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Vegetarian Diet Lowers Risk for Some Cancers, Study Finds

March 11, 2015

Vegetarians who also eat fish have even greater protection against colorectal cancers

 
According to the researchers, the additional benefit from fish probably comes from omega-3 fatty acids. However, they note that even the nonvegetarian group in the study consumed less meat than the average American.

SOURCE
http://www.wsj.com/articles/vegetarian-diet-lowers-risk-for-some-cancers-study-finds-1425913215


Dr Oz shares video on DHA structure and function

February 15, 2015

Dr Oz shares video on DHA structure and function 
http://www.sharecare.com/health/omega-3-fatty-acids/docosahexaenoic-acid-dha

Is Algae Oil a Sustainable Food or Fuel?

February 26, 2013

Is Algae Oil a Sustainable Food or Fuel?

[by Scott Doughman, PhD, et al., All Copyrights Reserved] 

ABSTRACT FOR CONFERENCE TALK: 
With respect to algae oils, we consider the word "sustainability" in current food and fuel models. Overviews discussed are intended as general contexts for 1) the planet, for 2) finished oils, and for 3) growing new innovations. Part of the discussion considers trophic (nutrient) classifications. Heterotrophic algae systems may be defined as carbon-carbon bond consumers. Autotrophic algae systems may be defined as carbon-carbon bond producers, but are also consumers of their self-made carbon-carbon bonds to produce oil. All other organisms are also carbon consumers. Efficiency models for algae oils are also based on systems theory, but isolated data may suggest theoretical systems that need further proven. Because algae are inherently part of a "food chain" or an "economy" of scale, algae sciences increasingly have discovered paradigms for primary roles for algae in the discussion of "sustainability". New technologies for biomass, waste mitigation, and food and feed products require direct consumers over passive applications, such as fertilizer, due to the difference between direct and indirect consumption, especially with respect to the sustainability of water usage to produce oils. We suggest identification of a proven oil product and the direct consumer first be established in a stable system of production and consumption of materials prior to the ability to discuss sustainability criteria. The discussion applies to both heterotrophic algae systems and autotrophic algae systems. The source of the carbon is not relevant to our equation for carbon-carbon bond flow as a measure of sustainability with respect to oil, unless further qualified. We conclude algae oil sustainability is fundamentally based on a controlled measure of carbon-carbon bond flow compared to the direct use of the target oil product for food or fuel. 

Join the LinkedIn discussion, for all the right reasons. http://www.linkedin.com/groups?gid=4330487&trk=hb_side_g

There are separate bodies of literature for fish oil and algae oil.

February 10, 2013

Fishing for Omega-3 supplements from marine algae
By the editors of Environmental Nutrition, Environmental Nutrition Newsletter
Q. Can marine algae omega-3s provide the same benefits as fish oil ?
Premium Health News Service SOURCE: chicagotribune.com, January 30, 2013;
 
Editorial Commentary By Scott Doughman, PhD  

  • There are two interesting points right off the bat. First is the consideration of algae as marine. Marine algae is a correct designation in general and with few exceptions.
  • Second, the supplement model is the only method of educating about the science of fish oil and algae oil and fish as food, all are separate. Combined algae DHA supplements with food is needed. Combined EPA supplements with food is needed. There is really no difference between the two. I concluded and have published that after 6 months of any EPA or DHA or EPA+DHA combination with any biologic fatty acid therapy that these are identical in relative omega-3 index and omega-3 physiology outcome. The differences are far more meaningless than the similarities. No one formula is superior, although products may compete for best. DHA inherently is EPA and EPA is inherently DHA as needed once in the body. Don't discount you have a healthy powerful liver for metabolism.
 
This article on the Tribune website is important. The basis of any omega-3 fat causing any change in LDL-C is a shared statistic. Stick the statistic in its place. It has a role. Why does this result happen, the LDL-C increase, a barely significant result and a barely significant point? Why, because consumed fat necessitates liver-VLDL budding, which is a particle that is processed into LDL-C particles: VLDL>>>Pre-LDL>>LDL-C>remnants. The metric for LDL-C has been standardized, just like the Omega-3 Index is becoming, but the LDL-C particle now is by law a disease marker.
 
Since adding omega-3 oils adds to total fat intake on a daily basis, this could add up to 5% more fat consumed per day. This is a metabolic challenge and, perhaps if you also control total fat intake by offsetting 5% of any other fats in the diet, you now have a controlled state. This is basically what Amarin did. That is all. So that means most all other data has the risk of showing omega-3 benefits in preferential lowering of steady state blood fats and increasing steady state waste removal via HDL-C, but a tiny LDL-C change may be seen as (not) a side effect. Not in me. I want my LDL-C to go up if I eat more fat.
 
Why does the doctor NOT want me to have a healthy fat metabolism? Does this not prove part of the high cholesterol problem is caused by the high fat problem in the blood (due to sugar and fat together) as a first indicator? In some people, not in all. But in general, high triglycerides will correlate with higher LDL-C.

ALGAE OIL OMEGA-3 CULTURE

February 9, 2013

by Scott Doughman, PhD

Join Algae Oil Omega-3 Today 
http://www.linkedin.com/groups?home=&gid=4330487&trk=anet_ug_hm&goback=%2Egmr_4330487 


ALGAE OIL OMEGA-3 CULTURE

First of all, consider me a full CSO and Regulatory QA/QC officer in operations and a CEO of Purity. For 5 years I have been seeking the holy grail of algae oil omega-3s and have emerged as Dr "DHA" Doughman. 

Everything comes down to one single concept here. Do YOU have the love it takes? Could YOU take a 99% pure DHA triglyceride oil and make something with it? I made DHAlicous(TM) and started researching how to develop this product for many different uses, now working on recipes. About half of product innovation is sparked by my customer's needs. You could also establish a ...founDHAtion...(TM) starting from our two ingredient DHA algae oil (DHA Chromista oil plus green tea antioxidants). 

It is my mission as PURE ONE(R) brand manager to make all our messages resonate with Peace and Love, all for the consumer and in the name of infants, families, the Public Health and Diabetes self-care programs. You are the PURE ONE(R) 

Also, we have made many PURE ONE(R) babies over the years. I call the babies born to mothers and families taking it... PURE ONE(R) babies http://www.facebook.com/pages/Pure-One-Omega-3/162198434028

What to Buy Now!? Mother Nature. Ever wonder what food consumers worldwide really want? Natural purity. Good news, you are in luck. PURE ONE® uses the original water extraction technique to give 99% natural triglycerides for the purest DHA oil on the planet. 

Now we can assure the mother of our water extraction process and absolute purity. The analysis we did shows it exceeds all fish oil or other algae oil purity standards in the world.You can really save your life, live longer healthy and enjoy life, including foods and drinks all along the way. 

Can you win on purity? Is it superior? Well, if you don't think so you will end up loving another, have less peace of mind, less comfortable living conditions, loss of wireless, fear and pain. No, really! 

Maybe we should cap and trade purity, like we do pollution. Think about it, if we cap purity levels then I can sell purity credits to my competitors. 

I'm strategically going in the direction of supporting life, preventing death and promoting conception. I'm interested in focusing on ideas related to birthing, beauty and body wraps. 

Call me if you need product or oil. http://www.source-omega.com/ 
Chief Scientific Officer/Consulting Available

POWER OMEGA: DHA SAVES LIVES, LIVE LONGER HEALTHY

January 15, 2013

POWER OMEGA: DHA SAVES LIVES, LIVE LONGER HEALTHY 

WHAT IS A POWER OMEGA?
A POWER OMEGA is an omega-3 fatty acid IN YOU found one order of magnitude more abundantly than any other omega-3 fat. That means there are several forms of omega-3 fats, but only one is found ten times higher in you as part of your distinctively human "omega-3 identity". The POWER OMEGA in you is DHA (docosahexaenoic acid).

Your omega-3 identity is part of your omega-3 physiology. Different parts of your body are separated into different organs and tissues similarly non-identical in omega-3 composition, ratio or abundance of DHA. But this one omega-3, the DHA, is always found most abundant in every single part of you.

