3/16/2009 10:11pm, #81
So nobody's decided to try to cash in on my offer of an e-high-five, eh? I'm probably too impatient. Anyways, here's what I missed.
If you look at this table, the only oil listed that has more long-chain omega-6 than long-chain omega-3 is cottonseed. A naive reading of this would indicate that if, as Sears argues, we're trying to avoid having an AA:EPA ratio that's too slanted towards AA, all we have to do is avoid cottonseed oil.
This, however, is not necessarily correct. Consider my reference to ALA as a potentially-pertinent substance - it's a short-chain omega-3 that, it appears, is partially converted to our relevant long-chain omega-3s. Could it be that there are analogous short-chain omega-6 fatty acids that the body can convert to arachidonic acid?
Human adults are shown to be capable of conversion of linoleic acid (LA, 18:2 n-6) to arachidonic acid (AA, 20:4 n-6) in vivo. It is confirmed that they can also convert alpha-linolenic acid (LNA, 18:3 n-3) to eicosapentaenoic acid (EPA, 20:5 n-3) and to docosahexaenoic acid (DHA, 22:6 n-3) in vivo.
I'm going to try to get a copy of that study to look at. Sears is pessimistic about rates of conversion of ALA to EPA/DHA, perhaps overly so. Here's what I found when I looked into it myself:
Hence, there is no assurance that increasing ALA intake will increase tissue levels of EPA or DHA; in fact, some studies show that DHA remains unchanged or even decreases after ALA supplementation
Said book also makes reference to competition between LA (linoleic acid, 18:2 n-6) and ALA for conversion into AA and EPA/DHA, respectively.
The plot thickens.
Edit: And to confuse things even more, there are reports of gender-based differences.
Increasing alphaLNA intake for a period of weeks to months results in an increase in the proportion of eicosapentaenoic acid (EPA; 20:5n-3) in plasma lipids, in erythrocytes, leukocytes, platelets and in breast milk but there is no increase in docosahexaenoic acid (DHA; 22:6n-3), which may even decline in some pools at high alphaLNA intakes. Stable isotope tracer studies indicate that conversion of alphaLNA to EPA occurs but is limited in men and that further transformation to DHA is very low. The fractional conversion of alphaLNA to the longer chain n-3 PUFA is greater in women which may be due to a regulatory effect of oestrogen. A lower proportion of alphaLNA is used for beta-oxidation in women compared with men.
3/17/2009 10:17pm, #82
So to add to my list of foul-ups...
I was going to start on creatine after the tournament, because I didn't want to wind up in +100kg. The weight classes were merged, so that's a moot point. And then I decided not to start supplementing with it afterwards because:
1) I wasn't in the gym, so what good would it do?
2) Would it damage my brain? I mean, creatine uptake -> water uptake to maintain homeostasis -> swelling -> increased ICP, right?
Well, guess what...
Results demonstrate that chronic administration of creatine ameliorated the extent of cortical damage by as much as 36% in mice and 50% in rats. Protection seems to be related to creatine-induced maintenance of mitochondrial bioenergetics.
Animals fed a 1% Cr-diet were afforded greater neuroprotection than animals fed a 0.5% Cr diet. These results support the idea that a Cr-enriched diet can provide substantial neuroprotection in part by suppressing secondary brain injury.
Although creatine did not attenuate gray matter loss in the NYU cohort, it significantly spared gray matter in the IH cohort with pre-fed and pre & post-fed regimens. Such selective sparing of injured spinal cord gray matter with a dietary supplement yields a promising strategy to promote neuroprotection after SCI.
The administration of creatine to children with TBI improved results in several parameters, including duration of post-traumatic amnesia (PTA), duration of intubation, intensive care unit (ICU) stay, disability, good recovery, self care, communication, locomotion, sociability, personality/behavior and neurophysical, and cognitive function. Significant improvement was recorded in the categories of Cognitive (p < 0.001), personality/behavior (p < 0.001), Self Care (p = 0.029), and communication (p = 0.018) aspects in all patients. No side effects were seen because of creatine administration.
Here, we review the roles of Cr and Cr-related enzymes and consider the potential
value of supplementation with Cr, a potent neuroprotective substance. As a hypothesis, we consider whether Cr, if given at an early time point of the disease, may prevent or delay the course of AD-related neurodegeneration.
