Linolenic Acid or “GLA” status? When you take fish oils, an omega 3 fatty acid, you have to also supplement with GLA (an omega 6 fatty acid) because high doses of fish oils will cause drug mugging of GLA. For example, if you take 1,000 mg of fish oil (EPA and DHA totaled together), you need 500mg GLA at the same time. Evening primrose oil supplements can provide this GLA. This is important because GLA deficiency can increase your tendency to form clots (bad). GLA is known to protect the heart, without adequate amounts, you could suffer cardiac consequences, and this was not even addressed.

Even the American Heart Association approves of fish oils for heart health. Think smart and don’t be fooled by a single study intended to sway you away from decades of positive research.
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READ THE COMPLETE ARTICLE HERE.
Also watch Suzy's video discussing this here.

Association Between Omega-3 Fatty Acid Supplementation & Risk of Major Cardiovasular Disease - Harris

Comment On JAMA publication by Rizo et.al: Association Between Omega-3 Fatty Acid Supplementation & Risk of Major Cardiovasular Disease

               

Written by William Harris PhD

 

 

Response on the JAMA publication: Association Between Omega-3 Fatty Acid Supplementation and Risk of Cardiovascular Disease Events: On September 12, 2012 Rizos et al. published a meta-analysis titled: “Association Between Omega-3 Fatty Acid Supplementation and Risk of Major Cardiovascular Disease Events” on fish oil and concluded no benefit. Spokespeople from the AHA have been on TV saying that omega-3 supplements clearly don’t ‘work’. here are some of my thoughts…

Positve view of the study

They included all relevant studies; they did not exclude (like the previous meta-analysis (Kwak) did) the non-placebo controlled trials (GISSI-Prevenzione and JELIS)

First negative view about the study

They showed in Figure 3 that there was a significant benefit of omega-3 on cardiac death, and trends towards benefit in total mortality, sudden death and MI (plus trends towards increased stroke). But in the text, they said that there was NO significant effect on cardiac death – this is because they set the p-value for significance at 0.006, a much higher hurdle (than the usual 0.05) for concluding benefit. In my view, this is completely inappropriate and excessively conservative, especially for a very safe intervention. In other words, if you are testing a new drug that has potential benefits AND side/adverse effects, then you want to be very conservative in concluding “benefit” (i.e., you want to require a very small p-value) since – if you’re wrong and the drug really isn’t helpful (false positive) - your ‘endorsement’ of the drug will lead to increased use and thus the potential for increased adverse effects. However, for very low risk interventions (n-3 fatty acids), you don’t worry about adverse effects… you want people to use the treatment even if there is only a trend towards benefit. A favorable benefit-risk ratio. (I’d even suggest that in this setting, a p-value for ‘significant effect’ should be 0.1 instead of the traditional 0.05). In addition, nobody I know of ever adjusts for multiple testing (sets a lower p-value than 0.05 as the target for significance) in a meta-analysis. Therefore, I believe that the authors were far too conservative in this analysis, which led to their “no benefit” conclusion.

Second negative view about the sudy

They should have been much more nuanced in their conclusions. They said, “Our findings do not justify the use of omega-3 in structured [?] intervention in everyday clinical practice or guidelines supporting dietary omega-3 PUFA administration.” They should have said, “In patients of average age 63, with existing cardiovascular disease and under optimal medical care (which, by the way, is very UNcommon), the administration of about 1 g of EPA+DHA for 4 years will not affect major clinical outcomes.” Their study does NOT show that treating with a higher dose for a longer period of time, or treating patients earlier in the disease process or those who are not receiving “optimal medical therapy” will NOT be beneficial.

There may (or may not!) be a slight silver lining to all of this: Here is what Tom Barringer and I ended a chapter on n3 and CVD with in an upcoming book on “Omega-3 Deficiency”:
It should be stressed that future research will be significantly hampered if clinicians and patients are dogmatic in their belief that the value of n-3 fatty acids in CVD is already well-established. If such unfounded certainty is widespread, it will become very difficult to find patients (and investigators and IRBs) willing to participate in or approve the placebo-controlled clinical trials that are so desperately needed to properly evaluate the value of these nutrients in the treatment and prevention of CVD.”
Clearly with Rizos’ paper, we now won’t have any problem convincing the world that the question of omega-3s and CHD risk is still open.

In summary, they were too conservative in their analysis and they were not thoughtful in drawing their conclusions. It’s quite likely true that 1 g of EPA+DHA won’t affect outcomes over a few years in older people started later in life who are well-treated pharmacologically – but that’s a far cry from USA Today’s Headline “Fish oil pills with omega-3 don’t help against disease”
==================================================================

William Harris PhD
Senior Scientist
William Harris holds a PhD in Nutritional Biochemistry from the University of Minnesota, and did 4 years of post-doctoral research at the Oregon Health Sciences University. He was Director of the Lipid Research Laboratories at the University of Kansas Medical Center (KUMC) and at the Mid America Heart Institute, both in Kansas City, MO, for 22 years, and was on the faculty at KUMC and at the University of Missouri-Kansas City School of Medicine. Between 2006 and 2011 was the Director of the Cardiovascular Health Research Center at Sanford Research/USD (Sioux Falls, SD).
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Read the complete article here.

