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zonelifter 
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| 01/06/2005 3:48 PM |
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| zoneadept - Thanks for the link. I haven't had a chance to look at it in detail, but it looks to be a very valuable source of AA content data. Do you know if it uses the USDA database for its data source? Or does it use data derived from testing independant from the USDA's testing?
Scott - Thanks for your comments. For the last 2 allergy seasons (Spring and Fall 2004), I have used 2400mg EPA and 1200mg DHA (6 capsules) daily to go along with the 440mg of GLA to get complete relief from allergy symptoms. My first experience with high dose fish oil was in 2003 immediately after I read the "OmegaRx Zone." I
immediately began using 7.5 g of EPA & DHA (1 tablespoon per day of the liquid OmegaRx). During that season, my allergy symptoms were dramatically reduced (though not completely relieved). Still, I was quite happy with the results until I began to experience extreme fatigue about 6 weeks after beginning supplementation. After doing
some research (primarily the Holub papers), I suspected that low DGLA levels might be the cause, so I bought some borage oil to try. I experienced a dramatic improvement in my fatigue after my very first borage oil dose (220mg GLA). That experience was very consistent with your comments that high dose fish oil can reduce GLA production as well as with Holub's research that indicated that 4g of EPA/DHA per day dramatically reduced DGLA levels.
Consistent with your comments, I am contemplating reducing fish oil supplementation levels further. I am curious to know if I can get the same results with the reduced EPA/DHA supplementation. Perhaps I can reduce my GLA supplementation accordingly and still get the same results. The next allergy season isn't for several months, so I
have a while before I can evaluate it. I'm also keeping my eye on the advancement of blood testing for AA, EPA, DHA, & DGLA levels. Ideally, I would like to do that on a regular basis if the cost and ease of performance continue to improve. I also use the eiconsanoid status report, but experience has taught me that a good eisosanoid status
report does not necessarily give me good allergy symptom relief once the allergy season hits - so I've come to rely on my allergy symptom relief as my primary indicator of my zone & fatty acid level status.
Thanks again for your comments. I appreciate your thoughts.
Terry |
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Scott
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| 01/06/2005 5:15 PM |
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| [quote:9a91d39f76="zonadept"]SCott,
Have a look at the AA content of common food:
http://www.nutritiondata.com/foods-000064000000000000000-w5.html
If the link doesn't work, do the search yourself.[/quote:9a91d39f76]
First--thanks for the link--pretty neat setup.
Second-the amounts on that table (highest in 20:4) were in 6-block portions--so I had to prorate to one block increments.
In choosing a few of what appeared to be [i:9a91d39f76]favorable[/i:9a91d39f76] choices (chicken/turkey)--a lot of unfavorables in the list-- it looks as if it comes to between 30-40mg AA per protein block. So let's say you have two meals per day that include these foods. At 8 blocks (average male for two meals) you'd get close to 280mg.
Next you fine tune with EPA and GLA such that along with your average dietary intake of AA coupled with your protein-carb ratio and its impact on D5D, you find your self checking off more positive marks on the ESR. Or you are more exact and get an AA/EPA test. It seems to me that since the amount of EPA and GLA arrived at was in conjunction with your current dietary AA intake--dietary sources become irrelevant provided you are consistent with your average AA intake. What IS relevant is the amount of GLA it takes to begin an [i:9a91d39f76]accumulation[/i:9a91d39f76] of AA in the phospholipids. Or if you happen to take in more AA on a certain day. There also may be an inherent difference in how the body metabolizes dietary sources of AA vs. AA derived from GLA in the cellular membranes. Is the excess dietary AA taken in on a given day (since your EPA/GLA was derived along with an average AA intake) incorporated into the cellular membranes to the same extent as the desaturation of DGLA.
Ultimately, one would think that as long as DGLA rises higher relative to any increase in AA, you should be ok. |
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Scott
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| 01/06/2005 5:48 PM |
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| [quote:aae8ffddcd="zonelifter"]After doing some research (primarily the Holub papers), I suspected that low DGLA levels might be the cause, so I bought some borage oil to try. I experienced a dramatic improvement in my fatigue after my very first borage oil dose (220mg GLA). That experience was very consistent with your comments that high dose fish oil can reduce GLA production as well as with Holub's research that indicated that 4g of EPA/DHA per day dramatically reduced DGLA levels.