Your omega-3 identity is defined. From the character of your red blood cells to the uniqueness of your organs, your individual DHA ratios are preset within each different part of you. But the range of total omega-3 levels in you will slowly build-up or go down in line with the DHA your system takes in. One conclusion is your DHA levels matter most.

It mainly matters how much omega-3 you are getting. Secondary to the problem is what type of omega-3 you are getting. Your body is pre-programmed to use the omega 3s you consume on a daily basis. Your liver will reshuffle the omega-3 fats in order to fulfill a preset fat delivery function it exists to perform for the rest of the body. 

The Great Balls of Fat

There is little any food or oil or drug can do to stop the liver from budding off droplets of fat filled during the hours after you eat, with or without an additional stick of butter added to your meal. Fortunately, the liver is a fat sponge that differentially uses, selects, pulls-out, picks-up DHA from liver membranes to form the budding fat droplets that traffic and transport fat out to the rest of the body. DHA is the fundamental omega-3 of that machinery in the liver that assembles the cargo packing material around the great balls of fat. 

This packing material is micelle-like; that is, it is a wrapper-like film on the surface of the fat ball. Like a shell. That shell has lots of DHA omega-3 in it, used by the liver to wrap fat. How this was learned is related to the scientific models of fat transport through the liver. Diving into the creation of these droplets is a mystery and a journey into science beyond the scope of this book. Several factors come together in the liver cell to make the great balls of fat inside special internal compartments. 

Think of budding fat droplets as packages going out through the mail. After wrapping, a stamp gets put on the package; it's the same case in the liver transport of fats. This is an example of reading into the detailed situation of what is happening to the omega-3 fats after you have eaten them. The liver controls and processes all the omega-3s. It re-bundles all of the omega-3s into a preset format, uses these for making fat packages ready to ship out. 

The liver is your first omega-3 processing organ. Other tissues are receivers of the shipments. At the other end of the package delivery, a cell will take in the package of fat by receptors. That means the cells see the stamp and swallows up the fat packet. After that the cell can incorporate the omega-3s into itself.

Fat transport functions are detectable and improved by virtue of what happens first in the liver cells to make the great balls of fat. Even if you don't eat omega-3, DHA mediated processes are still taking place in the liver, because that is how the liver works. But it seems that the liver works better when it has higher levels of DHA and other omega-3s available to do its work. In fact, this is clearly part of a physiology that lowers blood fats called triglycerides and reduces fatty liver syndromes. That omega-3 physiology is tied to the power of omega-3 DHA. 

Omega-3 Identity

Your omega-3 identity is part of your blueprint. DHA always present much more abundantly than all other omega-3 fatty acids in every tissue and cell in your body is not the only surprise. About 15 percent of your blood omega-3s are something called omega-3 DPA (docosapentaenoic acid). DPA is something most people have never heard of, which points to a need to know more about DHA as well.

Another important omega-3 fatty acid in the diet and the body is perhaps the most well-known. EPA (eicosapentaenoic acid) makes up about 5-10 percent of the omega-3s in you. 

DHA, the POWER OMEGA, is also the longest chain fat that directly improves total blood fat levels. This in turn improves your health, but what you need to know is that when it comes down to eating your omega-3 fats, you are NOT at all what you eat.  

The input of food and type of omega-3 does not define your primary omega-3 identity, your liver does. Unlike alcohol that is removed by the liver, omega-3s are saved by the liver. Unlike amino acids that get absorbed by your cells while in the blood, fats don't absorb into you until they are deposited into the liver first for processing and shipment. Unlike sugar, which is rapidly spiked into the blood within minutes and hours, omega-3 fatty acids slowly travel through the system over hours, days, weeks and months. Fat is different in how it moves around in your body, it is tightly controlled and largely independent of other systems' direct control, although integrated with those other systems.

The DHA Power Food Advantage

What are people asking online and on calls? Now it seems everybody has heard about omega-3 as an important way to improve your quality of life, so people ask if there are lots of omega-3 sources to choose from, isn't all omega-3 the same? Not anymore!

Introducing DHA algae oil as a power food! This means you get the first optimized omega-3 dietary oil developed from a pure culture, not harvested or caught. Even if other omega-3s are also good for you, DHA could be the best for you to get in the diet directly. What if you could get your POWER OMEGA directly? Now you can. Algae are the unique Kingdom of Life that makes DHA directly as an organism.

It has since been found that the DHA in algae oil will help give nutrition, structure and function to your liver, heart, eyes and brain. Does that mean you are taking a brilliant leap forward in omega-3 fatty acids with DHA algae oil? Yes! Fish and flax oil require a majority of what is taken to be modified by the liver before use by the body.

Derived from algae, DHA algae oil is different from ordinary fish oil because it eliminates the possibility of mercury and other contaminants. DHA algae oil boosts your intake of DHA, the clinically supported nutrient associated with cognitive health and liver function.

DHA algae oil gives you a more scientifically perfect omega-3 balance directly used first by the liver for lowering your blood fats and for giving you the EPA you want for your heart by keeping or making the DHA you need.

DHA can be made by your body from fish oil and flax oil, but these are low DHA suppliers and require internal processing in the liver, plus these are not where DHA comes from in nature. Without direct DHA intake you could be at higher risk. Fish oil is a good substitute, but DHA algae oil is a truly great addition, especially if taking only flax oil.


What can the POWER OMEGA do for you?

So what do you need to know? The omega-3s are good fats needed more than ever to ensure your quality of life. So you need to know that DHA from algae oil has the highest natural DHA level known on Earth for providing you the POWER OMEGA your body uses most.

After years of research at leading universities I'm convinced DHA algae oil is the most effective and sustainable way to get the benefits of omega-3 in a way that will help keep you metabolically healthy so you can live longer healthy.
In fact, the science suggests DHA is critical to keep you metabolically healthy regardless of your weight. This means DHA is also a power food that saves lives. When you put more omega-3 fats into the diet the more DHA is made in the liver, this leads to less total fat build up in the blood to help keep you metabolically healthy. 

Metabolic health is defined as normal levels of blood fats such as the good and bad cholesterol, total cholesterol and your triglyceride levels.

Recent studies of persons who were obese supported the theory of a reduced risk of dying by up to 40 percent from obesity if metabolically healthy compared to persons who were obese and metabolically unhealthy. 
You live a certain lifestyle, besides your weight, be honest, are you metabolically healthy? It may not be the calories only, rather the choice of lifestyle and foods. It is truly simple; the steady state of being metabolically healthy is linked to the sturdy art of normal living, plus the DHA levels in you.

Right now, at this very moment, how is your fat health? Not your weight, your blood fat levels. These are also called your plasma lipids. Like your blood pressure has a normal range, so too blood fats have a normal range.
Separate from your weight, you can control your blood fats to increasingly become metabolically healthy. At high levels DHA in particular, plus other omega-3 fatty acids, could cut almost half the risk of dying from all causes when combined with normal diet and exercise.

Not all studies will agree, yet most will give some measure of reduced risk. My role is to inform you of the range of possibilities. Of course you may choose to do nothing, but medical doctors, FDA officials, Sports Umpires, Republicans and Democrats will often themselves be consumers of omega-3 supplements.
Could this book help you learn how to live longer healthy? Could this book help save lives? Indeed, omega-3 fats will help save you from yourself becoming metabolically unhealthy. Could this add an average three years to your lifespan? Yes it can when used for the long-term.

You can now call DHA algae oil the next generation omega-3 and the next generation plant-based omega-3. Now you know, in order to work, the liver particularly uses the omega-3 called DHA. This all seems to say that DHA in the liver is the POWER OMEGA, DHA SAVES LIVES and you can live longer healthy.

COPYRIGHT NOTICE: 
Scott Doughman ©2009-2013; All Rights Reserved
The copyright to this work is retained by Scott Doughman for the education of Algae Oil DHA effective July 2nd, 2012.

What Causes Type 2 Diabetes, and How Can it be Prevented?

July 20, 2012

What Causes Type 2 Diabetes, and How Can it be Prevented?

