Omega-3
But what about n-6 fatty acids? The abstract tells us that n-6 PUFAs stimulate angiogenesis. Does that make n-6 one of the bad guys? That’s what I thought, at first. But no, we need both these fatty acids in order to be healthy, so eliminating n-6s from our diet would be a very VERY bad move.
What we lack is BALANCE between the two omegas. Read this: In terms of the consequences for human health, it has been shown that Japanese who migrated to the United States and acquired the local dietary habits leading to an increase in the dietary n-6/n-3 PUFA ratio of 16:1 resulted in health problems in the migrants similar to those that already existed in the local population. Sixteen to one! That’s astounding. Even more astounding: the ideal balance should be 1:1, at the most 4:1. But the average North American diet, and probably European by now, ranges from 11:1 to 30:1. Yikes!
According to Andrew Weil, M.D., This dietary imbalance may explain the rise of such diseases as asthma, coronary heart disease, many forms of cancer, autoimmunity and neurodegenerative diseases, all of which are believed to stem from inflammation in the body. The imbalance between omega-3 and omega-6 fatty acids may also contribute to obesity, depression, dyslexia, hyperactivity and even a tendency toward violence.(see: http://tinyurl.com/4s32fc; see also: http://tinyurl.com/565h8n).
Now, what happens when we ingest n-3s and n-6s? They get converted by so-called PUFA bioconversion enzymes. Otherwise, these fatty acids would not be of any use to us at all. The researchers state that their findings suggest that n-6 and n-3 PUFAs compete for enzymes involved in PUFA biotransformation. It is widely believed that PUFA bioconversion enzymes have a greater affinity for n-3 PUFAs so that their biotransformation is favored when the dietary n-3 PUFA intake is high. This simply means that the two omegas compete for the attention of these bioconversion enzymes, and n-3s happen to be the winners.
At any rate, our bodies are not able to produce these fatty acids from scratch, and in fact that is why they are called “essential” (essential for health, but cannot be made inside the body), so we need to get them from our food.
Dietary sources of n-3s: mainly cold water fish such as salmon, herring, anchovies, but be careful about the potential presence of heavy metals, PCBs and dioxin (!); also, but to a lesser degree, flax, pumpkin seeds, walnuts, pecans, butternuts, nut oils, as well as the seeds of: chia sage, kiwi, lingonberry, black raspberry. For more info: http://en.wikipedia.org/wiki/Omega_3. By the way, today I learned that mercury does not get stored in fish oil (only in the tissue). How about that? I also learned that some manufacturers are able to purify fish oil via molecular distillation, which increases the cost, but who wants to be swallowing dioxin or pesticides, after all? I would rather pay more for a high quality product. So, do your research, watch what you buy, and don’t go for el cheapo.
Dietary sources of n-6s: poultry, eggs, cereals, whole-grain breads, baked goods, most plant-based cooking oils (sunflower, corn etc.), nuts, borage oil. See also: http://en.wikipedia.org/wiki/Omega_6
The experts still do not completely understand why fish oil is so effective against inflammation: increased levels of omega-3 fatty acids are associated with lower asthma prevalence in people, but the mechanisms to support that observation are poorly understood.
But the main thing is: omega-3 fatty oils are effective against asthma.
One thing led to another, and I found myself involved in a bit of research that I hadn’t intended to do (happens a lot to me…
). Completely by chance, in fact, I came upon a study by a team of Japanese researchers on the same topic–asthma, mice and RvE1–a study published in March 2008 (see: http://tinyurl.com/6xaddo), that is, a few months before the publication of the study reported in Science Daily. The Japanese researchers discovered the exact same thing about RvE1.
So, just for the heck of it, I did a search on PubMed for RvE1 and asthma, and found another study (full version available for free here: http://tinyurl.com/5d64sa) published back in 2005 (!!!) on the protective anti-inflammatory effect of this molecule, and on the role it has in preventing (drum roll!) osteoclast-mediated bone destruction in periodontitis (= a severe form of gum disease).
Osteoclasts? Why, those are the hyperactive bone-destroyers in multiple myeloma…! At that point, I had a look at the full study, where I read that bone loss in periodontitis is caused by osteoclast activity. The researchers discovered that the animals (sigh) with periodontitis that were treated with RvE1 had only a few osteoclasts compared to the untreated ones. Conclusion: RvE1 inhibits osteoclasts. Well, well! (I just hope that the “animals” involved in this study were tiger mosquitoes…)
Another excerpt tells us that periodontitis has pathogenic features similar to those observed in other inflammatory diseases such as arthritis. And read this: Resolvins are a new family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammatory signals. Because it is now increasingly apparent that local inflammation plays a critical role in many diseases, including cardiovascular disease, atherosclerosis, and asthma, experiments were undertaken to evaluate the actions of the newly described EPA-derived Resolvin E1 (RvE1) in regulation of neutrophil tissue destruction and resolution of inflammation. The results were that RvE1, used as a topical pharmacologic agent, was found to prevent the progression of tissue destruction.
Treatment with RvE1 was more effective and less damaging than the chronic use of antibiotics. Interesting. The researchers propose that regulating inflammation with molecules such as RvE1 is a rational new therapeutic approach to the treatment of osteoclast-mediated bone disease. Aha!!!
It turns out that there are 32 studies in PubMed on RvE1. The earliest study dealing with the specific anti-inflammatory activity of these so-called resolvins, as far as I can tell, dates to 2004. But the above-mentioned Science Daily article led me to believe that RvE1 was a startling NEW discovery. Why would that be? Well, I have learned my lesson. From now on, whenever I see exclamations such as “exciting new discovery…,” I will do a background check. There just might be a less publicized precedent…as happened with the IRF4 studies…
Now for my own personal experience. I have suffered from asthma for years. I know the main source of my trouble: cats. I am very allergic to cats, but I am also a huge cat-lover (life is unfair, sometimes…!) and now have four cats. When Stefano and I went to Northumberland in April I didn’t have one asthma attack, not even with all the walking we did. I didn’t use my cortisone inhaler or my Ventolin. Why? No cats. Simple.
My non-cat loving friends think I’m nuts. They don’t understand that the benefits of having cats in my life far outweigh the inconvenience of having to use a cortisone inhaler once a day (I would like to mention that in the pre-curcumin period I was much worse off, and used cortisone and Ventolin quite a lot).
Recently, though, I haven’t needed to use my inhaler. As for Ventolin, well, I haven’t used it in a long time. Is it a coincidence that I have started taking a fish oil supplement in recent months? After reading about RvE1, I think the answer to that question is ”no.”
So my fish oil intake is probably inhibiting my overly eager osteoclasts…and it has gotten rid of my asthma…at least for now…brilliant!