Triglycerides: Mother of Meddlesome Particles - Davis

Triglycerides: Mother of Meddlesome Particles



Triglycerides are a crucial risk factor for coronary plaque growth, even at levels previously thought to be normal. Dr. Davis discusses why and how this oft-neglected factor can be harnessed to strengthen your program.

While the world obsesses over cholesterol, a potent stimulator of plaque growth is frequently ignored—triglycerides. A subject of controversy in past, the data are now clear: triglycerides spawn unwanted lipoprotein particles that trigger plaque growth. Track Your Plaque members are advised that control of triglycerides is essential to everyone’s plaque control program.

Triglyceride control is crucial if you are interested in gaining control over coronary plaque. Triglycerides should be brought under control at the start of your program. If you are experiencing plaque growth (increasing heart scan scores), seriously reining in triglycerides should be considered.

How important are triglycerides?

 

For years, the relationship between coronary heart disease and triglycerides remained muddled by the confounding effects of low HDL. In other words, increased triglycerides tend to occur alongside low HDL. This caused many to dismiss the importance of triglycerides. To make matters even murkier, high triglycerides in some situations generated high risk for heart disease, while in others it appeared unrelated to heart disease, even when markedly elevated (in the thousands!).

Thanks to the evolving science of lipoproteins, the issues are crystallizing. One important fact has emerged: triglycerides are a critical risk factor for coronary plaque growth, even at levels previously thought to be normal. Yes, high triglycerides frequently occur with low HDL, but they also behave independently. High triglycerides are a common cause of heart disease, even in people with low or normal cholesterol values. It is crucial that you (and your doctor) pay close attention to triglycerides if you are to succeed in controlling your plaque. We urge Members to make triglyceride control a priority in their program.

 

Where do triglycerides come from?

 

The liver produces a particle called “very low-density lipoprotein”, or VLDL, packed full of triglycerides. The higher your triglycerides, the more VLDL you will have. Sometimes triglycerides are increased due to genetic factors. More commonly, triglycerides are high due to excess weight, indulging in processed carbohydrates, and resistance to insulin (metabolic syndrome).

VLDL is like that bad kid on the block you want your kids to avoid. VLDL particles in the blood come into contact with LDL and HDL particles and they’re never quite the same. When a LDL or HDL particle meet VLDL, the triglycerides of VLDL are passed on. The result: LDL and HDL become bloated with triglycerides. Triglyceride-loaded LDL and HDL are a ready target for a set of enzymes in the blood and liver that reconfigure these particles into smaller versions, small LDL and small HDL. Recall that both small LDL and HDL are highly undesirable particles that stimulate plaque growth.

Although “official” (ATP-III) guidelines suggest that triglycerides over 150 mg are undesirable, we regard any value over 60 mg as high. An ideal level for an intensive Track Your Plaque approach is <45 font="font" mg.="mg.">

 

How will I know if I have this pattern?

 

On a conventional cholesterol panel, increased triglycerides and low HDL are tip-offs that excess VLDL are available to contribute to coronary plaque growth. At what triglyceride level does this cascade begin to take effect and create this collection of particles? Levels of 45 mg/dl or greater. In the Track Your Plaque program, we aim for zero plaque growth or reduction, and so we target triglyceride levels of 60 mg/dl or less.

You’ll notice that low HDL and increased triglycerides are also patterns that characterize the metabolic syndrome. In our experience, over 50% of adults show at least some of the characteristics of the metabolic syndrome. In our society of inactive, sedentary lifestyles and packaged, processed foods, metabolic syndrome is rampant. That means increased triglycerides from VLDL are also running rampant. The result: a 3 to 7-fold increase in risk for heart attack. Eliminating the metabolic syndrome is another battle we need to fight to conquer plaque. (See Shutting Off the Metabolic Syndrome.)

 

How can triglycerides be reduced?

