June Challenge - Omega 3

[Mitra]

There were some headlines recently reporting that a new study showed there was no benefit from taking fish oil.

Looking at 3,114 men with stable angina in 2003 it found that those given high amounts of oily fish were at a higher risk of heart attack and recorded an increased number of cardiac deaths.

The authors could not say why the results of this trial differed from other large studies in the field.

They therefore concluded that it was not clear whether omega-3 fatty acids reduced or increased total mortality, cardiovascular events, cancer and strokes.

http://news.bbc.co.uk/1/hi/health/4838086.stm

I decided this would be a good candidate for me to practise reviewing a scientific paper. First I'll give a bit of background info (which I've taken from The Skinny on Fats (http://www.westonaprice.org/knowyourfats/skinny.html), by Mary Enig, and the Fat of the Land chapter of PPLP.

Why Would You Take Fish Oil?

Fatty acids consist of chains of carbon atoms, with hydrogen atoms attached. If all the available slots are filled with hydrogen atoms, it's called saturated. If there is one empty slot, it's called mono-unsaturated, and if there are more, it's called polyunsaturated.

The length of the carbon chain can vary (you'll come across references to short, medium or long-chain fatty acids), and if there are missing hydrogen atoms (referred to as "unsaturations," or "double bonds") they can occur in different positions along the length of the chain. In older books, and popular works, you'll hear about "omega-3" (or 6, or 9). In more modern technical writing, they're usually called n-3 (or 6, or 9). "Omega" and "n" mean the same thing - that the first unsaturated position is 3 carbon atoms (or 6, or 9) from the end.

http://www.danam.co.uk/Images/Polyunsaturate.gif

The technical description of the fatty acid molecule shown above would be "18:2 n-6 c,c" which means that the chain is 18 carbon atoms long, there are 2 unsaturations, the first one happening at the sixth carbon atom, and both unsaturations are in the cis configuration. This particular molecule is also known as linoleic acid. There's a handy chart of all the fatty acid descriptions, together with the names that are used for them at http://www.nutritiondata.com/fatty-acids.html

Your body can make saturated fats from dietary carbohydrates, and they are also found in animal fats and tropical fats (coconut, palm). Your body can make mono-unsaturated fats from saturated fats, but some kinds of polyunsaturated fats cannot be made, and have to be obtained from food. These are the omega-3 and omega-6 "essential fatty acids."

The fats we actually need are the omega-6 arachidonic acid, and the omega-3 eicosapentanoic (EPA - 20:5 n-3) and docosahexanoic (DHA - 22:6 n-3) acids. It is possible to eat other fatty acids that are close enough that your body can convert them into these essential forms (linoleic acid for omega-6, and the alpha-linolenic acid found in flax oil for omega-3), but in some people the conversion process is inefficient, so taking the essential fatty acids themselves is more reliable.

http://www.westonaprice.org/images/challenge.gif

The diagram above shows the conversion stages, and how the fats are involved in the production of eicosonoids that regulate many bodily functions, the different enzymes involved, and sources of the various fats (there's more on this in PPLP, and Tripping Lightly Down the Prostaglandin Pathways).

Modern diets aren't usually short of omega-6s (seeds, grains, vegetable oils), but can be deficient in omega-3s. The essential forms EPA and DHA are found in oily fish, and that's why it's recommended as a supplement for those who don't eat lots of oily fish.

I couldn't find anything in PPLP about how much fish oil to take. In Know Your Fats, Mary Enig quotes a study (Connor & Connor, 1997) recommending that those who do not eat fish take 2-3g fish oil per day for maintaining health, and more if you have heart disease. I could only find an abstract online (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9322583&query_hl=1&itool=pubmed_DocSum), and there were no numbers in it.

Now I'll go and look at this study that's been in the news (http://bmj.bmjjournals.com/cgi/content/full/332/7544/752).

[mcsblues]

Now I'll go and look at this study that's been in the news (http://bmj.bmjjournals.com/cgi/content/full/332/7544/752).

You realise AC has already done that right? ;)

http://www.theomnivore.com/Straight%20out%20of%20my%20inbox%2012.html

[Mitra]

Yes, thank you Malcolm, but I'm trying to follow his advice to think for myself ;). (It probably won't last, I'm rapidly finding that letting someone else do it is much easier!)