SOURCE:http://wholehealthsource.blogspot.com/2012/07/what-causes-type-2-diabetes-and-how-can.html
by 
From July 19th, 2012
In the comments of the last post, we've been discussing the relationship between body fatness and diabetes risk.  I think this is really worth understanding, because type 2 diabetes is one of the few lifestyle disorders where 1) the basic causes are fairly well understood, and 2) we have effective diet/lifestyle prevention strategies that have been clearly supported by multiple controlled trials.

Insulin resistance is an inability of tissues to "hear" the insulin signal properly, leading to poor blood glucose handling and other metabolic problems in processes that depend on insulin.  In my interview with Aitor Calero, I made the statement that the main cause of insulin resistance is excess body fat.  To be more precise, body fatness is the main modifiable cause*-- genetic makeup is another major factor that you're stuck with regardless of lifestyle.  Diabetes is caused by insulin resistance plus the eventual failure of the insulin-secreting pancreatic beta cells.  Some people become obese and insulin resistant, but their beta cells never fail, and therefore they do not become diabetic.  This has a strong genetic component, as Gretchen mentioned in the comments.  If you look at genetic loci associated with type 2 diabetes risk, most of them are in genes that regulate the pancreas, although the strongest obesity locus FTO is also a diabetes risk factor (0).

Regardless, there can be no question that body fatness is tightly associated with diabetes risk.  For example, in the Health Professionals Follow-up study, among 52,000 men, body mass index (a rough estimate of fatness) predicted the risk of developing diabetes over five years (1).  A BMI of 25 or more suggests overweight, and a BMI of 30 or more suggests obesity.  The data are striking:

A person with a BMI over 35 in this study (solidly obese) had a 42 times higher risk of developing diabetes than someone with a BMI of less than 23 (lean but not skinny).  People who straddled the line of obesity had a 6.7 times higher risk.  Furthermore, this relationship was not restricted to the obese.  Let's blow up the first four points and take a closer look:

Having a BMI of 24-24.9, which isn't even considered overweight, was associated with a 50 percent higher risk of diabetes, and going just over the cusp of overweight yielded a 120 percent increase in risk.  Therefore at nearly all levels of BMI, higher BMI strongly predicted the risk of developing diabetes.  This has been repeatedly confirmed.  

As I've explained in the past, multiple lines of evidence suggest that this is because excess body fat causes insulin resistance, which in turn increases the risk of developing diabetes* (1A1B).  

I understand that this is frustrating to people who carry excess fat and have a hard time losing it.  For many people, fat loss is a real challenge, and achieving true leanness is unlikely.  If that's you, I have some good news.  First of all, you can reduce your diabetes risk without losing a pound, by exercising regularly, eating a whole food diet, and managing sleep and stress effectively.  Second, you can greatly reduce your diabetes risk by losing as little as 11 pounds (5 kg).

This was demonstrated by the striking results of the Diabetes Prevention Program study, involving 3,234 pre-diabetic volunteers (2).  In this study, a combination of weight loss (via calorie-restricted low-fat diet) and exercise reduced the risk of developing diabetes by a full 58 percent over 2.8 years.  A similar trial in Finland a year earlier produced a virtually identical result (3), and similar results have come from trials in India, Japan, and China (456).  This kind of risk reduction is virtually unheard of in lifestyle modification trials, particularly considering the typical half-hearted adherence-- this shows that the intervention was striking directly at the heart of the problem.  It's possible that weight loss via a different diet (e.g. Paleo) would have been even more effective, but we won't know for sure until it's tested.

A follow-up study tried to determine which aspect of the DPP intervention was most important for diabetes risk reduction (7).  Here's what they found:
Weight loss was the dominant predictor of reduced diabetes incidence (hazard ratio per 5-kg weight loss 0.42 [95% CI 0.35-0.51]; P less than 0.0001). For every kilogram of weight loss, there was a 16% reduction in risk, adjusted for changes in diet and activity. Lower percent of calories from fat and increased physical activity predicted weight loss. Increased physical activity was important to help sustain weight loss. Among 495 participants not meeting the weight loss goal at year 1, those who achieved the physical activity goal had 44% lower diabetes incidence.
There you have it, folks.  We know how to prevent type 2 diabetes, and it's not magic.  These simple steps will reduce your risk:
  1. If you're overweight, lose fat if you can, even as little as a few pounds
  2. Exercise regularly
  3. Eat a healthy diet

* I simplify for a general audience, but it's probably more complicated than this.  Cellular energy overload causes insulin resistance, and this occurs when fat tissue expands to the point where it no longer efficiently traps fatty acids, exposing tissues throughout the body to excess energy.  In addition, enlarged fat depots tend to become inflamed, and inflammation contributes to insulin resistance.  So the causality is probably something like this: excess energy intake leads to excess fat mass, which leads to poor fatty acid trapping and inflammation in fat cells, which leads to cellular energy excess and inflammation in lean tissues, which leads to insulin resistance.  Although the full story is more nuanced, it is nevertheless fair and accurate to distill this down to the statement that excess body fat causes insulin resistance and diabetes.  This is true even though there is not a 1:1 correspondence between obesity and insulin resistance.

Omega-3 Fatty Acid Recommendations for Vegetarians

April 22, 2011

Omega-3 Fatty Acid Recommendations for Vegetarians

Last updated: May 2009: SOURCE: http://veganhealth.org/articles/omega3#veganDHA

Contents

Summary & Recommendations for Vegetarians

Omega-3 fatty acids are important for preventing heart disease, depression, and possibly other problems. There are three important omega-3 fatty acids:

  • ALA - alpha-linolenic acid; found in a wide range of foods
  • EPA - eicosapentaenoic acid; found mainly in fish
  • DHA - docosahexaenoic acid; found mainly in fish and seaweed

The body can convert ALA into EPA and DHA. ALA is efficiently converted to EPA, but it may require large amounts of ALA to produce optimal amounts of DHA. Recent evidence has raised a potential concern that large amounts of ALA could be harmful to the eyes over the long term.

Without diet planning, vegans and vegetarians have low omega-3 intakes and blood levels; and in some cases, elderly vegans have close to none. Therefore, vegetarians and vegans should do all three of the following:

A word of caution:
Too much omega-3 can result in bleeding and bruising. If you have reason to believe you have problems with easy bleeding or bruising, or are already consuming plenty of omega-3s, consult a health professional before following these recommendations or adding more omega-3 to your diet.

Introduction to the Omega-3 Fatty Acids

For our purposes, there are three important omega-3 fatty acids:

  • ALA is a short chain (18 carbon) fatty acid. It is found in small amounts in animal flesh, in very small amounts in a variety of plant products, and in relatively large amounts in soy, walnuts, canola oil, flaxseeds and their oil, hempseed oil, camelina oil, and chia seed oil. The human body cannot make its own ALA - it must be obtained through the diet.
  • EPA is a long chain (20 carbon) fatty acid. It is found mostly in fatty fish, in small amounts in eggs, and in very small amounts in seaweed. Some EPA is converted into series 3 eicosanoids which can reduce blood clotting, inflammation, blood pressure, and cholesterol. The human body can produce EPA out of ALA and out of DHA.
  • DHA is a long chain (22 carbon) fatty acid. It is found mostly in fatty fish, in small amounts in eggs, and in very small amounts in seaweed. It is a major component of the gray matter of the brain, and also found in the retina, testis, sperm, and cell membranes. Low levels of DHA have been associated with depression, and high levels and intake are associated with lower rates of heart disease.

A chart showing the conversion pathways for the omega-3 and omega-6 fatty acids can be found in this article.

Recommendations for the General Population

Table 1. ISSFAL ALA / EPA & DHA Recommendations
  ALA (.7% of energy) EPA + DHA
160 lb Man (1,724 cal) 3.0 g 500 mg
120 lb Woman 2.5 g 500 mg
Pregnant or Lactating Woman N/A 500 mg (200 should be DHA)

There are many health organizations that give omega-3 intake recommendations. I have chosen to use the recommendations of theInternational Society for the Study of Fatty Acids and Lipids (ISSFAL) because they give recommendations for ALA together with EPA and DHA (rather than just DHA and EPA) with an explanation readily available and after considering recommendations of many other organizations. Table 1 summarizes the ISSFAL's recommendations.

