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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 8 of 8. This is the beginning of the thread.
Posted by joebob on August 15, 2004, at 0:00:29
question of ratio of epa to dha in fish oil..
i do know that you usually suggest the cheapest good brand, but there is a controversy on the ratio, and i would appreciate your inputi am sure you are aware of stoll and horrobin, etc.
what do YOU think? is the ratio important? got any citations either way? i've seen some but would like you HO
best,
joebob
Posted by Larry Hoover on August 15, 2004, at 14:02:54
In reply to larry, i can't remember you weighing in on the, posted by joebob on August 15, 2004, at 0:00:29
> question of ratio of epa to dha in fish oil..
> i do know that you usually suggest the cheapest good brand, but there is a controversy on the ratio, and i would appreciate your input
>
> i am sure you are aware of stoll and horrobin, etc.
>
> what do YOU think? is the ratio important? got any citations either way? i've seen some but would like you HO
>
> best,
> joebobI don't have an opinion on the validity of enhanced EPA formulations of fish oil. Frankly, I think your body knows what to do.
I'm concerned that manipulations of the EPA:DHA ratio are simply attempts to make a product patentable (and increase profits therefrom).
Seems to me, people did fine just eating fish, long before the scientists starting meddling around with what's in 'em.
Lar
Posted by joebob on August 16, 2004, at 11:02:55
In reply to Re: larry, i can't remember you weighing in on the » joebob, posted by Larry Hoover on August 15, 2004, at 14:02:54
have you seen the david horrobin research on ratios?
thanks
Posted by Larry Hoover on August 17, 2004, at 9:54:16
In reply to none of the high epa formulas i get are patented, posted by joebob on August 16, 2004, at 11:02:55
> have you seen the david horrobin research on ratios?
>
> thanksDo you have a link?
Patented forms include ethyl eicosspentaenoate, and ones in which the triglycerides have been manipulated. I'm not sure if preconcentration is patentable, or if it's just considered to be "public domain".
Lar
Posted by joebob on August 17, 2004, at 20:22:56
In reply to Re: none of the high epa formulas i get are patented » joebob, posted by Larry Hoover on August 17, 2004, at 9:54:16
i have files on my hard drive that i could send to you, but need more time to find more links
i note that this is horrobin mostly or only in '03, i saw him speak a few years ago when he presented the science behind his position
here's another one
http://www.fincastle.com/research.htmland one more with refs at end of article
http://www.psychiatrictimes.com/p030850.htmli also came across this recently:
The studies suggest that it is EPA that promotes positive emotions, rather than DHA (Nemets, Stahl et al. 2002; Peet and Horrobin 2002). Studies using pure DHA have shown it has no more effect than a placebo (Marangell, Martinez et al. 2003). In addition, a competition mechanism means DHA prevents EPA being completely assimilated and used (Horrobin, 2002), while by contrast, the body can transform EPA into DHA as required.
here's the link to the above:
http://en.isodisnatura.com/depression_omega-3.htmthis oughta get you going for now......gotta go and get my kid for dinner
thanks
joebob
Posted by Larry Hoover on August 19, 2004, at 10:46:07
In reply to lar heres a place to start...link to partial bibli, posted by joebob on August 17, 2004, at 20:22:56
> i have files on my hard drive that i could send to you, but need more time to find more links
>
> i note that this is horrobin mostly or only in '03, i saw him speak a few years ago when he presented the science behind his positionOK, I don't do names well. I didn't recognize Horrobin....he's the front man for Laxdale, the British chemical house pushing the patented (and expensive) ethyl-eicosapentaenoate. Basically, pure EPA, but in an unnatural form, so it can be patented.
Everything he says trumpeting EPA has to be taken with a grain of salt.
DHA may not be the front man in the EPA and DHA team, but it is probably the muscle. Consider this first abstract, which shows that postpartum depression is massively correlated to DHA concentrations, but is independent of EPA. The next abstract shows that Horrobin is full of BS about the conversion of EPA to DHA....after 16 months at 12-grams/day E-EPA, the DHA levels were not elevated. They should have been elevated above normal, if interconversion readily occurs.
Lar
J Affect Disord. 2002 May;69(1-3):15-29.
Seafood consumption, the DHA content of mothers' milk and prevalence rates of postpartum depression: a cross-national, ecological analysis.Hibbeln JR.