 

Our triglyceride target of 60 mg or less dramatically reduces triglyceride availability. Without triglycerides, LDL and HDL can’t be processed into undesirable small particles. Among the strategies we use to reach our triglyceride target of 60 mg or less:

• Fish oil—The omega-3 fatty acids in fish oil are our number one choice for substantially reducing triglycerides. Fish oil, 4000 mg per day, is a good starting dose (providing 1200 mg EPA+DHA); higher doses should be discussed with your physician, though we commonly use 6000–10,000 mg per day without ill-effect. Flaxseed oil, while beneficial for health, does not correct lipoprotein patterns. Consider a concentrated fish oil preparation (e.g., Omacor™, a prescription preparation, or “pharmaceutical grade” preparations from the health food store) if you and your doctor decide a high dose is necessary.
• Weight loss to ideal weight or ideal BMI (25). If achieved with a reduction in processed carbohydrates, the effect will be especially significant. Exercise will compound the benefits of weight loss, triggering an even larger drop in triglycerides.
• Reduction in processed carbohydrates—especially snacks; wheat-flour containing foods like breads, pasta, pretzels, chips, bagels, and breakfast cereals; white and brown rice; white potatoes. The reduction of high- and moderate-glycemic index foods is the factor that reduces triglycerides. High triglycerides are therefore a pattern that develops when someone follows a low-fat diet. For this reason, we do not advocate low-fat diets like the Ornish program. Reducing your exposure to wheat-containing snacks and processed foods is an especially useful and easy-to-remember strategy that dramatically reduces triglycerides.
• Elimination of high-fructose corn syrup—This ubiquitous sweetener is found in everything from beer to bread. High-fructose corn syrup causes triglycerides to skyrocket 30% or more.
• Niacin in doses of 500–1500 mg is an effective method of reducing triglycerides. Niacin also raises HDL, increases large HDL, reduces the number of small LDL particles, reduces VLDL, and modestly reduces total LDL. The preferred forms are over-the-counter Slo-Niacin® and prescription Niaspan®, the safest and best tolerated. Immediate-release niacin (just called niacin or nicotinic acid on the label) can also be taken safely, provided it is taken no more frequently than twice per day. Total daily doses of >500 mg should only be taken under medical supervision. Avoid nicotinamide and “no-flush niacin” (inositol hexaniacinate), neither of which have any effect whatsoever.
• Green tea—The catechins (flavonoids) in green tea can reduce triglycerides by 20%. Approximately 600–700 mg of green tea catechins are required for this effect, the equivalent of 6–12 servings of brewed tea. (Tea varies widely in catechin content.) Nutritional supplements are also available that provide green tea catechins at this dose. The weight loss accelerating effect of green tea may add to its triglyceride-reducing power.
• The thiazolidinediones (Actos®, or pioglitazone, and Avandia®, or rosiglitazone), usually prescribed for pre-diabetes or diabetes, can reduce triglycerides by 30%; Actos may be more effective than Avandia in this regard. However, these agents are accompanied by weight gain.
• The fibrate class of prescription drugs (fenofibrate, or Tricor®, and gemfibrozil®, or Lopid) reduce triglycerides 30–40%, i.e., almost as effectively as fish oil.

The evil influences of VLDL and triglycerides are therefore erased from your risk profile by achieving the Track Your Plaque target of triglycerides 60 mg/dl or less. One or more of these strategies are usually required to bring your triglycerides to target. 

        William Davis, MD


Selected references:

Packard CJ. Understanding coronary heart disease as a consequence of defective regulation of apolipoprotein B metabolism. Curr Opin Lipidol 1999; 10:237–244.

Otvos J. Measurement of triglyceride-rich lipoproteins by nuclear magnetic resonance spectroscopy Clin Cardiol 1999;22 (Suppl II) II-21–II-27.

Grundy SM. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol 1998;81(4A):18B–25B.

Zilversmit DB. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin Chem 1995;41(1):153–158.

Fish oil: The natural triglyceride form is better

Posted on February 2, 2011 by Dr. William Davis

If you have a choice, the triglyceride form of fish oil is preferable. The triglyceride form, i.e., 3 omega-3 fatty acids on a glycerol “backbone,” is the form found in the body of fish that protects them from cold temperatures (i.e., they remain liquid at low ambient temperatures).
Most fish oils on the market are the ethyl ester form. This means that the omega-3 fatty acids have been removed from the glycerol backbone; the fatty acids are then reacted with ethanol to form the ethyl ester.

If the form is not specified on your fish oil bottle, it is likely ethyl ester, since the triglyceride form is more costly to process and most manufacturers therefore boast about it. Also, prescription Lovaza–nearly 20 times more costly than the most expensive fish oil triglyceride liquid on a milligram for milligram basis–is the ethyl ester form. That’s not even factoring in reduced absorption of ethyl esters compared to triglyceride forms. Remember: FDA approval is not necessarily a stamp of superiority. It just means somebody had the money and ambition to pursue FDA approval. Period.
Taking any kind of fish oil, provided it is not overly oxidized (and thereby yields a smelly fish odor), is better than taking none at all. All fish oil will reduce triglycerides, accelerate clearance of postprandial (after-eating) lipoprotein byproducts of a meal (via activation of lipoprotein lipase), enhance endothelial responsiveness, reduce small LDL particles, and provide a physical stabilizing effect on atherosclerotic plaque.

But if you desire enhanced absorption and potentially lower dose to achieve equivalent RBC omega-3 levels, then triglyceride forms are better.