[mcsblues]

Yes, I just go with the flow ... I must admit those 'healthy complex' carbs are looking more appealing by the minute!:p

[Shadow]

It is possible to eat other fatty acids that are close enough that your body can convert them into these essential forms (linoleic acid for omega-6, and the alpha-linolenic acid found in flax oil for omega-3), but in some people the conversion process is inefficient, so taking the essential fatty acids themselves is more reliable.
Mitra - I'd be highly interested if, in your research, you come across an answer I've pondered since reading PPLP. The question is: how do you know if you have an efficient conversion process or not? I use flax (I personally love the taste and its thickening capability) but I have no idea if my body processes it like it should. And since you're researching this topic, it's far easier for me to ask you than to look for an answer myself :lol:!

[Mitra]

Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review (http://bmj.bmjjournals.com/cgi/content/full/332/7544/752)
Lee Hooper, lecturer, Rachel L Thompson, senior research fellow, Roger A Harrison, senior research fellow, Carolyn D Summerbell, professor, Andy R Ness, senior lecturer, Helen J Moore, research fellow, Helen V Worthington, professor, Paul N Durrington, professor, Julian P T Higgins, statistician, Nigel E Capps, consultant chemical pathologist, Rudolph A Riemersma, professor, Shah B J Ebrahim, professor, George Davey Smith, professor

The first thing to comment on is that this was not a report of a trial, but a "meta-analysis," a study of previous trials. The first task in such an analysis is to pick which trials to include.

We excluded trials if they were not randomised; they had no omega 3 arm; the participants were children or were critically ill; the duration was < 6 months; the intervention was multifactorial; or data on death, cardiovascular disease, or cancer were not available. We rejected cohort studies if they did not assess the intake of omega 3, follow-up was < 6 months, or the association between the intake of omega 3 and health was not investigated.

From 15,159 papers screened, they ended up with 48 randomised controlled trials, and 41 analyses of 26 cohort studies. Most of the trials involved involved oil supplements, but a few used dietary advice (to eat more fish), or both.

They analysed the trials for various effects - mortality, cardiovascular events, strokes, cancer and presented the results on charts. The cardiovascular one is here (http://bmj.bmjjournals.com/content/vol332/issue7544/images/large/hool301135.f3.jpeg). They show more clearly in the pdf download of the report. But it's worth looking at them. On the one I've linked, the top grouping is results for randomised controlled trials (RCT). The square shows the average result, and the line is the uncertainty. Points to the left of centre indicate a benefit from taking omega-3, and those to the right indicate a benefit to not taking it. The final combined result comes out ever so slightly in favour of omega-3, but with enough uncertainty that it could go slightly to the other side of the line. The next group down the page repeated the analysis without trials that the authors judged to be potentially biassed in some way. The answer shifted slightly against omega-3.

Looking at the individual studies, you can see that most of the results have very wide lines, indicating a high degree of uncertainty (generally indicates smaller numbers of people in the trials). The ones that stand out as having particularly short lines (the larger studies) are Burr (DART) 1989, GISSI-P 1999 and Burr 2003. It's notable that many of the comments on this study focussed on the selection of Burr 2003 (otherwise known as DART 2), which is a big enough trial to have a major impact on the results, and seems to have some major problems in its design.

The text of the study says that they also looked at whether the type of omega-3 supplement used had any effect on the outcome, but that it didn't significantly change things.

The major thing that I learned just from reading this paper (and from the reading I did on grains) is just how uncertain the science behind nutritional recommendations actually is! It's nice to read somebody confidently telling you to take this supplement and eat that food - but much of the science is murky and open to variable readings.

If I really wanted to dig into this subject I'd have to get and read each of the papers that went into the analysis - but especially the big ones, so I'd start with the three mentioned above. I did try to read the DART 2 report, since that seemed to be a major fly in the ointment, but only the abstract (http://www.nature.com/ejcn/journal/v57/n2/abs/1601539a.html) was available for free.

I read through the comments on the BMJ web-site (http://bmj.bmjjournals.com/cgi/eletters/332/7544/752) which largely dealt with the selection of trials to be included - whether some included were invalid, whether the differences were such that it was meaningless to combine them, how the analysis was carried out, whether the effects on genetically different populations were confounding the results; also a few people seemed to have personal hobby horses.

I was interested to see the authors' response:
We did not report that ‘long chain omega-3 does not offer any protection from heart disease’, that ‘omega-3 fats have no effect on total mortality, combined cardiovascular events, or cancer’ or that omega 3 fats are of ‘no benefit’ - this is not what we found, or what we reported (despite our being misquoted in much of the press).

