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Correcting high Omega 6/3 ratio

Discussion in 'Optimal Labs' started by Mark959, Mar 18, 2020.

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  1. Mark959

    Mark959 New Member

    Hey Dan,

    That is a very interesting idea, and I have actually been doing that instinctively on a periodic basis. Wouldn't be able to do those kinds of fasts for long periods of time, but I do do it a few times per month, so those changes are probably taking place.

    Looking back at my fatty acid panel from 2013, it's not clear exactly how high my linoleic acid was because I ate almond butter an hour before the test, not knowing that I needed to fast. Linoleic acid was right at the high end of the range. Some Omega 6 fatty acids were actually low. DHA and EPA were in the low ends of the ranges.

    First problem (I think): I wasn't digesting fats very well. I'm taking ox bile for now. Seems like it helps. Don't really know what the long term solution is for that problem though.

    I was using sunflower and safflower oil for a while and when I stopped doing this, I originally thought it was high in linoleic acid, but I was actually using the high oleic, so the linoleic content was the same or about the same as olive oil or most other common oils.

    Second problem: Not enough Omega 3.

    So I think my main two problems were that I wasn't digesting fats well, and I wasn't getting enough Omega 3. My body doesn't really like any of the fatty fish. I've been taking fermented cod liver oil (3 capsules per day), and that feels like it's doing the job. It does seem like it's assimilated better. I also eat grass fed meat all the time, including lamb a couple times per week.

    So I'm not even sure if my total Omega 6 was too high to begin with, but if it was, doing what you suggested is probably helping. Won't it also help with releasing and removing store toxins?

    P.S: Sorry for the late response. Notifications must be going to spam. I will check back tomorrow. Thanks for the replies.
     
  2. Dan2

    Dan2 New Member

    I've heard people say fasting, like water fasting, will help get fat-soluble toxins out of the system quickly but that it's not always the safest way, and that depending on (generally speaking here, I don't really know the details) the liver and digestive system health they can be mobilized but not excreted and so stored in nervous system tissue (which is fatty) instead of body fat, which is a worse place for them. I don't know how true that is, how exactly that might happen. In this case you're not water fasting for several days, you're doing a low-calorie, low fat and medium protein ketosis thing, and so that might affect the way the fat-soluble toxins are handled compared to an extended water fast. I wasn't thinking about the fat-soluble toxin mobilization when I made that post about the low-fat mid-protein fat loss and fat replenishing cycles, so uhhh now that I think about that, it might be a better idea unless you learn more about the risk of storage in nervous system tissue to just consistently eat fat in the ratios you want stored. And about the amount, there's two situations I'm thinking of and I don't know which would be better.

    You could eat maybe just a little less than the amount that would keep you having the same amount of body fat so that you'd be metabolizing a little of the stored body fat each day, allowing the release of fat-soluble toxins to be gradual for the liver, kidneys, digestive system etc to handle excreting. Or you could eat enough fat that you gain body fat even though you'd be metabolizing fat being in ketosis, with the intention being for the older fat stores to not need to be metabolized daily because of the cleaner new excess fats and for the speed of metabolizing the older fats and excreting the fat-soluble toxins to be decided by the body at its own safe pace, the safety of the pace the body would decide being the limiting factor in the preference of when those old fats are metabolized instead of the excess of new ones, and so you might want to gain some body fat to know you're eating a plentiful excess of fats each day, and the body might also barely or not at all be metabolizing the older fats sometimes, but there won't be pressure on the body to metabolize older fats at a speed that's risky for toxin excretion ability and nervous system tissue storage just for the sake of metabolizing the fats that are available (like stored body fat in the first situation of you eating less fat per day than what the body in ketosis would like to metabolize) to support energy requirements of organs detoxifying the stored body fats and so needing more of those fat stores metabolized and detoxified to support more of that cycle which could be a risky pace of detoxification.