Here are cut-and-pasted abstracts of two of the studies comparing forms of fish oil.

Bioavailability of marine n-3 fatty acid formulations.

Dyerberg J, Madsen P, Moller JM et al.

Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark.

Abstract

The use of marine n-3 polyunsaturated fatty acids (n-3 PUFA) as supplements has prompted the development of concentrated formulations to overcome compliance problems. The present study compares three concentrated preparations – ethyl esters, free fatty acids and re-esterified triglycerides – with placebo oil in a double-blinded design, and with fish body oil and cod liver oil in single-blinded arms. Seventy-two volunteers were given approximately 3.3g of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 2 weeks. Increases in absolute amounts of EPA and DHA in fasting serum triglycerides, cholesterol esters and phospholipids were examined. Bioavailability of EPA+DHA from re-esterified triglycerides was superior (124%) compared with natural fish oil, whereas the bioavailability from ethyl esters was inferior (73%). Free fatty acid bioavailability (91%) did not differ significantly from natural triglycerides. The stereochemistry of fatty acid in acylglycerols did not influence the bioavailability of EPA and DHA.

(Full text of the Dyerberg et al study made available at the Nordic Naturals website here.)

Eur J Clin Nutr 2010 Nov 10.

Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.

Neubronner J, Schuchardt JP, Kressel G et al.

Institute of Food Science and Human Nutrition, Leibniz Universität Hannover, Am Kleinen Felde 30, Hannover, Germany.

Abstract

There is a debate currently about whether different chemical forms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are absorbed in an identical way. The objective of this study was to investigate the response of the omega-3 index, the percentage of EPA+DHA in red blood cell membranes, to supplementation with two different omega-3 fatty acid (n-3 FA) formulations in humans. The study was conducted as a double-blinded placebo-controlled trial. A total of 150 volunteers was randomly assigned to one of the three groups: (1) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as reesterified triacylglycerides (rTAG group); (2) corn oil (placebo group) or (3) fish oil concentrate with EPA+DHA (1.01?g+0.67?g) given as ethyl ester (EE group). Volunteers consumed four gelatine-coated soft capsules daily over a period of six months. The omega-3 index was determined at baseline (t(0)) after three months (t(3)) and at the end of the intervention period (t(6)). The omega-3 index increased significantly in both groups treated with n-3 FAs from baseline to t(3) and t(6) (P < 0.001). The omega-3 index increased to a greater extent in the rTAG group than in the EE group (t(3): 186 versus 161% (P < 0.001); t(6): 197 versus 171% (P < 0.01)). Conclusion: A six-month supplementation of identical doses of EPA+DHA led to a faster and higher increase in the omega-3 index when consumed as triacylglycerides than when consumed as ethyl esters.

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Read the full article here.

Tip the scales towards plaque reversal

Tip the scales towards plaque reversalThere’s no one easy formula to achieve coronary plaque reversal: no single pill, supplement, food that guarantees that you drop your heart scan score.

But there are indeed factors which can work in favor or against the likelihood that you
gain control over your coronary plaque
.

Does everyone who tries to reverse coronary heart disease and reduce their heart scan score succeed? No, not everyone. There are indeed people who fail and see their heart scan score increase. There are usually identifiable and correctable reasons for this to happen. Occasionally, even someone who does everything right still sees their score increase. Thankfully, this is unusual.

There are a number of basic requirements that everybody needs to follow if you hope to gain control over your coronary plaque. There are also less common factors that need to be corrected only by some people. There are also factors that make it more difficult to drop your score.

What makes plaque reversal more likely?

Among the most important facets of the Track Your Plaque program are the recommended targets for conventional lipids: LDL 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl: 60-60-60. We call this the Track Your Plaque “Rule of 60”. (Refer to the Special Reports on each of these factors to see how we accomplish this. There’s no quick and dirty pill or supplement that immediately achieves these numbers, but there are indeed effective ways.)

The metabolic syndrome must be eliminated. This usually means weight loss, exercise, and reduction of high-glycemic index foods sufficient to achieve normal blood pressure (preferably 130/80 or less), normal blood sugar (≤100 mg/dl), a C-reactive protein <1.0 g/l. This is also good for your long-term health. The metabolic syndrome is a pre-diabetic condition. You can’t remain pre-diabetic for a lifetime. Unless corrective action is taken, you will convert to a full diabetic. You need to put a stop to this for lots of reasons, including gaining control over coronary plaque .

Lower scores are easier to control than higher scores. A level of 200 or less seems to represent a fairly distinct cut-off between easier and tougher. Having a higher heart scan score of, say 500, doesn’t means it’s impossible, but it will be somewhat tougher and may require a longer period. We’ve seen really high scores in the thousands take 2 to 3 years, for instance.

Taking fish oil. It’s truly shocking how few people take fish oil, even when they’ve suffered a heart attack. It’s simple, virtually harmless, and inexpensive. Yet the benefits are enormous. Fish oil is a crucial requirement for controlling coronary plaque.