The overall result from the meta-analysis was a relative risk suggesting benefit of omega 3 intake on mortality, but a confidence interval including unity (total mortality RR 0.87, 95% CI 0.73 to 1.03 with significant heterogeneity) so that we are not quite so sure. This raises the possibility that the protective effect of omega 3s may have been overestimated OR the heterogeneity may imply that omega 3s may be helpful in some people and less so (or even harmful) in others (perhaps men with angina or people with higher omega 6 intakes?). If the first is the case, this is not a big issue, and general advice on therapeutic doses of omega 3 fats should probably not alter. If the second is the case then we owe it to our patients to watch the unfolding evidence very carefully so we can react fast and alter our advice for specific groups if it proves necessary.

Clearly they didn't feel the media portrayal had done justice to their study, but you can see that "erm, well, we're not totally sure," doesn't make for great headlines :rolleyes: .

Malcolm's already pointed out that Anthony Colpo reviewed this paper (http://www.theomnivore.com/Straight%20out%20of%20my%20inbox%2012.html) before I got to it - he also clearly has much more knowledge of the individual studies involved than I do.

His view is that he'd only consider the randomised trials, not the cohort studies, and only the large ones, and not the one run by the Indian researcher who was recently found fiddling his data, and not the ones using much higher doses than he considers reasonable (not sure where his view of reasonable comes from, maybe it's mentioned in some corner of his site, but not on this page - pr maybe it'll be in the book ;)). That comes down to the three trials I mentioned: DART, GISSI-P and DART 2. He points out several problems with the DART 2 design (using more information than my level of trawling uncovered) and therefore sticks with the outcome from the other 2 in favour of fish oil.

Hooper et al (the authors of the report under review) replied to the letters to the BMJ with a defence of their inclusion of Burr 2003 (DART 2), and their view that it wasn't any worse than the other two studies, neither of which was perfect.

They summarised their view of how the results should be interpreted:

Like many of you, we had anticipated that our review would provide a simple comprehensive conclusion that omega-3’s are protective against cardiovascular disease. In fact this is not the case. Surely, however, it is more important to have a balanced and objective analysis of existing evidence so that we can be certain about what we do not know and be clear about what future trials should be designed to answer?

Our review has not questioned UK healthy eating advice suggesting that the public eat two portions of fish per week, one of which should be oily. This seems very sensible given the essentiality of omega 3 fats and evidence of wide ranging benefits of fish. It also suggests that low dose fish oil supplements in those not eating oily fish (the sorts of doses taken to help with arthritic symptoms for example) would cause no harm.

However we are less sure about the higher, therapeutic, doses of omega 3 - three or more large portions of oily fish each week or 1g+ of omega 3 fats daily. The evidence here is less clear. If high doses of omega 3 are not helpful for some people, or are even harmful for some groups of people, it is important that we recognise this and make sure that only the right people get the advice to take more oily fish or fish oil supplements. We need to keep watching the evidence as it emerges and adjust our advice as appropriate, for the best health of people everywhere.

So, keep taking the fish, or the oil, but not too much, and you probably don't need both, and watch this space (but since the trials take several years, don't hold your breath!).

[Mitra]

Shadow, I didn't see an answer to your question, though Anthony Colpo's article (http://www.theomnivore.com/Straight%20out%20of%20my%20inbox%2012.html) did make reference to testing blood levels of DHA and EPA which would obviously tell you if your body was making the conversion. Otherwise, just bite the bullet and add the occasional bit of tuna or salmon to your menu if you can't face sardines.

[Mitra]

If any brave souls have made it this far, here are a few more thoughts.

Some people have commented on the risk of taking too much omega-3. Russel Smith, in The Cholesterol Conspiracy, mentions the blood-thinning effect of fish oils, and comments that high rates of consumption lead to higher rates of death from internal bleeding following injury (in Eskimos) and higer rates of strokes (Eskimos and Japanese). He points out that polyunsaturated fats are highly immunosuppressive, and therefore there is a risk of cancer, and that fish oils interfere with the absorption of vitamin E, which is, in turn, a protector of vitamins A and C. This book was published in 1991, so although the claims list extensive references, fewer of them are on-line, and I gave up trying to track them down.

In the randomised controlled trials covered by the study I looked at, overall mortality was 960 deaths out of 16701 participants taking omega-3s (5.75%)and 1035 out of 16492 in the control groups (6.28%). This is quoted as a "relative risk" of 0.87, or a 13% reduction in relative risk, but, as you can see, if you look at absolute figures, the risk difference is about 0.5%. That's the risk of dying during the trial - but without correcting it for ages of participants, and the length of the trials, and taking into account that some had previous cardiovascular diseases, it's not possible to compare it with other mortality figures, just to see the change brought about by adding omega-3s in these particular trials.