Laboratory of Membrane Biophysics and Biochemistry, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Park 5, Room 150, 12420 Parklawn Drive, Rockville, MD 20892, USA. jhibbeln@niaaa.nih.gov
BACKGROUND: Mothers selectively transfer docosahexaenoic acid (DHA) to their fetuses to support optimal neurological development during pregnancy. Without sufficient dietary intake, mothers become depleted of DHA and may increase their risk of suffering major depressive symptoms in the postpartum period. We postulated that the DHA content of mothers' milk and seafood consumption would both predict prevalence rates of postpartum depression across countries. METHODS: Published prevalence data for postpartum depression were included that used the Edinburgh Postpartum Depression Scale (n=14532 subjects in 41 studies). These data were compared to the DHA, eicosapentaenoic acid (EPA) and arachidonic acid (AA) content in mothers' milk and to seafood consumption rates in published reports from 23 countries. RESULTS: Higher concentrations of DHA in mothers' milk (r=-0.84, p<0.0001, n=16 countries) and greater seafood consumption (r=-0.81, p<0.0001, n=22 countries) both predicted lower prevalence rates of postpartum depression in simple and logarithmic models, respectively. The AA and EPA content of mothers' milk were unrelated to postpartum depression prevalence. LIMITATIONS: These findings do not prove that higher omega-3 status cause lower prevalence rates of postpartum depression. Data on potentially confounding factors were not uniformly available for all countries. CONCLUSIONS: Both lower DHA content in mothers' milk and lower seafood consumption were associated with higher rates of postpartum depression. These results do not appear to be an artifact of cross-national differences in well-established risk factors for postpartum depression. Interventional studies are needed to determine if omega-3 fatty acids can reduce major postpartum depressive symptoms.
Prostaglandins Leukot Essent Fatty Acids. 2003 May;68(5):301-4.
The effects on plasma, red cell and platelet fatty acids of taking 12 g/day of ethyl-eicosapentaenoate for 16 months: dihomogammalinolenic, arachidonic and docosahexaenoic acids and relevance to Inuit metabolism.Horrobin D, Fokkema MR, Muskiet FA.
Laxdale Ltd, Kings Park House, Laurelhill Business Park, Stirling, FK7 9JQ, Scotland, UK. agreen@laxdale.co.uk
A patient with mantle cell lymphoma took 12g/day of ethyl-eicosapentaenoate for 16 months. Compared to reference values, eicosapentaenoic and docosapentaenoic acids were elevated in plasma, red cells and platelets but docosahexaenoic acid levels were in the normal range. Arachidonic acid levels were moderately reduced but dihomogammalinolenic acid levels remained in the normal range. In spite of a long chain n-3 fatty acid intake higher than in most Inuit populations, arachidonic acid levels remained considerably higher in this patient than in the Inuit. The implications for understanding of fatty acid metabolism in humans are discussed.
Posted by joebob on August 19, 2004, at 12:31:03
In reply to Re: lar heres a place to start...link to partial bibli » joebob, posted by Larry Hoover on August 19, 2004, at 10:46:07
directly to the need for dha by the fetus and suckling infant?
and it seems to me that the implication re epa conversion to dha might also imply that there was no increased need for dha, so no conversion takes place
the research about epa conversion to dha did not come from horrobin, as was cited later in my post, and i am sure i recall a replication study more recent than the one i copied in my post
thanks so much, i value your opinion highly and enjoy the exchange/debate aspect, as i am a curious boy and like to get informed
one last thing did you follow the selegine/phenalynine post? see below....
do you think that the phenalynine would compete for absorption with other aminos, like tyrosine,taurine, theanine? is this combo worth a try? actually i tried 5mg sele and 500 mg phenal this morning and will report subjective results as i become clear on what i experience....Selegiline + Phenylalanine « nemesis
Posted by Dr. Bob on August 14, 2004, at 13:20:16
In reply to Selegiline + Phenylalanine, posted by nemesis on August 14, 2004, at 1:42:44
Posted by nemesis on August 14, 2004, at 1:42:44
> I was first diagnosed with major depression 13 years ago, and have had some form of depression endlessly since (and likely prior, too). I've never been able to tolerate the side effects of pure SSRIs (headache, foggy head, feeling drugged and "on another planet", sexual dysfunction, etc.) for long. The SSNRI Effexor took me from major depression, to completely flat and apathetic, and abandoned me there. I couldn't feel any emotion at all. I've taken Wellbutrin for several different courses and always tolerated it well (only side effect, increases my pre-existing anxiety), but found it to lift mood only very slightly. The only TCA I have tried is Pamelor, which markedly and surprisingly helped my anxiety, and made a mild to moderate dent in my depression, but the side effects piled up over time (weight gain, tiredness, dry mouth, dry skin, constipation, hemorrhoids from constipation in spite of fiber supplements), with the side effects counteracting my gains in getting less depressed. I also tried SAM-E (did nothing except give me a headache), and St. John's wort (did it help mildly sometimes? I'm still not sure).
>
> My best response, on a response to side effect ratio has still been to Wellbutrin, but it never gave me nearly enough of a kick; it was like one bite of an appetizer, with no more food to follow. I read that it somewhat inhibits dopamine reuptake, but then cripples itself by reducing the amount of dopamine your body produces. "Stronger" dopaminergic drugs are illegal, have been removed from the market (e.g., Survector), and/or are potentially addictive and not generally prescribed for depression anymore (e.g., Dexadrine). I read that old-school MAOI Parnate reputedly has a dopaminergic effect, too, but within a smorgasboard of effects and side effects.