Reaching a blood 25-OH-vitamin D3 level of 50 ng/ml. Though our appreciation for this fact is recent, it’s among the most exciting developments in coronary plaque reversal. In fact, we would rank vitamin D as among the most important heart health discoveries of the last 40 years, along with CT heart scanning and fish oil.

Having an optimistic attitude that allows you to see the bright side of problems, overcome difficulties, and engage in healthy relationships with family and friends. Optimists have an easier time in life and they seem to reduce their heart scan scores much more readily.

What makes plaque reversal tougher?

There are some obvious factors that make it less likely that you will drop your heart scan score: cigarette smoking; an unrestricted diet rich in donuts, fried chicken, spare ribs, and cookies; diabetes; uncontrolled high blood pressure; kidney disease. Chances are that, if these factors are uncorrected, you will simply not drop your heart scan score. It is much more likely that your score will increase, sometimes substantially, year after year. Eventually, heart attack or a major heart procedure (actually a lifetime series of procedures) will catch up to you.

More recently, we have seen several well-established diabetics drop their score, sometimes as much as 30%. However, it still remains more difficult if diabetes is part of the picture, as compared to a non-diabetic.

Pre-diabetes represents an intermediate between full-blown diabetes and non-diabetes. However, from a plaque reversal viewpoint, it does make it substantially tougher to drop your score.

Having lipoprotein(a), or Lp(a), also makes it more difficult. We have had more success in halting the increase in heart scan scores (i.e., holding the score steady without increase or decrease) in people with Lp(a), less success in dropping scores. Though our track record with Lp(a) is getting better and better, it still remains a tough nut to crack. With Lp(a), it is clear that you’ve got to work harder to succeed.

Higher scores are tougher to drop than lower scores. Someone with a starting score of, say, 1800, will have to try harder and for a longer period than someone starting with a score of 70. This holds true even if they share the same set of lipoprotein causes. The person with the higher score may even require 2 or 3 years before they see the score stop increasing or decrease, while the person with the lower starting score may drop their score in the first year. People with scores of <100 can even occasionally see zero again. This is not possible (with present-day knowledge) with high scores.

We’ve recently begun to appreciate that a pessimistic attitude may play an important role in your program. People who are angry, critical, see the bad in everything, are isolated and lack social involvement, have a much more difficult time reducing their scores.

Coronary plaque in the balance

In the Track Your Plaque program, we try to help you achieve as many advantages as possible to gain control over coronary plaque. While not perfect, the Track Your Plaque approach is, without question, the most effective program available anywhere.

Obviously, we can do nothing about our genetics, but we can identify and correct as many factors as possible. In this way, we tilt the scales heavily in favor of dropping your heart scan score.

Copyright 2007, Track Your Plaque, LLC
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5 Steps You Can Take To Reduce Your Heart Scan Score

By William Davis,MD

CT heart scans are booming in popularity. With over 300 scanners nationwide,
over one million Americans have now been scanned since the introduction of this
technology 10 years ago.

In some cases, lives have been saved. People with high scores (e.g., over
1000) can end up with lifesaving procedures like bypass surgery or stents.

But what about the majority of people who don't have a life-threatening
score?

Too often, people in this very large group are prescribed a cholesterol drug
and patted on the back with advice to cut the fat in their diet. According to
several recent studies, that's a recipe for failure. Do nothing, and you can
expect your score to increase 30% per year. Take a cholesterol drug and cut your
fat, and you can still expect your score to grow 30% per year!

Surely there's a lot more you could do to gain control over your score.

Here's our list of 5 easy yet crucial steps you can take that tip the odds in
your favor that you will not just stop your score from increasing, but perhaps
even reduce it.

1. Take fish oil

Fish oil is among the few breakthrough discoveries of the past 20 years that
has altered the course of cardiovascular illness, slashing risk of death, heart
attack, and stroke. The mis-guided advice of the 1980s that polyunsaturated oils
were healthy has left us appallingly overloaded with omega-6 fatty acids, and
omega-3 supplementation from fish oil has become increasingly important.

The 11,000-participant GISSI-Prevenzione trial brought any remaining
naysayers to their knees. Participants taking fish oil experienced 30% reduction
in cardiovascular death and an astounding 45% reduction in sudden death.

Fish oil provides anti-inflammatory benefits, plaque-stabilizing effects, and
corrects many genetic and acquired causes for heart attack. Fish oil helps
correct the triglyceride and small LDL abnormalities triggered by metabolic
syndrome, the collection of pre-diabetic abnormalities now afflicting 59 million
Americans. Fish oil also accelerates clearance of abnormal fat particles in the
blood that persist after eating. All of this adds up to a dramatic reduction in
cardiovascular "events" and greater control over coronary plaque. In our heart
disease reversal program, we start with 4000 mg of standard fish oil capsules
per day provide 1200 mg of omega-3 fatty acids, EPA + DHA.