Within this slight reduction in overall mortality, cardiovascular deaths were slightly reduced compared to the controls, while cancer and stroke deaths were very slightly increased. All of these effects were so small that the confidence limits include the possibility of the opposite effect being true!

It wasn't at all clear from the report what the doses of omega-3 were in the various trials, and whether the effects were sensitive to dose.

On Shadow's question, Smith (Cholesterol Conspiracy) also says that no studies have been able to show that plant-based linolenic acid is converted to EPA and DHA in humans. Again, he gives references, but I haven't tracked them down yet - or only an abstract, that doesn't mention this claim.

[Gaelen]

Well...while I was still capable of sustained analytical thought, I *did* make it 'this far' but got hung up yesterday arguing with insurance companies. ;)

However...re: the over-intake of Omega-3s...this is something I pay a bit of attention to since, while the studies aren't conclusive that this contributes to enhanced blood thinning, stroke risk and issues with cancer, I do have enhanced risks in all of those areas. I don't buy omega-3 enhanced eggs, I stopped adding in 'extra' sources of omega-3s and I try to keep omega-6 intake low so it doesn't overwhelm the 0mega-3 consumption I take in during the course of normal eating.

And I keep my fingers crossed, wear gemstones reputed to enhance personal auras, avoid sidewalk cracks and always toss spilled salt over my shoulder...;) Sometimes, the published science just hasn't caught up with the questions and you have to make consumption decisions based on a 'best guess' until it does

Gaelen, checking in from life on the edge :p

[mcsblues]

One thing that I'd like to know is the relationship between blood thinning nutrition and medication and the potential for strokes. On the one hand people particularly the elderly are put on low dose aspirin to thin the blood to prevent strokes (and possible heart attacks) by thinning the blood to prevent clotting (ie "ischemic" strokes). Omega 3 oils do the same thing as I would imagine does improving the omega 6 : omega 3 ratio generally by the eicosanoid pathways the Eades talk about.

On the other hand though, the thinning of the blood potentially leaves you open to a higher chance of bleeding of blood vessels in the brain ... which would of course also bring on a "hemorrhagic" stroke.

I guess this comes back to fish oil dosage as well, but since aspirin therapy is so common place, presumably this quandary has been addressed elsewhere?

[Mitra]

I'm not sure, but as well as aspirin, it seems that a very high proportion of people I know who are over 60 are also taking warfarin, which would be another interaction to beware of.

This info sheet (http://healthlibrary.epnet.com/GetContent.aspx?token=7e9094f4-c284-4b3a-8f7c-867fd12b36ee&chunkiid=21684) (which I probably should have read sooner) says:

Fish oil has a mild "blood-thinning" effect, and in one case report it increased the effect of the blood-thinning medication Coumadin (warfarin). 199 Fish oil does not seem to cause bleeding problems when it is taken by itself 142 or with aspirin. 143 Nonetheless, people who are at risk of bleeding complications for any reason should probably consult a physician before taking fish oil.

[mcsblues]

Mitra - I'd be highly interested if, in your research, you come across an answer I've pondered since reading PPLP. The question is: how do you know if you have an efficient conversion process or not? I use flax (I personally love the taste and its thickening capability) but I have no idea if my body processes it like it should. And since you're researching this topic, it's far easier for me to ask you than to look for an answer myself :lol:!
I think the general answer is you don't (have an efficient conversion process) and although this may vary slightly from person to person, this was the basis of the anti flax oil comments in PP - only slightly modified in PPLP. But these papers will get you started! (what do you mean, 'you haven't specified who "you" is?' :p)

1. Gerster H. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? International Journal for Vitamin and Nutrition Research, 1998; 68 (3): 159-173.

2. Pawlosky RJ, et al. Physiological compartmental analysis of alpha-linolenic acid metabolism in adult humans. Journal of Lipid Research, 2001; 42: 1257–1265.

(btw I probably should come with a health warning myself now that I have 1400 indexed and critically assessed references at my disposal!! - the review? ... its coming! :))

[Mitra]

Looking forward to that review :). It must be a fairly technical one if you're looking at all those references, too!

Here's the abstract (http://verlag.hanshuber.com/Zeitschriften/IJVNR/98/vn9803.html#vn9803_01) to the Gerser paper, and full text of the Pawlosky paper (http://www.jlr.org/cgi/content/full/42/8/1257).

