A little over a year ago, I remember doing some research on the three different types of omega-3, but for some reason I have completely neglected this topic since starting CR. I think I was distracted by other topics. I tend to follow my compulsions when it comes to research; I wouldn’t do it if it was a chore. Anyway, as I was reading a thread on healthy fats over at imminst, I was linked to an older topic on fats at the CR Society archives. I saw a line on long-chain omega-3s (found in animal sources) and short-chain omega-3s (found in plant sources), and realized I needed to refresh my knowledge since almost all of my omega-3s are now from plant sources.

The Three Types of Omega-3: Basic Chemistry
alpla-Linolenic acid (ALA)

ALA is an 18 carbon polyunsaturated fatty acid found in plant sources. The most common dietary sources include: chia seed, flax seed, hemp, rapeseed (canola), walnuts,  and soy beans. Since ALA is an essential omega-3 fatty acid, it cannot be produced within the body and must be consumed. The other two types of omega-3s can be synthesized from ALA within the body or can be consumed.

Eicosapentaenoic acid (EPA)

EPA is a 20 carbon polyunsaturated fatty acid that is obtained primarily by eating fish or fish oils, but can also be found in microalgae. EPA can also be directly synthesized from ALA in the body, but this process reportedly has much lower yields than directly consuming it. EPA is essential within the body, and acts in the body to counteract the inflammatory effects – particularly from the consumption of the omega-6 fatty acid “arachidonic acid”. EPA is also a precursor for prostaglandin-3, thromboxane-3, and leukotriene-5.

Docosahexaenoic Acid (DHA)

DHA is 22 carbon polyunsaturated fatty acid that is dietarily obtained from fish, fish oils, or mircoalgae. DHA is also directly synthesized from EPA within the body. In the body, DHA is the major fatty acid component in sperm, brain phospholipids, and the retina.


The Omega-3 Debate
Currently, there seems to be a debate on whether ALA alone is sufficient enough to produce the required amount of EPA and DHA in the body. This is particularly of interest in the veg*n community where no animal sources of EPA or DHA are consumed. I remember concluding from the research I did back in the summer of ’08 that the body has an inefficient conversion rate of ALA to EPA and an even less efficient rate of DHA conversion from EHA – implying some sort of supplementation would be optimal for veg*ns. However, I want to re-verify that conclusion by digging deeper because my dietary goals and motivations were different then – I want to make sure I wasn’t biased or misunderstanding something.

Currently my diet containes a nice amount of omega-3, mostly in the form of ALA. However, I have been buying flax oil enhanced with a vegan source of DHA. My shrimp and salmon consumption has also been declining, and unless I can find sufficient reasoning to continue with these foods, I will likely progress to a majority vegan (mostly raw too) diet. I won’t be fundie about it or anything, but that would become the best way to describe my eating practice.

**Tangent**
On the topic of eating meat or not eating meat, or even a generic form of that argument – just substitute meat for some other food. The reasons I eat, or do not eat, certain foods are decided through a pro/con type rationalization with my choices. Not only do I just consider the pro’s and con’s, but I also consider if the pro’s of a food can be obtained via a different, less harmful route. My carnosine supplementation and meat reduction is a great example of this thought process.

The omega-3 debate also fits into this category. Speaking hypothetically, if DHA really is a necessary supplement, then one could simply supplement with EPA/DHA instead of eating fish or taking fish oil.

Another side rant: I have noticed a sub-group of people in the “health” community that think taking any sort of “pill” is just unnatural and a sign you are doing something wrong in your diet. These also tend to be the people that do not monitor nutrition and “let their body” tell them what to eat every day. I’m sorry, but until you get off your health food throne and actually do some research and *real* diet tracking, I don’t want to be preached to. Some people take this “natural”, “back to the earth” mentality a little too far, and there are plenty of “guru’s” leading the way (and they are conveniently profiting too). Now, I’m not saying all supplementation is good, I am just griping about a particular black and white mindset I have observed recently.
****

PUFAs and Peroxidation

Back to the omega-3 topic. In the context of CR, analyzing the omega-3 issue is of importance because of the anti-aging implications. This concern was brought to my attention via two different post, one from the Inhuman Experiment blog I follow, and the other from an older post in the CR Society Archives. After seeing this twice in a week, I realized it was time to do some reading.

Remember, omega-3s are PUFAs (poly unsaturated fatty acids), and being a lipid they can undergo lipid peroxidation when exposed to heat or air (some lipids are more fragile than others). Also, just as with AGEs, lipid peroxidation can occur internally just as glycation can endogenously occur. Glycoxidation products can also be formed during lipid peroxidation. Below is an interesting excerpt from the paper I just linked:

Obviously, in the effort to construct a low AGE (exogenous and endogenous) diet, lipid peroxidation must be carefully considered. This is a major factor in my reasoning to eat my fats raw. I now avoid roasted nuts and seeds, and avoid cooking with oil when I do cook. However, just as we observed with AGEs, endogenous reactions must also be considered. Fructose seems to be a major culprit in endogenous AGE production, but what about endogenous ALE (advanced lipoxidation end-products) production?

So, now the question becomes: Which fats are the ones most likely to produce endogenous ALEs? According to the paper “Modifications of proteins by polyunsaturated fatty acid peroxidation products“,

This basically states that saturated fats and mono-unsaturated fats were not observed to form ALEs, and PUFAs were the major culprit behind formation of advanced lipoxidation products. It was also observed that more ALEs were formed as the number of double bonds in the PUFA increased. Now, take a look at the structures of ALA, EPA, and DHA above. Notice that ALA has 3 double bonds, EPA has 5 double bonds, and DHA has 6 double bonds. Therefore, from a peroxidation perspective, EPA and DHA theoretically have a greater potential to cause oxidative stress —> think age related damage. O.o

Now I see the omega-3 issue from a completely different perspective. I’m not sure if being so selective would benefit the al lib population, but from a CR perspective, this is definitely worth considering.

I am now forced to probe the situation further: What is the “safe” ingestion limit with these omega-3s before they cause more harm than good? I suspect this is not known. However, it would still seem that some ingestion of these my have benefits if our bodies cannot efficiently convert the ALA, but maybe I am not giving enough credit to our bodies. In healthy bodies, this conversion rate may be ideal. The problem may arise only in unhealthy individuals.

Now that I have presented the dilemma, I am quite aware of the need for further research. I intend on exploring the topic of EPA/DHA conversion in the body as well as lipid peroxidation in other PUFAs, so expect further lipid posts in the near future.