    I don't know how palatable, how appetizing it'd be to eat enough fat to get fatter from fat. I guess it depends on the way you eat it. It reminds of what I was thinking about if a woman eating a zero carb/carnivore diet wanted to stay kind of fat instead of having a lean muscular kind of build. If you get raw cream, you can churn it or shake it in a jar to get a chunk of raw butterfat and some buttermilk. If I were to eat that amount of the butterfat that's in a quart of cream in one meal, it wouldn't be very appetizing, especially not by itself. But I could easily drink a quart of the cream, which has that same amount of butterfat plus the little bit of buttermilk, and want more. And people have different tastes about eating lots of flesh fats, like whether it's raw suet or melted just a little in a pan quickly or rendered all the way. So depending on the taste for it, a woman could maybe eat enough fat, in addition to plenty of relatively leaner meat and fish, that she wouldn't get a lean muscular toned look. It seems to me like raw cream would be the most appetizing way to do that. Hopefully raw grass fed cream has a good 6:3 ratio. So maybe you could try a healthy fat girl diet. Or eat lots of bone marrow and kidney suet like a Sasquatch. And even if the 6:3 ratio of the excess of fats you eat is high in the 6, if you're maintaining good redox and not eating much heavy metals while eating and storing those fats, there shouldn't be much toxicity stored in those new fats, and so they could both help the nervous system be able to slowly remove or avoid storing metals and to be clean fat stores that would further reduce the risk to the nervous system tissues when they become the older fats getting metabolized slowly. And then you could focus more on the 6:3 ratio a little better proportioned after the older stored fat should be relatively clean, since not risking the nervous system tissue is probably more important than having the 6:3 ratio just right. And if you're eating grass fed flesh fat and maybe cream plus some cod liver oil it shouldn't be so disproportionate in 6s that the symptoms would be worse than risking metals in the nervous system from eating too little fat (although I don't know enough about that to know the risks specifically). And maybe the quality of the fish has something to do with digesting the cod liver oil better than fish. Almost all cod liver oil other than a couple more expensive brands are heated and processed in similar ways, and Jack has said about the DHA being in sn-2 position makes it more bioavailable and most cod liver oils have a little sn-2 position DHA but mostly sn-1 and sn-3 whereas fish has mostly sn-2 (if I remember right the processing methods of the fish oil can change the sn position from more 2 to more 1 and 3). What kind of fish have you tried, like species, fresh or canned, brand?
     
    Last edited: May 19, 2020
  3. Mark959

    Mark959 New Member

    As far fatty fish go, I don’t like many except for squid and clams, but that’s a start. I’ve never liked salmon, tuna, or anchovies, raw or cooked. Which are the more expensive brands of cod liver oil you are speaking of? I’ve been taking Green Pasture for the past 3 months, switching from Carlson’s. I can’t really find any information on whether DHA in Green Pasture is in SN-2 position or not. Do you know? Do the brands you were talking about have it in SN-2? I think it’s possible I have an allergy to many fatty fish. I’ve done LDI in the past for other allergies with very quick success, so I may go back to that doctor and have him test me for fish allergies among other things.
    I understand what you are saying about nervous system toxicity. Two different doctors gave me homeopathic detox protocols to follow and they were a disaster; and I bet it was because of the very situation you described where toxins move from body fat to nervous system fat. My body couldn’t handle excreting that much at once. If it could, I would think the toxins never would have been stored in fat in the first place.
    Luckily, I don’t think my Omega 6 is a problem right now or ever was; only low Omega 3. I didn’t analyze the FA analysis I had gotten correctly. Linoleic acid was the only high omega 6 on my FA analysis, and like I said, I had eaten some almond butter shortly before the test. Just need to figure out the best way to get DHA into my body and brain now. I will find out if an allergy is the issue, but it would be good to use the best possible fish oil to make up for the dietary deficit right now.
    Also, when I had that test done that showed DHA in the low normal range, I was looking at an unfiltered computer screen and television screen for several hours a day. I imagine that was a large factor as well. My blue light exposure is far less now.
    Please tell me about those fish oil brands you mentioned. Another I found is called Marinol. They claim their oil has more DHA in the SN-2 position than others. Going to look into it more after I post this. https://www.stepan.com/uploadedFile...Pre-Metabolized Presentation January 2015.pdf
     
  4. JanSz

    JanSz Gold

    Talking in a general way about omega6 or omega3
    is the same as talking about light and not getting into light frequencies.
    Sounds good
    but only to someone who wants to sell you (highly suspicious) stuff.
    Because most of the time current discussions about omegas are similar misinformation as currently happens with covid-19.
    Everybody talking have some other motives than the topic which is (supposedly) discussed.
    ....
    I wish that one-day @Jack Kruse got seriously into individual fatty acids and peroxisomes.