My reading list seems to be getting longer - now I'll have to read these, and probably some of the references, and also chase up some of the references on bleeding, and other possible side effects of fish oils, as well as the differences between the effects of DHA and EPA. If The Book arrives as well, I'm not sure I'll manage a new subject next week! (I've been thinking of CoQ10.)

[Gabriel Guzman]

I think the general answer is you don't (have an efficient conversion process) and although this may vary slightly from person to person, this was the basis of the anti flax oil comments in PP - only slightly modified in PPLP. But these papers will get you started! (what do you mean, 'you haven't specified who "you" is?' :p)

1. Gerster H. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? International Journal for Vitamin and Nutrition Research, 1998; 68 (3): 159-173.

2. Pawlosky RJ, et al. Physiological compartmental analysis of alpha-linolenic acid metabolism in adult humans. Journal of Lipid Research, 2001; 42: 1257–1265.

(btw I probably should come with a health warning myself now that I have 1400 indexed and critically assessed references at my disposal!! - the review? ... its coming! :))

Besides the studies done in healthy humans, there is also evidence from animal studies that link delta-6 and delta-5 desaturase modulation by hormons. R. Brenner Prostaglandins, Leukotrienes and Essential Fatty Acids[/I] [B]68 (2003) 151–162] discussed the relationship between insulin and proper function of the desaturase system. Those studies show that the desaturase system is depressed during experimental diabetes and are restored upon insulin treatment. When we think of diabetes also as part of the insulin resistant syndrome, then it comes to mind what we read in PPLP about people that are already insulin resistant not having a well oiled desaturation system.

If we connect what is known about the efficiency of the desaturase system in healthy humans and the already depressed system in insulin resistant individuals, then is easy to think that under insulin resistant conditions, not even the low efficiency of the desaturase system may be achieved. Thus the importance of providing the body with pre-manufactured EPA and DHA instead of precursors that may or not be efficiently transformed. Also, another inference would be that reverting insulin resistance restores the capacity of the desaturation system to work properly, even if the process per se is not 100% by nature.

[Missy]

Holy COW this is way far over my head....:suspicious: :eek: but, I just need to ask a question, not knowing if it's relating to this subject or not?? Forgive me if it's not. :o

My compounding pharmacist is added DHEA to my treatment...along with my progesterone, pregnenolone, naltrexone cream. Is this related to this subject that you all are talking about??

I take fish oil(10 caplets a day), and within the last month added CoQ10 too along with vitamin E. I'm fairly certain I'm on the right track with all that...but? I'm always curious to learn more. Once again, I like to know WHY I'm doing what I'm doing sometimes to help keep me motovated and confident in what I'm doing, if that makes any sense?

I think my system is depressed certainly, and am looking for ways to boost it...and I think DHEA is the missing link?? ...but, as I admit, I'm quite clueless.

[Mitra]

DHEA (dehydroepiandrosterone - and no, I didn't just happen to know that name, but I did just happen to have a book with it in just next to me ;) ) is a hormone produced by the adrenal glands. It's a precursor to other hormones such as estrogen and testosterone.

DHA (docosahexanoic acid) is an omega-3 essential fatty acid found in fish oils (also egg yolk and organ meats).

So DHEA isn't what we've been talking about in this thread, but it makes sense that your pharmacist has given it to you in trying to help your hormones back into balance.

10 caplets of fish oil sounds quite a lot. Did s/he suggest you needed so many?

[Missy]

Thanks Mitra for helping me understand better. :o I think you should have just let me be IMPRESSED with you in knowing it! LOL

To be honest with you, I'm not entirely SURE of how I ended up on so many...other then comparing with another friend of mine who's taking it too.... AND the owner of the health food store that seems quite knowledgable suggested it. (Granted she SELLS the stuff!:eek: ) I will contact my Dr. and/or run it past my compounding pharmacist when I pick up my latest additional prescriptions and see what he says. I'll make a list of all of my supplimentations and get thier approval.

I do know that at one time my personal Dr wanted to make sure I was taking some fish oil...I just don't think I recall discussing with him "how much". That was before I upped it to ten a day.

[Shadow]

(btw I probably should come with a health warning myself now that I have 1400 indexed and critically assessed references at my disposal!! - the review? ... its coming! :))
Malcom - Thanks for the references but all the more I'm inclined to read scientific studies, I must say you'll most likely get your review done before I get the papers read :o. Especially if I read them over and over enough times to understand them :lol:! (Seriously, I will get to them if things ever slow down here and I can actually concentrate on trying to understand them.)