The recommendations are based largely on studies showing a lower risk of heart disease in people who have a relatively high intake of EPA and DHA. Table 2 summarizes ISSFAL's more detailed table.

Table 2. EPA and DHA Effects on Heart Disease
Study Highest EPA + DHA Intake Group (mg) Risk Compared to Lowest Intake Group Statistically Significant?
Dolecek 664 0.61a Y
Hu, Bronner et al. 533 0.62 Y
Albert, Campos > 246 0.43 N
Siscovick et al. 455 0.40 N
Mozaffarian et al. 919 0.47 Y
Ascherio et al. 580 1.03 N
a0.61 means a 61% risk compared to the lowest intake of EPA and DHA

This table shows a fairly consistent trend for ~500 mg of EPA plus DHA being associated with a ~40% reduced risk of heart disease.

A 2006 systematic review by Wang et al. found that EPA and DHA were beneficial in preventing cardiovascular disease (11). Another 2006 review by Hooper et al. concluded that omega 3 fats do not have a clear effect on total mortality, combined cardiovascular events, or cancer (26). Hooper found that among randomized controlled trials, there was great variability in the results among different studies. However, the studies with a strong methodology had more consistent results with a pooled relative risk of .98 (.70, 1.36). In cohort studies analyzed by Hooper, there was a benefit to omega 3s with a significant risk ratio of .65 (.48, .88). RCTs are considered stronger evidence than cohort studies and so it could be that the benefit found in cohort studies were due to other lifestyle factors that correlate with omega-3 intake but for which the results were not adjusted because they are not clearly known.

Vegetarians and vegans already have about a 24% lower risk of heart disease (5), and there is a question as to whether EPA and DHA could further benefit them.

Table 3. ALA Intake of Vegetarians
Study Population Intake (g/day)
Australia, 1999 (15) 17 vegetarian men, ~26-42 yrs 1.9
UK, 1984 (25) 10 vegan men 1.8
UK, 1984 (25) 10 vegan women 1.2
UK, 2010 (28) 5 vegan men 1.0
UK, 2010 (28) 5 vegan women .9

Omega-3 Intakes of Vegetarians

According to the USDA nutrient database, a medium egg contains about 2 mg of EPA and 16 mg of DHA. That provides lacto-ovo vegetarians with very small amounts of dietary EPA and DHA. Vegans who are not supplementing have an intake of zero EPA and DHA.

Three studies have listed the amount of ALA intake for vegetarians (who were presumably not purposefully adding rich sources of ALA to their diets). See Table 3.

Table 4. EPA & DHA Levels in Vegans
  Number EPA DHA
1981 UK17     %PCPG %PCPG
  Vegans 4 0.3 1.3
  Non-Veg 5 1.4 4.1
      %PP %PP
  Vegans 4 0.3 0.9
  Non-Veg 5 0.8 2.8
1992 UK16     %PTPG %PTPG
  Vegans 20 0.2 0.8
  Non-Veg 20 0.9 2.1
1999 Chile18     %PFA %PFA
  Vegetarians 26 0.35 1.56
  Non-Veg 26 0.79 2.58
2005 UK19     mg/l mg/l
  Vegan 232 8 16
  Lacto-Ovo 231 14 31
  Non-Veg 196 23 53
2010 UK28     µmol/l µmol/l
Men Vegan 5 65 195
  Lacto-Ovo 25 56 222
  Meat Eaters (no fish) 359 47 215
  Fish Eaters 2,257 58 240
Women Vegan 5 50 286
  Lacto-Ovo 51 55 224
  Meat Eaters (no fish) 309 57 241
  Fish Eaters 1,891 65 271
%PCPG - percentage of plasma choline phosphoglycerides
%PFA - percentage of plasma fatty acids
%PTPG - percentage of platelet phosphoglycerides

It appears that vegetarians meet about 50 to 60% of the daily ALA recommendations without special diet planning.

Vegans and vegetarians have been shown in many studies to have lower levels of long chain omega-3 fatty acids (EPA and DHA) than meat eaters. Table 4 shows the results of some of these studies. The general trend is that lacto-ovo vegetarians and vegans have lower levels of EPA and DHA in their blood. One exception were the 5 vegan women in the 2010 UK study who had, on average, higher DHA levels than even the fish-eaters. This is probably an anomaly for a few reasons. First, "vegan" was simply defined as someone who did not list eating animal products in their 7-day diet diaries. These vegans might have only been vegan for one week. Second, there were only 5 vegan women in the study making the finding unlikely to be statistically significant. Third, the standard deviation for the DHA levels of the vegan women was very high at 211 ?mol/l. That means that one or two of the vegan women had very high levels of DHA but some have very low levels.

Lower blood levels of EPA and, especially, DHA in vegetarians doesn't necessarily mean that they have lower levels of EPA or DHA in other tissues such as the brain. We do not know if these lower levels of DHA in the blood are harmful, but we should be careful because they might be.

Effects of Low EPA and DHA on Vegetarians

One of the main things that long chain omega-3 fatty acids do, particularly EPA, is reduce blood clotting which protects against heart attacks. There have been some differences noted in blood clotting between vegetarians and meat-eaters.

A 1999 Chile study (18) found that vegetarians had significantly more platelets (242,000 per ul) than non-vegetarians (211,000 per ul) and a shorter bleeding time (4.5 vs. 7.3 min).

In a follow-up 2000 Chile study (4), vegetarians were given 700 mg EPA and 700 mg DHA for 8 weeks. EPA went from .2 to 1.8% and DHA went from 1.1 to 3.0%. Some clotting factors did change, but bleeding time stayed at 5-1/2 minutes.

In a 1992 UK study (16), only one of eight platelet aggregation parameters in the men (but not the women) was different from the non-vegetarians. Bleeding times were similar.

Thus, of two studies that looked at these factors, vegetarians were doing worse than meat-eaters in one, but not much in the other.

In the one study looking at vegans' risk of death from heart disease (5), vegans had a 26% reduced rate which was not statistically significant (95% CI: .46, 1.21). Although these rates were not based on lifelong vegans, this finding was disappointing considering a 1987 prediction that lifelong vegans would have a 57% reduced incidence of heart disease based on cholesterol levels (6). Omega-3 status might be a reason why vegans did not have lower heart disease rates.

We do not really know whether low blood DHA levels reflect lower levels in other tissues in vegetarians, though it seems like a reasonable assumption. It seems more prudent to raise blood EPA and DHA levels than it is to hope that there is no damage from lower levels.

Traditional Remedy: Take more ALA, Reduce LA

Table 5. Effects of ALA Supplementation: 1999 Australian Study
  Baseline After 4 wks of 3.7 g ALA per day After 4 wks of 15.4 g ALA per day
  %PTPL %PTPL %PTPL
ALA 0.1 0.1 0.3
EPA 0.3 0.3 0.5
DHA 1.1 1 0.9^
  %PPL %PPL %PPL
ALA 0.3 0.4 1.4^
EPA 0.8 0.9 1.4^
DHA 2 2.1 1.9
  %PTG %PTG %PTG
ALA 1.2 2.5^ 7.4^
EPA 0.2 0.3 .4^
DHA 0.2 0.2 0.2
%PTPL - percentage of platelet phospholipids
%PPL - percentage of plasma phospholipids
%PTG - percentage of plasma triglycerides
^Statistically significant result compared to baseline

The traditional way that vegetarians were encouraged to raise EPA and DHA levels was by increasing ALA and decreasing linoleic acid (LA), a short chain omega-6 fatty acid. The body can convert ALA into EPA and DHA. The enzymes that do this conversion also convert LA, into longer chain omega-6s, and can be saturated with omega-6s due too so much in the diet. If they are saturated with omega-6s, they are not able to convert omega-3s.