>
> Suspecting that, for me, I needed to elevate dopamine levels moreso than serotonin levels, I did a ton of research and somehow stumbled across information on a couple of studies done on a combination of selegiline (Eldepryl) and phenylalanine. The studies, although not placebo-controlled, appeared to show rapid and dramatic results. Other sources attributed this to a dopaminergic effect coming from accumulation of the "chocolate amphetamine", phenylethylamine (PEA). The phenylalanine breaks down in part into PEA, and the selegiline keeps the PEA from dissipating too quickly to have an effect.
>
> Tired of seeing HMO doctors who were always just pushing the next SSRI, or putting me back on Wellbutrin, I located a highly regarded private practice psychopharmacologist, and paid out of pocket to see him. At first he didn't put much stock in my thought of wanting to try selegiline + phenylalanine. He said selegiline isn't an effective antidepressant until you take enough that it becomes a nonselective MAOI similar to Parnate or Nardil. I didn't want to argue on my first visit, that the primary effect was purportedly coming from the phenylalanine (creating PEA) and that selegiline's "low-dose" role was to keep the PEA from metabolizing too quickly.
>
> Over eight months or so, he eventually became open to letting me try the selegiline + phenylalanine combo. He prescribed 10 mg selegiline + 500 mg DL-phenylalanine just yesterday. While it's far too soon to come to any conclusions, I have to say I'm nothing short of amazed less than 12 hours into this. I "felt something" within three to four hours of taking my first selegiline + phenylalanine dose. My energy level, sense of balance, clarity, and focus, are already up, and my mood is noticably elevated. (The only similar experience I can relate, is the amazing "relief" I felt the first time I ever took a Xanax for anxiety.) It will be interesting to see how this progresses. Right now I'm just thrilled after 13 years of unsuccessfully fighting depression, that anything could have a positive effect this quickly.
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· Selegiline + Phenylalanine « nemesis Dr. Bob 8/14/04
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Posted by Larry Hoover on August 20, 2004, at 8:21:24
In reply to thanks, but doesn't the post partum thing relate, posted by joebob on August 19, 2004, at 12:31:03
> directly to the need for dha by the fetus and suckling infant?
And adult women, too.
DHA is a structural component of, among many other sorts of membranes, the membranes covering nerve cells and brain cells.
When a cell senses certain kinds of signals from the environment, it snaps off a piece of the membrane, and that membrane fragment is broken, to release a fatty acid. If that fatty acid is DHA, it goes down to the DNA, and changes the "volume control" on the synthesis of all sorts of different proteins, including receptors. If that fatty acid is AA (arichidonic acid), then different things happen altogether (a whole different group of genes are up- and down-regulated). When you are DHA deficient, your body substitutes arichidonic acid, but that changes the other things that happen afterwards. Your body might 'want' the DHA-mediated effect, but it gets the AA-mediated effect, instead.
> and it seems to me that the implication re epa conversion to dha might also imply that there was no increased need for dha, so no conversion takes place
That is a plausible rationale, but it doesn't fit the science. Enzymes are "stupid little machines". If they get more raw material, they make more product. As simple as that. There ought to have been *some* increase, for two reasons: a) feedback regulation (the signal that would shut down the stupid little machines) only occurs if the body has enough of the substance; b) what are thought of as "normal concentrations" of DHA are not normal. They are *typical* concentrations, and the typical person is DHA deficient (unless you are Inuit, and eat whale blubber all the time).
That's my interpretation, anyway. Others are certainly going to differ.
> the research about epa conversion to dha did not come from horrobin, as was cited later in my post, and i am sure i recall a replication study more recent than the one i copied in my postThe references at the bottom of the page had Horrobin as first or second author. <shrug> In any case, most nutrition scientists are now recognizing that the interconversion argument is a straw-man argument. If you obtain DHA from diet, and EPA from diet (or supplements), interconversion is not a factor. Period. Recent thinking is that EPA and DHA are at least "conditionally essential nutrients". Some are starting to call them "essential nutrients", in their own right. Just like the essential fatty acid alpha-linolenic acid, I believe that DHA and EPA are themselves essential (or so darn close to it that the ability to make a little bit inside our own bodies is a trivial consideration).
> thanks so much, i value your opinion highly and enjoy the exchange/debate aspect, as i am a curious boy and like to get informedMe too, dude.
> one last thing did you follow the selegine/phenalynine post? see below....
> do you think that the phenalynine would compete for absorption with other aminos, like tyrosine,taurine, theanine? is this combo worth a try? actually i tried 5mg sele and 500 mg phenal this morning and will report subjective results as i become clear on what i experience....I didn't comment because this is a preliminary trial. We'll see what comes of it. Theories do not substitute for empirical evidence. In other words, having an idea why something may or may not work is not the same thing as what is confirmed in an experiment. An experiment might work, but for a completely different reason than that in the hypothesis. "This works" is a different entity than "This works because..."
Lar
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