2. Take vitamin D

Imagine over half the adults in the U.S. were toothless and had open skin
sores covering their bodies from vitamin C deficiency, or "scurvy. Well, that's
the situation, though less graphic, with vitamin D. Deficiency is rampant in the
U.S., particularly in northern climates where sun exposure is in short supply
for long periods. It's not uncommon even in southern climates, given indoor
workplaces and lifestyles. Vitamin D deficiency has been implicated in
osteoporosis, prostate and colon cancer, hypertension, multiple sclerosis, and
heart disease.

The higher your heart scan score, the more likely you are deficient in
vitamin D. Consider taking a minimum of vitamin D 1000 units per day. Even
better, have your doctor check a blood level (25-OH-vitamin D3) and the dose can
be adjusted accordingly. In our heart disease reversal program, most women
require 2000 units per day, most men 3000 units per day to achieve the desirable
blood level of >50 ng/ml.

3) Boost your HDL cholesterol to 60 mg/dl

Raise this simple value to 60 mg/dl or greater, and you will have
accomplished a huge improvement in a whole constellation of health effects.

This is because HDL is a gauge of many things: body weight, your body's
ability to respond to insulin, potential for hypertension, and the presence of
hidden causes of heart disease, especially the dreaded small LDL. The higher
your HDL, the less likely other undesirable phenomena are present. HDL is the
blood particle that is responsible for regression, or shrinkage, of plaque. The
more, the better.

Boost HDL by losing excess weight, reducing processed carbohydrates like
breads and breakfast cereals, exercise, 4-8 oz of red wine per day, and fish
oil. Raise it even further by considering niacin (vitamin B3), 500-1000 mg.
(Discuss niacin use with your doctor.)

4) Have a colorful lifestyle

Deeply colored foods are rich in flavonoids, naturally-occurring substances
that pack broad, powerful health effects and include blood pressure-reducing and
anti-inflammatory benefits.

Add more deeply colored foods to your day, especially blueberries,
pomegranates, plums, black grapes, spinach, green peppers, and red wine. Drink
green tea whenever possible. Use cocoa powder (unsweetened) in your protein
shakes or add a daily two-inch square of dark chocolate. Add capers, fresh basil
and other herbs to your salads and dinner dishes. All are rich in
naturally-occurring flavonoids, destined to become health champions of the 21st
century. Among their myriad benefits, flavonoids are natural artery relaxing
agents and add another healthy dimension to your heart scan control program.

5) Substitute raw nuts for unhealthy snacks

Dump the chips, pretzels, and crackers. Replace them with raw almonds,
walnuts, and pecans. (Not "party mix", "honey-roasted", mixed nuts, etc., all no
better than other unhealthy snacks.) Raw and whole (unshelled) are the keys,
bought bulk in most supermarkets or health food stores. This simple substitution
reduces LDL cholesterol 20 points, reduces blood sugar, reduces small LDL,
raises HDL, and boosts your energy level. Don't sweat the fats--the
monounsaturated fat in raw nuts are the source of much of the benefit.
One-quarter to one-half cup per day provides maximum benefit.

Stopping your heart scan score from increasing may be among the most powerful
ways to sharply reduce, perhaps even eliminate, risk for heart disease in your
lifetime. There's no single strategy that guarantees you stop your heart scan
score from increasing―it's all your efforts combined, followed consistently over
time.

Dr. William Davis is a cardiologist and expert in reversal of heart disease. He is author of “Track Your Plaque: The only heart disease prevention program that shows you how to detect, track, and control coronary plaque.” Dr. Davis also makes his book, “What Does My Heart Scan Show?” available for free at www.trackyourplaque.com. Article Source: http://EzineArticles.com/?expert=William_Davis,MD

Article Source:
http://EzineArticles.com/297354

Dr. Dwight Lundell on omega-3s and CLA

Thursday, September 06, 2007

Dr. Dwight Lundell on omega-3s and CLA

An interview with Dr. Dwight Lundell, cardiac surgeon and author of the new book, "The Cure for Heart Disease."

Dr. Lundell comes to us with a unique pedigree. He is a cardiothoracic surgeon practicing in the Phoenix, Arizona, area. Despite having performed thousands of coronary bypass operations, including numerous "off-pump" procedures earning him a place in the Beating Heart Hall of Fame and a listing in Phoenix Magazine’s Top Doctors for 10 years, more recently Dr. Lundell has turned his attentions away from traditional surgical treatment and towards prevention of heart disease and.

In particular, Dr. Lundell is a vocal advocate for omega-3 fatty acids from fish oil and conjugated linoleic acid, or CLA.

When I heard about Dr. Lundell’s unique perspectives, I asked him if he’d like to tell us a little more about his ideas. Here follows a brief interview with Dr. Lundell.