Most vegetable oils are high in omega-6s. Most people, and especially vegetarians, tend to get plenty of LA in their diets. A 1981 UK study (17) showed that the dietary ratio of omega-6 to omega-3 fats was 16 for vegans and 6 for meat-eaters. A 1992 UK study (16) showed a ratio of 15.8 for vegan men vs. 10.2 for meat-eating men, and 18.3 for vegan women vs. 8.2 for meat-eating women. An ideal ratio is thought be about 3 or 4.

To deal with this problem, in the late 90s and 00s, vegetarian health professionals recommended increasing ALA intake and decreasing LA intake. Unfortunately, there are no real long-term studies looking at vegetarians' blood EPA and DHA after following these recommendations. But we do have some related studies.

A 1999 study (Table 5) of 17 vegetarian men in Australia (15), aged about 26 to 42 years old, showed that four weeks of 3.7 g of ALA per day (the equivalent of about 1.5 teaspoons of flaxseed oil) did not significantly increase the percentages of EPA or DHA in various blood lipids (fats). The same study showed that four weeks of 15.4 g of ALA (the equivalent of about 6.5 teaspoons of flaxseed oil) did increase EPA levels, but still did not increase DHA levels. There was no change in clotting factors (bleeding time was not reported).

Table 6. Effects of ALA Supplementation: 1981 UK Study
  Baseline 2 weeks of 6.5 g ALA per day
  %PCP %PCP
EPA 0.3 1.4^
DHA 1.3 1.3
  %PTPG %PTPG
EPA 0.3 0.3
DHA 0.9 1.2^
%PCP - percentage of plasma choline phosphoglycerides
%PTPG - percentage of platelet phosphoglycerides
^Statistically significant result compared to baseline

A 2000 study from The Netherlands (20) showed no change in EPA or DHA after 4 weeks of 2.0 g of ALA per day in 9 vegans aged 20 to 60 years old. By adding that much ALA, the ratio of dietary ALA:LA went from 13.7 to 6.7.

In a 1981 UK study (17), 4 vegans aged 26 to 37 years took 6.5 g of ALA per day for 2 weeks. They had some increase in EPA and DHA levels. See Table 6.

A 1992 study from India (21), in which 5 vegetarians aged 25 to 40 years old were given 3.7 g of ALA per day, showed an increase in EPA and DHA, and a reduction in LDL cholesterol and blood aggregation. See Table 7.

Table 7. Effects of ALA Supplementation: 1992 India Study
  Baseline After 6 weeks of 3.7 g ALA per day
  PPL (umoles/dl) PPL (umoles/dl)
EPA 0.6 2.7^
DHA 2.1 3.0^
  %PTPL %PTPL
EPA TR .4^
DHA 1.5 2.2^
LDL Cholesterol (mg/dl) 106 71^
Blood aggregation (%) 72.2 38.8^
PPL - plasma phospholipids
%PTPL - percentage of platelet phospholipids
TR - trace amount
^Statistically significant result compared to baseline

The Indian study was the longest length of time for any trial where the participants were vegetarian, but still wasn't that long (6 weeks). They also took a decent amount of ALA (the equivalent of about 1.5 teaspoons of flaxseed oil per day).

In summary, it appears that 3.7 grams of ALA per day minimum is needed for vegetarians to see an effect in blood DHA percentages in the short-term. But, there isn't any research in which participants were asked to cut their LA intake at the same time that they increased ALA intake. So we don't really know if doing that would be enough to boost DHA levels in the blood, not to mention the other tissues which we know nothing about.

Non-vegetarian Conversion Rates

In order to figure out what the ALA to EPA/DHA conversion rates are for vegetarians, it may be particularly important to stick with studies that use actual vegetarians rather than meat-eaters who might have a dietary source of EPA and DHA. Because there is a lack of long term studies on vegetarians, we should look at some of the research on meat-eaters.

There have been many studies on meat-eaters' conversion rates, and for the most part they have shown good conversion of ALA to EPA, but very little to DHA. Because small amounts or short terms do not appear to be promising, I will limit my review to two studies that used larger amounts and longer time periods.

A 2008 study on meat-eaters from Canada (22) who took 1.2, 2.4, and 3.6 g ALA per day for 12 weeks resulted in an increase in percentage of EPA in red blood cell fatty acids for the 2.4 and 3.6 ALA groups, but no increases in DHA. This study used an "intention to treat" method, which means that subjects who did not comply with the regimen were still included in the results. I'd like to know the results only for the people who stuck with the regimen, but there was little information given on the level of compliance.

A 1999 study on Japanese (23) elderly subjects gave subjects 3 g ALA per day and reduced the omega-6 to omega-3 ratio to 1:1. After 3 months, there was no difference in EPA and DHA levels, but after 10 months, EPA levels had risen from 2.5 to 3.6% of serum lipids, and DHA levels rose from 5.4 to 6.4 (both findings statistically significant).

Welch et al. (24) reported that non-fish eaters (both vegetarians and meat-eaters) convert ALA to long chained omega-3s at a slightly greater rate than do meat-eaters, so conversion rates of vegetarians might be greater than these studies on meat-eaters show.

In summary, it appears that 3 g (equivalent of about 1-1/2 teaspoons of flaxseed oil) per day of ALA cannot increase blood percentages of DHA in three months time, but can increase blood percentages in 10 months time, assuming intake of omega-6 is low.

Table 8. Foods with Lowest Omega-6 to Omega-3 Ratios
Food n-6:n-3 ratio ALA
flaxseeds 1:4 1.6 g / tablespoon
flaxseed oil 1:4 2.5 g / teaspoon
chia seeds 1:3 5 g / oz
camelina oil 1:2  
canola oil 2:1 1.3 g / tablespoon
English walnutsa 4:1 - 5:1 2.6 g / oz (14 halves)
walnut oil 5:1 1.4 g / tablespoon
soybean oil 7.5:1 .9 g / tablespoon
black walnuts 10:1 .9 g / oz
aEnglish are the typical walnuts found in most grocery stores.

Low Omega-6 to Omega-3 Ratio Foods

Table 8 lists foods with the lowest omega-6 to omega-3 ratios.

More information on omega-3 sources can be found in the articles "The Fatty Acids" and "High ALA Sources".

Vegetarian Children

I am not aware of studies measuring the EPA or DHA levels of vegetarian or vegan children. However, we do know that many children have been raised vegan without supplementing with DHA, or even ALA, and most of these children have developed well. It appears that not supplementing with ALA, EPA, and DHA might not be an issue for someone who is born vegan. It could be that their bodies are very efficient at converting the dietary ALA they receive into EPA and DHA. However, judging from the above studies, people who become vegan or vegetarian as adults might have less ability to make this conversion. Until we know more, I would encourage parents of vegetarian children to supplement their diets with DHA at 200 mg per day.

Retroconversion of DHA to EPA

A 1996 Canadian study (2) showed an 11 - 12% conversion rate of DHA to EPA after 6 weeks of 1,620 mg of DHA in vegetarians. See Table 9 for more details showing that EPA levels increased.

Table 9. Conversion of DHA to EPA: 1996 Canadian Study
  Baseline 6 weeks of 1.62 g DHA per day
  %SPL %SPL
EPA 0.57 1.3
DHA 2.4 8.3
  %PTPL %PTPL
EPA 0.21 0.58
DHA 1.2 3.9
Thrombogenic risk factors   No differences
%SPL - percentage of serum phospholipids
%PTP - percentage of platelet phospholipids
^statistically significant from baselines

A 1997 Canadian study (1) of vegetarians and meat-eaters showed a conversion rate of 9.4% of DHA to EPA from a dose of 1,620 mg DHA per day for 6 weeks, with no differences between groups.

A 1996 French study (3) fed three people 123 mg of DHA one time and found a conversion rate to EPA of 1.4%.

I could not find any other studies looking at DHA amounts less than 1,620 mg per day.

Health Benefits and Concerns of ALA

As described above, vegetarians on average meet about 50 - 60% of the ISSFL's daily recommendations. In recent years, there have been numerous studies that have shown benefits of a high ALA intake, and have also shown potential problems with a high ALA intake. I would like to quickly review those areas.