Consistent with your comments, I am contemplating reducing fish oil supplementation levels further. I am curious to know if I can get the same results with the reduced EPA/DHA supplementation. Perhaps I can reduce my GLA supplementation accordingly and still get the same results. [/quote:aae8ffddcd]
I am very interested in your results. Further to your experience, Holub published a paper in 2003 which looked at 4g EPA/DHA coupled with 0gGLA, 1gGLA, 2gGLA, and 4gGLA. The 4:2 group experienced a decrease in LDL. Prostaglandin E1 is known to increase the receptor binding for LDL, so it seems that a 4:2 ratio of EPA/DHA to GLA provided the greatest increase in "good" eicosanoids. EPA/DHA alone did not increase DGLA signifcantly, and 4:4 may have increased AA more so than the rise in DGLA.
Now these were women probably on a standard western diet so the relative of amounts needed would change following Zone principles (most likely less GLA given increased enzyme activity), but it does highlight the importance of finding that optimal GLA/EPA balance.
Laidlaw M, Holub BJ [i:aae8ffddcd]"Effects of supplementation with fish oil-derived n-3 fatty acids and gamma-linolenic acid on circulating plasma lipids and fatty acid profiles in women." [/i:aae8ffddcd]American Journal of Clinical Nutition 2003 Jan;77(1):37-42 |
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Scott
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| 01/07/2005 1:35 AM |
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| [quote:8e1ee2e216="zonelifter"]Still, I was quite happy with the results until I began to experience extreme fatigue about 6 weeks after beginning supplementation. After doing
some research (primarily the Holub papers), I suspected that low DGLA levels might be the cause, so I bought some borage oil to try. I experienced a dramatic improvement in my fatigue after my very first borage oil dose (220mg GLA). [/quote:8e1ee2e216]
I'm curious whether the extra GLA eliminated the fatigue due to higher DGLA, or what ultimately would be come more AA. Too many vasodilating (ie "good") eicocanoids that can occur from higher omega-3s can promote electrolyte loss and induce fatigue.
[quote:8e1ee2e216] I'm also keeping my eye on the advancement of blood testing for AA, EPA, DHA, & DGLA levels. Ideally, I would like to do that on a regular basis if the cost and ease of performance continue to improve. [/quote:8e1ee2e216]
When my wife had the AA/EPA test, I asked for a breakdown of all the fatty acids and was able to get numbers for DGLA, GLA, DHA etc. Unfortunately, I havn't see much data on an optimal serum DGLA/AA ratio |
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Dennis
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| 01/07/2005 12:46 PM |
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| [quote:4d4ae3bddd="zonelifter"]In my own experience, I have found increased GLA supplementation (up to 440mg/day) to be very beneficial. Using GLA supplementation at that level along with high dose fish oil has given me considerably better results than high dose fish oil alone. So much so, in fact, that I have been able to completely eliminate allergy symptoms for the last couple of seasons. Still, I worry about the spillover effect since Dr. Sears seems to emphasize it so much. Based on my experience, I speculate that I may have a reduced D6D activity (even when following the zone dietary principals) - which may explain the discrepancy between my experience and zone theory.[/quote:4d4ae3bddd]
Quite interesting. I had the opposite experience with my seasonal allergies and fatigue. I had been taking high dose GLA for years to no benefit. When I started the Zone diet, I started on high dose PGFO. After feeling good for a week, I would become fatigued. I found that I had to keep increasing my PGFO and decreasing dietary sources of GLA to continue to feel better. Finally with 27g of PGFO and minimal GLA, my allergy symptoms have virtually vanished and I never feel fatigued now. |
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Gent
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| 01/07/2005 1:23 PM |
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| Hi to all,
some considerations come to mind:
a) in a calorie restriction regime diet, like in the Zone, the activity of D6D increases up to 300%;
b) Horrobin et al.*) have shown that linoleic acid may be rapidly converted to arachidonic acid by a tightly linked enzyme sequence: GLA, in contrast, may be rapidly converted to DGLA but then only slowly on to arachidonic acid. However in some other studies assumption of GLA without EPA has been shown to increase AA serum levels.