You’re a vocal advocate of the role of omega-3 fatty acids from fish oil in heart disease prevention. Can you tell us how you use it?

In my book, I recommend 3 g of fish oil daily. This would normally yield about 1000 mg of EPA and DHA depending on the concentration of the supplement. This is approximately the dose that reduced sudden cardiac death by 50%, and all cause death, by 25% in patients with previous heart attack.

In patients with signs of chronic inflammation such as heart disease, obesity, arthritis, metabolic syndrome or depression or in those patients with elevation of CRP, I would recommend higher doses, 2000 to 3000 mg per day of EPA and DHA. The FDA has approved up to 3400 mg for treating patients with severely elevated triglycerides.

I personally take a 2000 mg EPA and DHA per day because I have calcium in my coronary arteries.

Of course, in the Track Your Plaque program we track coronary calcium scores. Do you track any measures of atherosclerosis in your patients to chart progression or regression?

Carotid ultrasound with measurement of IMT [intimal-medial thickness] has been shown to be a good surrogate marker for coronary disease, as has vascular reactivity in the arm. CT scanning with calcium scoring is a direct marker of coronary disease. CT does not differentiate between stable or unstable plaque but there is no good noninvasive way of doing this.

The dramatic value of CT scan calcium scoring is to demonstrate to people that they actually do have coronary disease and to motivate them to make the necessary lifestyle and nutritional changes to reduce it. CT scan with calcium scoring is a direct way to measure the progression or regression of coronary artery disease. If there is a choice between a direct measurement and indirect measurement, always choose the direct method.

Every patient treated with CLA in my clinic, experienced significant reductions in C-reactive protein. These patients were also on a weight-loss program, so I can't prove whether it was the CLA or the weight-loss that improved their inflammatory markers. In the animal model for arteriosclerosis, CLA has a dramatic effect of reducing and preventing plaque. This has not yet been proven in humans.

Normally, when people lose weight 20% or more of the loss is lean body mass (muscle) this lowers the metabolic rate and frustrates further weight-loss. My patient, from teenagers to retirees, lost no lean body mass and continued to have satisfactory weight-loss when CLA was used as part of the plan.

In reading your book, your use of conjugated linoleic acid (CLA) as a principal ingredient struck me. Can you elaborate on why you choose to have your patients take CLA?

My enthusiasm for CLA is based on:

1) Safety―this is of paramount importance. Animal toxicity studies have been done, as well as multiple parameters measured in human studies, both of these are well reviewed recently in the American Journal of Clinical Nutrition (2004:79(suppl)1132s). CLA, a naturally-occurring substance, is not toxic or harmful to animals or humans. The only negative report is by Riserus in Circulation (2002), where he found an elevated c- reactive protein; however, he used a preparation that is not commercially available and not found in nature as a single isomer.

2) Effectiveness―also critically important. A recent meta-analysis [a reanalysis of compiled data] in the American Journal of Clinical Nutrition (2007; 85:1203-1211) demonstrated the effectiveness of CLA in causing loss of body fat in humans. The study also reconfirmed the safety of CLA.

Since we now know that atherosclerosis is an inflammatory disorder, any strategy that reduces low-grade inflammation without significant side effects would seem to be beneficial in the treatment and prevention of atherosclerosis. CLA not only has antioxidant properties, but it modulates inflammatory cascade at multiple points. CLA reduces PGE2 (in much the same way as omega-3) CLA also has been shown to reduce IL-2, tumor necrosis factor-alpha and Cox–2. It reduces platelet deposition and macrophage accumulation in plaques. It also has some beneficial effect in the PPAR [peroxisome proliferator-activated receptors, important for lipid and inflammatory-mediator metabolism] area.

Part of the effect of CLA may be because it reduces fat mass and thus the amount of pro-inflammatory cytokines produced by fat cells.

I reiterate and fully admit that CLA has not been shown to have any effect on atherosclerosis in human beings. However, the results in the standard animal models for atherosclerosis (rabbits, hamsters,APO-E knockout mice) are very dramatic.

From all I know, it appears that the effective dose for weight loss and the animal studies in atherosclerosis would be equal to about 3 g of CLA per day. The anti-inflammatory properties of CLA seem to work better in the presence of adequate blood levels of omega-3.

I’m curious how and why a busy cardiothoracic surgeon would transform his practice so dramatically. Was there a specific event that triggered your change?

The transition from a very busy surgical practice to writing and speaking about the prevention of coronary disease has not been particularly easy, but it has been very interesting. I can't really point to any specific epiphany, it was a general feeling of frustration that we were not making any progress in curing heart disease, which is what I thought I was doing when I began my medical career.

Of course, I enjoyed the technical advances, the dramatic life-saving things that you do and I did on a daily basis. American medicine is spectacularly good at managing crises and spectacularly horrible at preventing those crises.