Heart Disease

A meta-analysis of five prospective studies of ALA intake published in 2004 (7) suggested that high ALA intake was associated with reduced risk of fatal heart disease (relative risk 0.79, .60-1.04). This finding was not quite statistically significant. The average highest level of intake was 2.0 g per day versus the lowest of .8 g per day.

Depression

A 2007 meta-analysis from Taiwan (8) and a 2006 review from Canada (9) found that supplementation with EPA and DHA improved depression, but a 2006 review from the UK (10) found that it did not.

Prostate Cancer

In contrast to the findings on heart disease which have been fairly consistent in favor of a modest benefit, ALA intake and blood levels have been associated with the risk of prostate cancer in a number of studies, and not associated in a number of other studies. Reviewing this material is beyond the scope of this article, but if you are interested in reading more details, a good review starts on p. 80 of Chapter 6: Flax and the Prevention of Cancer from FLAX - A Health and Nutrition Primer (Fourth Edition, 2007) published by the Flax Council. The following paragraph does a good job in summarizing the literature:

Otherwise, there are too many inconsistencies among the research findings to be confident that any one fatty acid contributes to cancer development in humans. These inconsistencies apply to most fatty acids, not just ALA. For instance, among the studies summarized in Tables 17 and 18, LA was associated with an increase in prostate cancer risk in 2 studies, had no association with prostate cancer in 7 studies and had an inverse relationship with prostate cancer in 5 studies.

I would not be worried about increasing the risk of prostate cancer with an intake of 2.0 g per day of ALA that is associated with a reduced risk of heart disease.

A 2004 review concludes that, "More research is needed in this area before it can be concluded that there is an association between alpha-linolenic acid and prostate cancer." A 2009 systematic review and meta-analysisstates:

When examined by study type (ie, retrospective compared with prospective or dietary ALA compared with tissue concentration) or by decade of publication, only the 6 studies examining blood or tissue ALA concentrations revealed a statistically significant association. With the exception of these studies, there was significant heterogeneity and evidence of publication bias. After adjustment for publication bias, there was no association between ALA and prostate cancer (RR: 0.96; 95% CI: 0.79, 1.17).

Eyesight

There have been three studies looking at age-related eye damage and fatty acids, all coming from the Nurse's Health Study.

A 2005 analysis (12) of a group of women from the Nurse's Health Study found that both the highest intakes of ALA and LA were associated with an increase in lens opacity, which can lead to cataracts. Interestingly, neither total fat, animal fat, vegetable fat, saturated fat, nor trans fats were associated with an increase in lens opacity. For ALA, the risk ratio was 2.2 (1.2, 4.5) for about 1.26 g compared to .86 g per day.

Table 10. ALA Effects on AMD: 2007 Nurse's Health Study
  Lowest fifth (g per day) Highest fifth (g per day)
Men 0.76 1.44
Women 0.78 1.49

A 2007 analysis (13) of the same group found that the highest category of ALA intake (about 1.26 g per day) was linked to a 16% increase in eye lens nuclear density compared to the lowest category (about .84 g per day) over five years. In this case, no other fat category was associated with an increase, including total, animal, vegetable, saturated, monounsaturated, polyunsaturated, trans, LA, arachidonic acid, or long chain omega-3s.

A 2007 analysis (14) of men and women in the Nurse's Health Study over the age of 50 years old found that those in the highest fifth of ALA intake had an increased risk of age-related macular degeneration (AMD). The risk ratio was 1.41 (1.00, 1.98). Rough estimates of intake are shown in Table 10

Total fat, saturated, monounsaturated, and trans fat were all associated with an increase in AMD. In contrast, the highest intakes of DHA tended to be protective. The authors state,

To evaluate further the association with linolenic acid, the major food sources of this fatty acid were examined (Table 5). These foods provided 38% of linolenic acid intake in women and 46% in men at baseline. Of the food sources of linolenic acid, intake of beef, pork, or lamb as a main dish appeared strongly positively related to AMD. More than 1 serving/wk of beef, pork, or lamb as a main dish was associated with a 35% increased risk of AMD compared with <3 servings/mo (pooled RR: 1.35; 95% CI: 1.07, 1.69). A high intake of margarine was also significantly related to an increased risk of AMD. Because these food items were also major contributors of trans unsaturated fat, we adjusted further for quintiles of trans unsaturated and other fats in models with linolenic acid; the relation with linolenic acid was slightly attenuated but remained significant (Table 4). Other high-fat foods were not associated with risk of AMD (data not shown).

The fourth quintile of animal fat was associated with a statistically significant increase in AMD (1.36, 1.03 - 1.79).

In the case of AMD, it appears that ALA might serve as a marker of certain animal fats and the ALA itself might not be the cause. Or, it could also be that cooked ALA is the cause, since ALA can be damaged during cooking at high temperatures. Unfortunately the analyses of lens opacity and nuclear density did not show any correlation with animal fat and so it is hard to dismiss all of these findings as simply due to ALA being a marker for animal fat intake.

These studies were done on only one population by one group of researchers, and more information is needed before we should draw conclusions. I consider it likely that further studies will show inconsistencies and until plant and/or uncooked sources of ALA are examined, I am skeptical that uncooked, plant sources of ALA are harmful to the eye.

According to the Canola Council, canola oil should be safe for use in cooking. Based on the results of the above studies on eye lens damage, make sure you use low heat and limited cooking times when cooking with canola oil until more is known about ALA and eye damage.

Table 11. Omega-3 Recommendations
  >Grams per day
ISSSFAL recommendations 2.5 (F), 3.0 (M)
Vegetarian intakes 1.2 (F), 1.8 (M)
Additional amounts needed for conversion to DHA 3 - 3.7
Protective against heart disease 2
Possibly cause eye problems 1.25 - 1.5
Teaspoon of flaxseed oil 2.5
F - female, M - male

Summary of Omega-3 Benefits and Concerns

What we know about ALA is summarized in Table 11.

If it weren't for the (small chance) for potential eye problems, I would suggest either adding 3 g of ALA per day, or taking DHA supplements. Because of the eye issues, that much ALA is not worth the risk when DHA supplements are available. I would still recommend adding about .5 g of ALA per day for its own benefits on heart disease and to help increase EPA levels. If using such small amounts of uncooked, plant sources of ALA, the risk to the eyes should be very minimal.

It is not clear what amount of DHA is best to supplement. 500 mg might be ideal, but that is an expensive amount and in the face of no compelling evidence that vegans are being harmed by lower blood levels of DHA, it seems unnecessary. Based on the amounts of vegan DHA that are available, I would recommend 200 to 300 mg per day.

If you are getting the recommended ALA and DHA, EPA should not be a problem. It should be pointed out that fish contain about twice as much DHA as EPA (27), so it's not unusual to get more DHA than EPA in the diet. 

Vegan DHA & EPA Supplements

Table 12. Vegan DHA Supplements
Brand Approx price per 300 mg DHA Available From
NuTru's O-Mega-Zen3 $ .47 Pangea
Vegan Essentials
V-PURE
25 mg EPA and 90 mg DHA per capsule
$1.10 Pangea
Pure One
10 mg EPA and 300 mg DHA per capsule
   
Opti3 Complete Omega-3
20 mg EPA and 100 mg DHA per capsule
  Opti3omega.com
Deva Vegan Omega-3 DHA $ .67
$ .50
Pangea
Amazon (% goes to Vegan.com)
Dr. Fuhrman's DHA Purity $ .86 DrFurhman.com
Spectrum Vegetarian DHA $ .51 whole foods Stores
Futurebiotics NewHarvest Omega-3 Vegetarian EPA $16.99 per bottle of 30 (600 mg EPA) capsules
Neuromins©   Most whole foods stores, in gelatin capsules

Human Ancestors and DHA

If humans require a significant dietary source of DHA for optimal health, it could imply that our ancestors have always had a source of fish in their diet. And this would imply that we must have evolved close to water.