[Shadow]

When we think of diabetes also as part of the insulin resistant syndrome, then it comes to mind what we read in PPLP about people that are already insulin resistant not having a well oiled desaturation system.
Gabe - Forgive me if I'm about to ask a stupid question :o, but are you still insulin resistant even if you've followed this WOE several years? I mean, do you ever get over insulin resistance or if you've fallen prey to it, are you that way for life?

If we connect what is known about the efficiency of the desaturase system in healthy humans and the already depressed system in insulin resistant individuals,
Uh, I can't connect something I don't know or understand :lol:! Sorry, couldn't resist :p...

Thus the importance of providing the body with pre-manufactured EPA and DHA instead of precursors that may or not be efficiently transformed.
So, am I going to cause more harm than good (or vice versa) if I start using fish oil but continue eating flax meal?

Also, another inference would be that reverting insulin resistance restores the capacity of the desaturation system to work properly, even if the process per se is not 100% by nature.
Okay - now I'm back to my first question :lol:...

Sorry - I do try to read and understand the research and science but... give me office equipment any day - it's much easier to understand and deal with ;).

[Missy]

Shadow, honey, lol ...I just wanted to add that I PERFECTLY UNDERSTOOD YOU!!!! :D lol

My question is what is a "desaturase system"? :rolleyes: :jawDrop: poor Gabe....poor poor guy....:o

[LisaS]

desaturase is the class of enzyme that changes one kind of fatty acid into another by desaturating it (removing a H+/causing a C=C to form).

Remember, saturated fats have 2H per C, no C=C double bonds (every carbon is saturated with hydrogens). Monounsaturated fats have 1 instance of a C=C double bond. Polyunsaturated fatty acids (PUFA) have more than one (poly) C=C double bond. EPA and DHA are types of PUFAs

Now, look at the flowchart Mitra posted originally - near the top you'll see steps where D5D is referenced and where D6D is referenced.

If those enzymes are not working up to snuff the product won't get made and the chain of events will stop. If they work, but not very well - you'll only get a little product to continue down the chain.

[Missy]

How do you get them to work better??

Can you suppliment with enzymes to improve it???

Is this TOO something that can be IMPROVED or once your not doing it is it gone forever???

[Mitra]

The studies Malcolm referred to seem to suggest it's "normal" for the conversion to be very inefficient:

Gerster: "... with a background diet high in saturated fat conversion to long-chain metabolites is ~6% for EPA and 3.8% for DHA. With a diet rich in n-6 PUFA, conversion is reduced by 40 to 50%."

Pawlosky: "Only about 0.2% of the plasma 18:3n-3 [that's the one in flax] was destined for synthesis of 20:5n-3 [EPA], approximately 63% of the plasma 20:5n-3 was accessible for production of 22:5n-3, and 37% of 22:5n-3 was available for synthesis of 22:6n-3 [DHA].

The inefficiency of the conversion of 18:3n-3 to 20:5n-3 indicates that the biosynthesis of long-chain n-3 PUFA from {alpha}-linolenic acid is limited in healthy individuals. In contrast, the much greater rate of transfer of mass from the plasma 20:5n-3 compartment to 22:5n-3 suggests that dietary eicosapentaenoic acid may be well utilized in the biosynthesis of 22:6n-3 in humans."

So, Missy, I don't know if the mechanism can be improved, but it seems to be pretty inefficient in any case.

Shadow, I don't have my books in front of me, but I think the text around the "dance with him that brung you" quote in Staying Power was suggesting that if you've been insulin resistant you'll always retain the tendency, though I think some of the graphs in Life Without Bread suggest improvement - I'll look later to see the timescales, and how many people improved.

[mcsblues]

Not quite sure where to put this, but it does claim some ... erm ... very special benefits to low carbing and omega 3 supplementation in particular ...

(btw - probably should come with a possible TMI warning for some readers!)

I'll have what she's having
June 22, 2006

http://www.smh.com.au/news/womenshealth/ill-have-what-shes-having/2006/06/21/1150845239029.html?page=fullpage#contentSwap2

Women are at the forefront of new research into the female orgasm, writes Samantha Selinger-Morris.

When Marrena Lindberg stumbled upon a sure-fire way to reach orgasm four years ago, she had no idea she was part of a new wave of women revolutionising the face of sexual health research.

Rather, her fortuitous discovery - that the high doses of fish oil she took in preparation for pregnancy and the kegel exercises she practised afterwards to restore lost vaginal muscle strength led her to easily achieve vaginal orgasm - was simply an unexpected boon.