c) in the Zone OmegaRX LA and AA assumption with diet is at low-moderate levels and insulin, a major D5D stimulating factor, is kept under control; adeguate amounts of EPA further inhibit D5D activity.
d) Rubin D, Laposata M. **) have shown that:
1) n-6 fatty acids markedly stimulated the elongation of EPA to 22:5 whereas n-3 fatty acids inhibited the delta 5 desaturation of DHLA to AA and the elongation of AA to 22:4; 2) n-6 fatty acids caused a specific redistribution of cellular EPA from phospholipid to triacylglycerol; 3) n-3 fatty acids reduced the mass of DHLA and AA only in phosphatidylinositol whereas n-6 fatty acids reduced the mass of EPA to a similar extent in all cellular phospholipids; and 4) n-3 fatty acids caused an identical (33%) reduction in the bradykinin-induced release of PGE1 and PGE2, whereas n-6 fatty acids stimulated PGE3 release 2.3-fold.
The Sears' anectodical evidence on the "spill-over effect" was observed in people that were taking supplements with a fairly high GLA:EPA ratio, while not following the Zone and not controlling their overall LA intake.
I believe that in a diet with the maintenance EPA+DHA level (2,5g), unless large amounts of GLA are assumed on a continuous basis with diet, it should be difficult to observe any "spill-over" effect.
*) Horrobin DF, Ells KM, Morse-Fisher N, Manku MS. The effects of evening primrose oil, safflower oil and paraffin on plasma fatty acid levels in humans: choice of an appropriate placebo for clinical studies on primrose oil.Prostaglandins Leukot Essent Fatty Acids. 1991 Apr;42(4):245-9.
**) Rubin D, Laposata M. Cellular interactions between n6 and n3
acids: a mass analysis of fatty acid elongation/desaturation, distribution
among complex lipids and conversion to eicosanoids. J Lipid Res
1992;33:1431–40. |
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zonadept
Posts:0
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| 01/07/2005 3:18 PM |
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| [quote:787eaf7e6f="Gent"]I believe that in a diet with the maintenance EPA+DHA level (2,5g), unless large amounts of GLA are assumed on a continuous basis with diet, it should be difficult to observe any "spill-over" effect.
[/quote:787eaf7e6f]
I spill-over very easily even with 2.5g of epa+dha.
Now, I think that the spill-over effect has nothing to do with the plasma AA. The reason is that we get around 400mg a day on a zone diet. Anecdotally, with 50mg a day of GLA, I spill over, but not with 450mg of AA, to make it short.
I'm sorry to say again that the 2mg of GLA twice a day in the form of a bowl of oatmeal doesn't make any sense at all.
From USDA, here's a list of food containing GLA (GLA in mg for 100g of food):
Lean beef : 13
avocado : 15
pine nuts: 52
peanuts: 38
brazilnuts: 17
turkey saussage: 13
Chicken, pork : 50 |
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Gent
Posts:0
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| 01/07/2005 4:55 PM |
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| Hi zonadept,
[quote:df01f685f5="zonadept"]
I spill-over very easily even with 2.5g of epa+dha.
Now, I think that the spill-over effect has nothing to do with the plasma AA. The reason is that we get around 400mg a day on a zone diet. Anecdotally, with 50mg a day of GLA, I spill over, but not with 450mg of AA, to make it short.
[/quote:df01f685f5]
but that's the point: are you sure you're "spilling-over" i.e. increasing AA concentration at the expense of DGLA?
Horrobin has shown in an animal model that when the activity of D6D was at its peak , supplementation with GLA didn't bring significant changes in DGLA, GLA and AA concentrations. It was only in the elderly that such supplementation did make a difference.
In my personal experience, when I've supplemented with around 50mg of GLA taking 3,6g of EPA+DHA I've noticed that the eico-signals were more in the sense of too many "goods" around. |
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Scott
Posts:0
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| 01/07/2005 5:14 PM |
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| Thanks for your insights, Gent.