Because our omega-6 to omega-3 ratios were probably much lower in pre-historical times, conversion of DHA from ALA might have been much greater. But even so, some researchers believe humans did evolve close to water, as described in this excerpt from a 2004 article in the Journal of Nutrition, Is Docosahexaenoic Acid (DHA) Essential? Lessons from DHA Status Regulation, Our Ancient Diet, Epidemiology and Randomized Controlled Trials:

It is as yet unclear what enabled us to expand our brains during evolution. About 60% of our brain dry matter is lipid, and AA and DHA are among the most abundant fatty acids of brain phospholipids. This raises the question as to how we have been able to meet the increasing LCP demand. Future elucidation of the 1.24% difference of our genome with that of chimpanzees will undoubtedly provide us with at least part of the answer, and many candidate genes either involved in LCP transport, binding or metabolism have already been postulated. Regarding the origin of the LCP there is little doubt, because they derive either directly from the diet or become synthesized from LA or ALA. As outlined above, predominant derivation from synthesis seems unlikely, but if we need LCP from the diet, what did our ancestors eat to support a brain growth from 450 to 1300 g. African hominids have long been assumed to have been hunter-gatherers who obtained a great deal of their food from the open savanna. Meat from savanna animals is a poor DHA source, but savanna meat does have higher (n-3)/(n-6) ratios compared with domestic animals. Savanna hunting is, however, not easy even with modern tools. Hunting hominids at that stage of human evolution would have possessed unimaginable complex cognitive functions for planning, stalking, coordinating and communication. It is more likely that they lived at the margins of lakes and rivers or at the seashore because that is where most of their remains and tools have been discovered. Examples of these locations are to be found in the East African Rift Valley, e.g., lake Turkana in the present Kenya (e.g., "Turkana boy," a Homo erectus), but also in the South African Cape and the Central African Chad Basin. From these breeding nests of the new hominid species they may have spread in at least three "out of Africa" waves to colonize the entire world. "We may have to trade the picture of our African ancestors from a brawny hunter who brings home the wildebeest to butcher it with stone tools into that of a fisherman who wades the placid lakes and comes home with easily caught fish, seabird eggs, mollusks and other marine foods". Many fishes from tropical warm waters, including those in lakes Nyasa and Turkana, are rich sources of AA and DHA, as opposed to their EPA- and DHA-rich counterparts from the more Northern climates.
For more information see
See summary of cooking oils

References

1. Conquer JA, Holub BJ. Dietary docosahexaenoic acid as a source of eicosapentaenoic acid in vegetarians and omnivores. Lipids. 1997 Mar;32(3):341-5.

2. Conquer JA, Holub BJ. Supplementation with an algae source of docosahexaenoic acid increases (n-3) fatty acid status and alters selected risk factors for heart disease in vegetarian subjects. J Nutr. 1996 Dec;126(12):3032-9.

3. Brossard N, Croset M, Pachiaudi C, Riou JP, Tayot JL, Lagarde M. Retroconversion and metabolism of [13C]22:6n-3 in humans and rats after intake of a single dose of [13C]22:6n-3-triacylglycerols. Am J Clin Nutr. 1996 Oct;64(4):577-86.

4. Mezzano D, Kosiel K, Martinez C, Cuevas A, Panes O, Aranda E, Strobel P, Perez DD, Pereira J, Rozowski J, Leighton F. Cardiovascular risk factors in vegetarians. Normalization of hyperhomocysteinemia with vitamin B(12) and reduction of platelet aggregation with n-3 fatty acids. Thromb Res. 2000 Nov 1;100(3):153-60.

5. Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G, Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J, McPherson K. Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies. Am J Clin Nutr. 1999 Sep;70(3 Suppl):516S-524S.

6. Thorogood M, Carter R, Benfield L, McPherson K, Mann JI. Plasma lipids and lipoprotein cholesterol concentrations in people with different diets in Britain. Br Med J (Clin Res Ed). 1987 Aug 8;295(6594):351-3.

7. Brouwer IA, Katan MB, Zock PL. Dietary alpha-linolenic acid is associated with reduced risk of fatal coronary heart disease, but increased prostate cancer risk: a meta-analysis. J Nutr. 2004 Apr;134(4):919-22.

8. Lin PY, Su KP. A meta-analytic review of double-blind, placebo-controlled trials of antidepressant efficacy of omega-3 fatty acids. J Clin Psychiatry. 2007 Jul;68(7):1056-1.(Abstract)

9. Sontrop J, Campbell MK. Omega-3 polyunsaturated fatty acids and depression: a review of the evidence and a methodological critique. Prev Med. 2006 Jan;42(1):4-13. Epub 2005 Dec 7. (Abstract)

10. Appleton KM, Hayward RC, Gunnell D, Peters TJ, Rogers PJ, Kessler D, Ness AR. Effects of n-3 long-chain polyunsaturated fatty acids on depressed mood: systematic review of published trials. Am J Clin Nutr. 2006 Dec;84(6):1308-16. (Abstract)

11. Wang C, Harris WS, Chung M, Lichtenstein AH, Balk EM, Kupelnick B, Jordan HS, Lau J. n-3 Fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review. Am J Clin Nutr. 2006 Jul;84(1):5-17.

12. Lu M, Taylor A, Chylack LT Jr, Rogers G, Hankinson SE, Willett WC, Jacques PF. Dietary fat intake and early age-related lens opacities. Am J Clin Nutr. 2005 Apr;81(4):773-9.

13. Lu M, Taylor A, Chylack LT Jr, Rogers G, Hankinson SE, Willett WC, Jacques PF. Dietary linolenic acid intake is positively associated with five-year change in eye lens nuclear density. J Am Coll Nutr. 2007 Apr;26(2):133-40.

14. Cho E, Hung S, Willett WC, Spiegelman D, Rimm EB, Seddon JM, Colditz GA, Hankinson SE. Prospective study of dietary fat and the risk of age-related macular degeneration. Am J Clin Nutr. 2001 Feb;73(2):209-18.

15. Li D, Sinclair A, Wilson A, Nakkote S, Kelly F, Abedin L, Mann N, Turner A. Effect of dietary alpha-linolenic acid on thrombotic risk factors in vegetarian men. Am J Clin Nutr. 1999 May;69(5):872-82.

16. Sanders TA, Roshanai F. Platelet phospholipid fatty acid composition and function in vegans compared with age- and sex-matched omnivore controls. Eur J Clin Nutr. 1992 Nov;46(11):823-31. (Same study population as citation 25.)

17. Sanders TA, Younger KM. The effect of dietary supplements of omega 3 polyunsaturated fatty acids on the fatty acid composition of platelets and plasma choline phosphoglycerides. Br J Nutr. 1981 May;45(3):613-6.

18. Mezzano D, Munoz X, Martinez C, Cuevas A, Panes O, Aranda E, Guasch V, Strobel P, Munoz B, Rodriguez S, Pereira J, Leighton F. Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine. Thromb Haemost 1999 Jun;81(6):913-7.

19. Rosell MS, Lloyd-Wright Z, Appleby PN, Sanders TA, Allen NE, Key TJ. Long-chain n-3 polyunsaturated fatty acids in plasma in British meat-eating, vegetarian, and vegan men. Am J Clin Nutr. 2005 Aug;82(2):327-34.

20. Fokkema MR, Brouwer DA, Hasperhoven MB, Martini IA, Muskiet FA. Short-term supplementation of low-dose gamma-linolenic acid (GLA), alpha-linolenic acid (ALA), or GLA plus ALA does not augment LCP omega 3 status of Dutch vegans to an appreciable extent. Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):287-92.

21. Ghafoorunissa IM. n-3 Fatty acids in Indian diets - comparison of the effects of precursor (alpha-linolenic acid) vs. product (long chain n-3 polyunsaturated fatty acids). Nutrition Research. 1992;12:569-82.

22. Barcelo-Coblijn G, Murphy EJ, Othman R, Moghadasian MH, Kashour T, Friel JK. Flaxseed oil and fish-oil capsule consumption alters human red blood cell n-3 fatty acid composition: a multiple-dosing trial comparing 2 sources of n-3 fatty acid. Am J Clin Nutr. 2008 Sep;88(3):801-9.