The lipid hypothesis is old and tired, even the most aggressive statin therapy reduces risk of heart attack by about 30% in a relatively small subset of people. It's interesting that we're now looking at statins as an anti-inflammatory agent.


Thanks, Dr. Lundell. We look forward to future conversations as your experience with CLA and heart disease prevention and reversal develops!


More about Dr. Lundell's book, The Cure for Heart Disease can be found at http://www.thecureforheartdisease.net.

Another reason not to get sick in a hospital

Hello, this is William Davis (I usually go by Bill) blogging.
Why does that matter? Well because on the not-so-coincidental article by Dr. William Davis on his Heart Scan Blog that I am going to quote and link here on my health related blog. I find it contains some excellent information on Vitamin D and hospitals.



Hospitals are a hell of a place to get sick
via The Heart Scan Blog by Dr. William Davis on 10/28/09

I answered a page from a hospital nurse recently one evening while having dinner with the family.

RN: "This is Lonnie. I'm a nurse at _____ Hospital. I've got one of your patients here, Mrs. Carole Simpson. She's here for a knee replacement with Dr. Johnson. She says she's taking 12,000 units of vitamin D every day. That can't be right! So I'm calling to verify."

WD: "That's right. We gauge patients' vitamin D needs by blood levels of vitamin D. Carole has had perfect levels of vitamin D on that dose."

RN: "The pharmacist says he can replace it with a 50,000 unit tablet."

WD: "Well, go ahead while Carole's in the hospital. I'll just put her back on the real stuff when she leaves."

RN: "But the pharmacist says this is better and she won't have to take so many capsules. She takes six 2,000 unit capsules a day."

WD: "The 50,000 units you and the pharmacist are talking about is vitamin D2, or ergocalciferol, a non-human form. Carole is taking vitamin D3, or cholecalciferol, the human form. The last time I checked, Carole was human."

RN: (Long pause.) Can we just give her the 50,000 unit tablet?

WD: "Yes, you can. But you actually don't need to. In fact, it probably won't hurt anything to just hold the vitamin D altogether for the 3 days she's in the hospital, since the half-life of vitamin D is about 8 weeks. Her blood level will barely change by just holding it for 3 days, then resuming when she's discharged."

RN: (Another long pause.) Uh, okay. Can we just give her the 50,000 units?"

WD: "Yes, you can. No harm will be done. It's simply a less effective form. To be honest, once Carole leaves the hospital, I will just put her back on the vitamin D that she was taking."

RN: "Dr. Johnson was worried that it might make her bleed during surgery. Shouldn't we just stop it?"

WD: "No. Vitamin D has no effect on blood coagulation. So there's no concern about perioperative bleeding."

RN: "The pharmacist said the 50,000 unit tablet was better, also, because it's the prescription form, not an over-the-counter form."

WD: "I can only tell you that Carole has had perfect blood levels on the over-the-counter preparation she was taking. It works just fine."

RN: "Okay. I guess we''ll just give her the 50,000 unit tablet."

From the alarm it raises trying to administer nutritional supplements in a hospital, you'd think that Osama Bin Laden had been spotted on the premises.

I laugh about this every time it happens: A patient gets hospitalized for whatever reason and the hospital staff see the supplement list with vitamin D, fish oil at high doses, iodine, etc. and they panic. They tell the patient about bleeding, cancer, and death, issue stern warnings about how unreliable and dangerous nutritional supplements can be.

My view is the exact opposite: Nutritional supplements are a wonderful, incredibly varied, and effective array of substances that, when used properly, can provide all manner of benefits. While there are selected instances in which nutritional supplements do, indeed, have interactions with treatments provided in hospitals (e.g., Valerian root and general anesthesia), the vast majority of supplements have none.

Fish Oil is Better Than Drugs for Preventing Heart Failure

Dr. Mercola writes "Fish oil supplements appear to work better than a popular cholesterol-reducing drug to help patients with chronic heart failure, according to recently released research."

The research Dr Mercola sites is from Lancet published Aug 31, 2008. Actually two articles,

one titled "Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial"

and the other titled "Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial".

Key words in the non-layman friendly medical journal lingo:
"n-3 polyunsaturated fatty acids" describes what we commonly call Fish Oil and

"rosuvastatin" which we know as Crestor, a powerful statin drug used to reduce cholesterol.

The study results, which were in part sponsored by Pfizer and AstraZeneca, were I'm sure, not what they would have liked the the tests to show because they're in the business of selling cholesterol lowering drugs which is a multi-billion dollar business . This comes on top of the studies showing increase of cancer due to cholesterol lowering drugs.

And you may want to read the articles listed under Credible Evidence to the right titled "NEW - Vytorin Rides Out Choppy SEAS from Medscape Today HeartWire " and "Pfizer's Cholesterol Drug Boosts Death Rate by 58 Percent.

Read the studies in Lancet here and here.