"I noticed that something was different," Lindberg says over the phone from her Boston home.

That's an understatement. When the computer programmer had fine-tuned her recipe (see breakout), she claimed a whopping personal best of 52 vaginal orgasms in one session.

"It gives a certain confidence to a woman," she says. "Now when I walk around, I get noticed."

And how. She has wrangled a publishing deal with a branch of Random House to release her book in the United States next year and been profiled by American Elle and London's Telegraph Magazine. Meanwhile, she has joined the growing ranks of women spearheading a new era of orgasm research that is characterised by astonishingly diverse approaches.

Gone are the days of Alfred Kinsey and Desmond Morris and their focus on the sociological and biological impacts of female orgasm. In their place are researchers who look at the psychological, physiological, anatomical and, yes, dietary factors behind what causes orgasm.

Last year, Helen O'Connell, a urological surgeon at Melbourne Private Hospital, became the first person to accurately map the clitoris.

University of New England physiologist Dr Gemma O'Brien - hailed by Wired magazine as "perhaps the only orgasm theorist in the world" - is working on a hypothesis that understimulation of a girl's reproductive tract during puberty could account for her difficulty, or inability, to achieve orgasm later.

Overseas, Dr Elisabeth Lloyd, a biology professor at Indiana University, rocked the talk-show circuit with her 2005 book The Case of the Female Orgasm, which rejects the theory that a woman's orgasm exists to facilitate reproduction. (Nonsense, she says, it's all about fun.)

Vivienne Cass, a Perth clinical psychologist and author of The Elusive Orgasm, says it's no surprise that women are generating headlines with their findings, rather than men.

"A few years ago, I was at a conference and these male researchers are standing up and talking about how they have been investigating sexual arousal in women," Cass says.

"They had been putting various sorts of probes into women's vaginas, measuring blood flow and lubrication, but they got confused. Because when they spoke to the women, who said, 'Oh, I'm not actually turned on', these researchers were saying, 'Well, yes you are'.

"The women sexologists in the audience were going, 'They just don't get it, do they?' What researchers now understand is that you can have a physical arousal and you can have psychological arousal and, in women, they are two quite different processes."

This is why the so-called Pink Viagra, marketed by pharmaceutical giant Pfizer after the male version was so successful, was pulled a few years ago after it was discovered that simply increasing blood flow to the clitoral region gave little or no relief to the majority of women with female sexual dysfunction.

There are new drugs in the pipeline, of course - a recent Reuters Business Insight report estimated that the market to treat so-called female sexual dysfunction could approach $1 billion by 2008.

Proctor and Gamble is developing a testosterone patch in the hopes that increasing women's libido will do the trick. Palatin Technologies in New Jersey is working on a new class of drugs, called melanocortin agonists, to target a woman's central nervous system and spark both genital arousal and sexual desire.

O'Brien and Cass, among other experts, think these approaches are misguided.

"Drug companies put a lot of money into trying to develop [the drugs but they] would be better off finding out how orgasm works and then develop drugs," says O'Brien, who believes there's no reason that women shouldn't be as sexually satisfied as men.

Cass is wary of the increasing medicalisation of women's sexuality - supported by a controversial and often-quoted 1999 study by The Journal of the American Medical Association that estimated 43 per cent of women suffered from sexual dysfunction. She says the renewed focus reflects a positive shift towards taking female sexual pleasure seriously, but fails to acknowledge that "the psychological aspect of a woman's life can very quickly override sexuality".

Her book details 25 causes of orgasm difficulty, with only a few linked to medical conditions (such as diabetes, multiple sclerosis and depression). The rest, she says, can be chalked up to a woman's mental state - from resentment or loss of physical attraction towards a partner to sexual abuse, boredom and even dysfunctional fantasies.

Contrary to the popularly held belief that it's women's lack of interest in sex that leads them to be, well, undersexed, Cass has found that there are certain fantasies that can inhibit orgasm.

"I had a woman who used to fantasise about almost being raped, and she could actually orgasm through masturbation quite happily with that fantasy," she says.

"But then when she met a nice man in real life that she actually wanted to be with, all of a sudden, the sex thing didn't happen for her. She had psychologically conditioned herself to only get aroused to one kind of sex."

(Cass trained her patient to swap this fantasy for another.)

The discrepancy between male and female ability to orgasm is well established. Doing it Down Under, a 2004 study of Australian sexuality, found that 29 per cent of women, compared with 6 per cent of men, had trouble reaching orgasm.