[quote:6734c72ef3="zonadept"]
Now, I think that the spill-over effect has nothing to do with the plasma AA. The reason is that we get around 400mg a day on a zone diet. Anecdotally, with 50mg a day of GLA, I spill over, but not with 450mg of AA, to make it short.[/quote:6734c72ef3]
Again, there may be a difference in AA derived from the desaturation of DGLA already withing the cellular membranes, then from dietary AA.
[quote:6734c72ef3]
From USDA, here's a list of food containing GLA (GLA in mg for 100g of food):
Lean beef : 13
avocado : 15
pine nuts: 52
peanuts: 38
brazilnuts: 17
turkey saussage: 13
Chicken, pork : 50[/quote:6734c72ef3]
The composition of the fatty acids within a food can impact how GLA is incorporated. |
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zonelifter
Posts:0
Newbie
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| 01/07/2005 7:28 PM |
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| Scott wrote:
[quote:fb1a397897]
I'm curious whether the extra GLA eliminated the fatigue due to higher DGLA, or what ultimately would be come more AA. Too many vasodilating (ie "good") eicocanoids that can occur from higher omega-3s can promote electrolyte loss and induce fatigue.
[/quote:fb1a397897]
Scott,
I think you may be on to something here. At the time, I did not consider this possibilty since I didn't seem to have any other vasodilating symptoms per the eicosanoid status
report. Now, a year and 1/2 wiser/more experienced in the zone, I see the possibility. I'll need to give it some more thought now (while keeping that possibility in mind).
Thanks for the thought!
Terry |
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Gent
Posts:0
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| 01/12/2005 10:38 AM |
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| Hi Zonadept,
[quote:81f79511ca="zonadept"][quote:81f79511ca="Gent"]I believe that in a diet with the maintenance EPA+DHA level (2,5g), unless large amounts of GLA are assumed on a continuous basis with diet, it should be difficult to observe any "spill-over" effect.
[/quote:81f79511ca]
I spill-over very easily even with 2.5g of epa+dha.
Now, I think that the spill-over effect has nothing to do with the plasma AA. The reason is that we get around 400mg a day on a zone diet. Anecdotally, with 50mg a day of GLA, I spill over, but not with 450mg of AA, to make it short.
[/quote:81f79511ca]
there are ways other than “spill-over” on how GLA would affect the eicosanoid equilibrium 1-2).
It is known that the elongation of GLA to DGLA occurs more rapidly than the successive desaturation step, the more so in the presence of EPA.
Maintaining the same levels of EPA assumption and increasing those of GLA, the phospholipids concentration of DGLA might slightly increase, at the expense of EPA phospholipids concentration - given a preferential cellular retention capacity of AA. - via shifting more EPA to triacylglycerol fraction and stimulating its elongation to DPA (22:5).
The ratio AApl/AAtg : DGLApl/DGLAtg i.e. the distribution of AA between the phospholipids and triglyceride cellular fractions [i:81f79511ca]versus [/i:81f79511ca]that of DGLA remains stable at an average level of 5,39.
Moreover AA is mostly concentrated in the phosphatidylinositol (PI) fraction of the phospholipids pool, while DGLA and EPA are fairly equally distributed in all the fractions. A reduction in the EPA concentration would eventually allow a slightly greater amount of DGLA being converted on to AA, and, more importantly, allow a greater up-take of AA into phospholipids pool. Thus, as an effect of increased assumption of GLA, the respective ratios DGLA/AA and EPA/AA in the PI fraction may worsen.
Given that the PI fraction is one of the major donors of eicosanoids' precursors, the end result may be a worsening of the eicosanoid equilibrium (more bad v. good) perceived as a "spill-over" effect.
1) Rubin D, Laposata M. Cellular interactions between n 6 and n 3
acids: a mass analysis of fatty acid elongation/desaturation, distribution
among complex lipids and conversion to eicosanoids. J Lipid Res
1992;33:1431–40.
2) Rubin D, Laposata M. Regulation of agonist-induced prostaglandin E1 versus prostaglandin E2 production J. Bio. Chemistry 1991 |
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