3/18/2009 8:43am, #83
Given that, whats your view on the anabolic diet and creatine supplements. I guess you're going to get increased creatine on the AD anyway from the amount of red meat you're meant to eat.
3/18/2009 2:10pm, #84
3/18/2009 9:50pm, #85
At least people are paying attention to it now.
I'm still kind of paranoid about whether it'll affect my brain geometry while I'm still showing symptoms, though.
---------- Post added at 08:50 PM ---------- Previous post was at 07:24 PM ----------
Also, for anyone waiting on my "verdict" re: fish oils, there are a few problems.
1) I got bloodwork done today, but no AA:EPA ratio, so I'd be working blind.
2) Given that I eat two cans of salmon a day (and have been eating at least one a day for the last year), I'm already getting more EPA/DHA daily than most of my sources recommend supplementing with.
3) There are plenty of studies about EPA/DHA supplementation, but it looks like the people running them are screwing them up in one way or another, because review efforts like Cochrane Collaboration aren't drawing any conclusions based on them.
4) The lipid chemistry governing the conversions between short-chain and long-chain polyunsaturated fatty acids is... well, whether it's not well understood or not in general, it's not well understood by me.
That said, I've still got a container of concentrated EPA/DHA caps from Costco, so I may still give it a shot. Right now, though, it looks like you're better off just eating canned wild Pacific salmon, from both a nutritional (hooray, bonus protein) and financial perspective.
3/18/2009 10:33pm, #86
So how does an average serving of, say, canned chunk tuna stack up next to an average serving of canned wild Pacific salmon in regards to daily amount of EPA/DHA? Did you choose wild Pacific salmon because it's got mo' fish oil than other types of canned fish products, or is it just a matter of taste?
3/18/2009 10:46pm, #87
Tuna, light, canned with water, drained, salted:
Total fat per 100g: 0.82g, 0.33g of which is polyunsaturated.
That should actually answer both of your questions (that is, no fat = the stuff tastes like cardboard).
3/18/2009 11:02pm, #88
3/18/2009 11:07pm, #89
http://webprod.hc-sc.gc.ca/cnf-fce/index-eng.jsp and search for salmon (or 3081, if you want to skip the alternatives).
There's also an American version: http://www.nal.usda.gov/fnic/foodcomp/search/
Oh, and a warning... grocery stores tend to have nearly a 100% markup on cans of salmon over Costco ($7.99/6 cans at last visit)/Wholesale Club ($6.99/6 cans at last visit). Wal-Mart had relatively cheap keta salmon last time I was there ($1.25/can), but keta tends to be lower in fat and blander.
3/21/2009 4:48pm, #90
So I got my bloodwork back. Some oddities in there, but nothing my doctor seemed overly concerned with. Because this thread so far is about lipids (when it's not about **** happening)...
Sears on triglyceride/HDL ratio:
>= 4 is diseased, 3 is poor, 2 is good, 1 is ideal.
Mine is 0.65.
Report on cholesterol ratio (total / HDL):
Average risk is 3.5-5.0, 2x risk is 5.1-10.0, 3x risk is 10.0-23.4.
Mine is 3.0.
So that's kind of neat. I also do not have hepatitis B or C, which I'm sure is a great relief to all of you.
Anyways, I have for-real referrals to a neurologist, ophthalmologist, and surgeon re: my brain, eyes and elbow respectively (no appointments yet, though), and I'm going to see a well-regarded physio about my knee (and probably neck and everything else too) next month.
And because my graphs-per-post average is veritably plummeting, here's Figure 1 from Harnack et al., "Quantitation of alpha-linolenic acid elongation to eicosapentaenoic and docosahexaenoic acid as affected by the ratio of n6/n3 fatty acids"
Because "the total concentration of LCPUFA administered was the same for all experiments", the scales of these graphs are a bit misleading for our purposes - the bars are ratios of AA/EPA/DHA vs. the recovered LA or ALA, which themselves are administered such that the total LA+ALA is constant. I'd probably have done a two-dimensional analysis instead (vary both LA and ALA concentrations independently), but that'd probably have made things more expensive.
Still, though, it's interesting to see the in vitro performance of the conversions - the relationship between SCPUFA ingestion and LCPUFA creation is probably greater than linear because of its effects on the competition between LA and ALA.