Unlike the medical companies, which are still shooting in the dark for a "cure", specialists such as O'Connell and Cass are making major headway into improving the sex lives of women.

O'Connell's new map of the clitoris and the nerves that supply it - she found the organ comprises not just the external "head", but also a larger structure that wraps around the vagina and urethra - will save women from having crucial genital nerve endings cut unnecessarily during surgery.

Her study has also shed new light on the "vaginal versus clitoral orgasm" debate.

"I think if you're trying to separate the two of them it's probably, you know, like barking up the wrong tree; I think they're clearly one and the same structure," she told the ABC.

She also thinks the elusive G-spot is the erectile tissue on the outside of the urethra.

Assuming O'Brien's research supports her theory - that lack of stimulation of the reproductive tract during puberty could lead to the "trimming" of unused nerve connections in the brain and inhibit the ability to climax later on - a little sex education could be all it takes to prevent women from being dissatisfied.

"Society is more successful at discouraging girls, rather than boys [from using their reproductive tracts around puberty], and when we get to adulthood, who is it that has the greater proportion of sexual problems? It's the girls.

"[So] it will be up to sex educators to come up with some really clever ways that society will accept to teach our teenagers how to have a healthy sex life during adolescence. Because if we can prevent orgasm problems in adults, it's better than being able to cure them."

Regardless of where research takes the debate, there can be no doubt that the tide of sexual research has shifted from the early days, when men's needs were the primary agenda.

"There's been more focus on men [in the past], because of the HIV epidemic and male-to-male communication [of the disease]," says Dr Chris Rissel, associate professor in public health at the University of Sydney, and the co-author of Doing It Down Under.

"[Now] we're looking for a sexually healthy society where men and women equally enjoy sex and know what to do to please their partners."

His intention, he says, is for his team to repeat the study in 10 years, to see whether the goal has been reached.

Until that time, it's likely that women from all walks of life - both sex experts and members of the public - will fight to ensure that the current agenda sticks.

Cass says: "What we've got coming up is a generation of women who are used to having orgasms, used to having some reasonably decent sex, unlike previous generations.

"So the trend here is a bunch of women saying, 'I don't like this', and they'll actually come to me and be absolutely furious and frustrated, [saying] 'I'm not going to put up with this'."

Better than chocolate?
So, does Marrena Lindberg's so-called orgasm diet really work?

There's no doubt that the diet itself is simple.

The first step is to "improve libido" by adopting a high-protein, low-carb diet "full of good fats", consuming a combination of high-dose fish oil ("an extremely unusual amount"), calcium, magnesium, zinc and 15 grams of dark chocolate every day and avoiding stimulants such as caffeine. (Lindberg refuses to give exact amounts of her ingredients for fear of jeopardising a book deal.)

The second step is to do regular kegel exercises to develop PC (pubococcygeus) muscle strength.

"I used myself as a guinea pig," Lindberg says of the diet, She says it has helped her go from having great difficulty reaching orgasm to achieving 27 consecutive clitoral orgasms with use of a vibrator.

But aside from a handful of women who have tried the diet after finding it on Lindberg's web-based forum, no scientific study has been conducted. (She is currently lobbying fish oil companies to fund a study in conjunction with a scientist at Columbia University).

Local experts are sceptical about its effectiveness.

University of New England physiologist and sex researcher Dr Gemma O'Brien says: "Since we don't know how [orgasm] works, it's difficult to see how we would know which nutrients would help."

Sydney dietitian Susie Burrell agrees: "There is no scientific evidence that links any particular food to orgasm."

She adds that achieving orgasm "is a lot about how psychologically comfortable [women] are ... It is probably just a feel-good diet just being sold on orgasm to get everyone's attention."

Burrell concedes, though, that, with dark chocolate increasing circulation of the feel-good hormone serotonin in the body and fish oil providing anti-inflammatory benefits, women are more likely to feel better in general, which could lead them to become more likely to achieve orgasm.

Caffeine also dehydrates the body, which can wreak havoc with a woman's lubrication.

Vivienne Cass, a clinical psychologist, sex therapist and author of The Elusive Orgasm, doesn't doubt that the diet has improved Lindberg's sex life, but says this would likely be due to a placebo effect.

"When we give women a placebo in a sexual trial, we know this will improve [their] sex lives by 40 per cent. [Because] if you get women to focus on their sexuality in any sense of the word, they will actually become more aroused," she says.

Marrena Lindberg's forum:
http://zaneblue.org/groupee

[banshee]

Heehee. It's fun to see a posting like this among all the super-intellectual scientific stuff. :D