23. Ezaki O, Takahashi M, Shigematsu T, Shimamura K, Kimura J, Ezaki H, Gotoh T. Long-term effects of dietary alpha-linolenic acid from perilla oil on serum fatty acids composition and on the risk factors of coronary heart disease in Japanese elderly subjects. J Nutr Sci Vitaminol (Tokyo). 1999 Dec;45(6):759-72. /p>

24. Welch AA, Bingham SA, Khaw KT. Estimated conversion of alpha-linolenic acid to long chain n-3 polyunsaturated fatty acids is greater than expected in non fish-eating vegetarians and non fish-eating meat-eaters than in fish-eaters. J Hum Nutr Diet. 2008;21:373. (Abstract)

25. Roshanai F, Sanders TA. Assessment of fatty acid intakes in vegans and omnivores. Hum Nutr Appl Nutr. 1984 Oct;38(5):345-54. (Same study population as citation 16.)

26. Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, Worthington HV, Durrington PN, Higgins JP, Capps NE, Riemersma RA, Ebrahim SB, Davey Smith G. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ. 2006 Apr 1;332(7544):752-60. Epub 2006 Mar 24.

27. Kris-Etherton PM, Grieger JA, Etherton TD. Dietary reference intakes for DHA and EPA. Prostaglandins Leukot Essent Fatty Acids. 2009 Jun 12. [Epub ahead of print]

28. Welch AA, Shakya-Shrestha S, Lentjes MA, Wareham NJ, Khaw KT. Dietary intake and status of n-3 polyunsaturated fatty acids in a population of fish-eating and non-fish-eating meat-eaters, vegetarians, and vegans and the precursor-product ratio of alpha-linolenic acid to long-chain n-3 polyunsaturated fatty acids: results from the EPIC-Norfolk cohort. Am J Clin Nutr. 2010 Nov;92(5):1040-51. Link

Reviewed

Kornsteiner M, Singer I, Elmadfa I. Very low n-3 long-chain polyunsaturated fatty acid status in Austrian vegetarians and vegans. Ann Nutr Metab. 2008;52(1):37-47. Epub 2008 Feb 28. 10:1 n-6/n-3 for vegetarian diets and lower LC n-3 levels. (Abstract only).

Kris-Etherton PM, Hill AM. N-3 fatty acids: food or supplements? J Am Diet Assoc. 2008 Jul;108(7):1125-30. (No abstract available.)

Mangat I. Do vegetarians have to eat fish for optimal cardiovascular protection? Am J Clin Nutr. 2009 May;89(5):1597S-1601S. Epub 2009 Mar 25.

Williams CM, Burdge G. Long-chain n-3 PUFA: plant v. marine sources. Proc Nutr Soc. 2006 Feb;65(1):42-50. Review.

Omega-3 DHA+EPA are Complementary To AHA Triglyceride Lowering Dietary Target

April 18, 2011

AHA Targets Elevated Triglycerides; Sees Fructose Among Culprits

OMEGA SOURCE: By: JENNIE SMITH, Internal Medicine News Digital Network; 04/18/11

Triglyceride levels, which play a large role in both atherosclerotic risk and metabolic health, are highly responsive to decreases in dietary sugar intake and saturated and trans fat intake, along with increases in omega-3 acid intake and exercise, according to a scientific statement from the American Heart Association.

 

    

Fructose in excess of 100 g/day, and possibly in excess of 50 g/day, has been associated with raised triglyceride levels. A typical can of cola or lemon-lime soda contains more than 20 grams of fructose.

"What's new is that we point out that triglycerides might be considered a marker for metabolic health," said Dr. Neil J. Stone of Northwestern University, Chicago, vice chair of the statement's writing group, in an interview. "If you have a country where you're seeing more obesity and more diabetes, it becomes important for people to start asking themselves 'are there signs that I should be doing something different?' and this is one," he said.

 

The scientific advisory, published online April 18 in the journal Circulation and citing some 528 sources, was not presented as a clinical guideline so much as a distillation of 30 years worth of evidence on the complex relationship among lifestyle factors, triglycerides, and cardiovascular and metabolic health (Circulation 2011 [doi:10.1161/ CIR.0b013e3182160726]).

However, the statement's authors, led by Dr. Michael Miller, director of the Center for Preventive Cardiology at the University of Maryland, Baltimore, included a number of recommendations on diagnosing and treating hypertriglyceridemia, focusing on dietary and lifestyle changes.

The statement emphasizes the "increasingly crucial role" of triglycerides in the evaluation and management of cardiovascular disease, and the importance of diet including consumption of sugars common in beverages in contributing to unhealthy triglyceride levels.

Reductions of 50% or more are achievable without the use of medication indeed medication is not a widely accepted strategy for reducing triglycerides except among people with extremely high values of greater than 500 mg/dL. "The subject of medication and triglycerides is still lacking crucial clinical trial evidence," Dr. Miller and colleagues wrote in their analysis, noting that certain medications, including hormonal treatments, can also contribute to elevated triglycerides.

About a third of American adults have elevated triglyceride levels, which are defined as fasting triglyceride of 150 mg/dL or higher. The authors recommended that optimal fasting triglyceride levels now be defined as 100 mg/dL and that clinicians screen initially for nonfasting triglyceride, defining normal at below 200 mg/dL. People with higher nonfasting levels may then be further screened for fasting triglyceride.

The new dietary recommendations include restricting added dietary sugar to 5%-10% percent of calories consumed. In support of this, the authors cited a study of 6,113 U.S. adults showing that the lowest triglyceride levels were observed when added sugar represented less than 10% of total energy, and that higher triglyceride levels corresponded with added sugar accounting for a greater proportion of energy intake (JAMA 2010;303:1490-7).

The authors singled out fructose, a type of dietary sugar increasingly common in processed foods and soft drinks, as particularly problematic. Fructose in excess of 100 g/day, and possibly in excess of 50 g/day, has been associated with raised triglyceride levels. A typical can of cola or lemon-lime soda contains more than 20 grams of fructose, the authors noted.

Dr. Miller and his colleagues advocated weight loss of 5%-10% of body weight, which is associated with a 20% reduction in triglycerides, and regular aerobic exercise, to reduce triglyceride levels closer to optimal.

They also promoted increasing dietary fiber, keeping saturated fat below 7% of calories, eliminating trans fat from the diet, and increasing omega-3 polyunsaturated fatty acid consumption in the form of marine fish, though the authors said more research was needed to determine whether supplementing with fish-oil capsules provided equivalent benefits. Complete abstinence from alcohol was also recommended for people with very high triglycerides.

"Overall, optimization of nutrition-related practices can result in a marked triglyceride-lowering effect that ranges between 20% and 50%," they concluded.

Funding for the scientific advisory statement was provided by the American Heart Association. Dr. Miller declared no conflicts of interest affecting the drafting of the statement. However, Dr. Stone and the report's third author, Dr. Christie Ballantyne of Baylor College of Medicine in Houston, disclosed support from pharmaceutical industry sources. Other coauthors and some reviewers disclosed additional support from pharmaceutical and agricultural firms.

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Omega-3 Sources - DHA Algae Oil

February 17, 2011

Algae, Latin for "seaweed" are a large and diverse group of simple, typically autotrophic organisms, ranging from unicellular to multicellular forms, such as the giant kelps that grow to 65 meters in length. The US Algal Collection is represented by almost 300,000 accessioned and inventoried herbarium specimens.[3] The largest and most complex marine forms are called seaweeds. They are photosynthetic like plants, and "simple" because their tissues are not organized into the many distinct organs found in land plants.


Though the prokaryotic cyanobacteria (commonly referred to as blue-green algae) were traditionally included as "algae" in older textbooks, many modern sources regard this as outdated[4] as they are now considered to be bacteria.[5] The term algae is now restricted to eukaryotic organisms.[6] All true algae therefore have a nucleus enclosed within a membrane and plastids bound in one or more membranes.[4][7] Algae constitute a paraphyletic and polyphyletic group,[4] as they do not include all the descendants of the last universal ancestor nor do they all descend from a common algal ancestor, although their plastids seem to have a single origin.[1] Diatoms are also examples of algae. SOURCE: http://losts.net/Dha_algal_oil

 

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