    ..
     
    Last edited: May 23, 2020
  5. Dan2

    Dan2 New Member

    That PDF is a good find, but I don't understand it enough to say whether it's misleading somehow.

    That company has two kinds of cod liver oil, Marinol C-38 and Marinol D-40.
    C-38:
    https://www.stepan.com/Products/Specialty-Products/MARINOL®/MARINOL®-C-38.aspx

    D-40:
    https://www.stepan.com/Products/Specialty-Products/MARINOL®/MARINOL®-D-40.aspx


    C-38 has 210 mg/g of EPA and 150 mg/g DHA.

    Marinol C-38.png
    https://www.stepan.com/uploadedFiles/Literature_and_Downloads/Product_Bulletins/Specialty_Products/MARINOL®/MARINOLC38.pdf


    Marinol D-40 has 60 mg/g EPA and 340 mg/g DHA.

    Marinol D-40.png
    https://www.stepan.com/uploadedFiles/Literature_and_Downloads/Product_Bulletins/Specialty_Products/MARINOL®/MARINOLD40.pdf


    _____

    This is the expensive cod live oil I was thinking of, Rosita Extra Virgin,
    150 ml/~5 oz for $50:
    https://www.corganic.com/products/evclo#556f563aed228

    From "Description" and then "Learn more" button:
    "Gives you 443 mg EPA and 605 mg DHA per teaspoon, along with a full spectrum of omega fats, including 3, 4, 6, 7, 9 and 11.
    Not winterized like other oils in order to preserve full spectrum of nutritious fats that protect against oxidation...
    No heat, bleach, solvents, mechanization, winterization or chemicals are used."

    Scroll down and click the FAQs link below the "Add to cart" button:
    "Rosita EVCLO is most unique in its production. 99% of all cod liver oil production is created using processes that severely damage the vitamins inherent in the oil, such as freezing, winterization, degumming, bleaching, and deodorizing. Because the fragile nutrients in the oil are destroyed during this time, most of the producers will then fortify it with synthetic vitamins and market the oil as natural."

    Here's an article from a company that sells the Rosita brand, about the details of processing methods,
    "Industrial Production of Cod Liver Oil":
    https://www.corganic.com/blogs/news/industrial-production-of-cod-liver-oil

    Full nutrient and fatty acid details:
    https://evclo.com/faqs/nutrient-results/

    Screen shot 2020-05-23 at 5.43.09 PM.png


    "Gadoleic acid (20:1 n−11) is an unsaturated fatty acid. It is a prominent component of some fish oils including cod liver oil.[2] It is one of a number of eicosenoic acids." (https://en.wikipedia.org/wiki/Gadoleic_acid)

    __

    "Other major species of fatty acids in brain include vaccenic acid [18:1(n-7)], oleic acid [18:1(n-9)], and gadoleic acid [20:1(n-9)] (5)." (https://academic.oup.com/jn/article/136/8/2236/4664825)

    __

    The long-chain monounsaturated cetoleic acid improves the efficiency of the n-3 fatty acid metabolic pathway in Atlantic salmon and human HepG2 cells

    https://www.cambridge.org/core/jour...-hepg2-cells/1DAD2BDFE82B86BB58397A3F0EA2CB22

    "The present study aimed to determine if the long-chain MUFA cetoleic acid (22 : 1n-11) can improve the capacity to synthesise the health-promoting n-3 fatty acids EPA and DHA in human and fish models. Human hepatocytes (HepG2) and salmon primary hepatocytes were first enriched with cetoleic acid, and thereafter their capacities to convert radio-labelled 18 : 3n-3 (α-linolenic acid, ALA) to EPA and DHA were measured. Increased endogenous levels of cetoleic acid led to increased production of radio-labelled EPA + DHA in HepG2 by 40 % and EPA in salmon hepatocytes by 12 %. In order to verify if dietary intake of a fish oil rich in cetoleic acid would have the same beneficial effects on the n-3 fatty acid metabolic pathway in vivo as found in vitro, Atlantic salmon were fed four diets supplemented with either sardine oil low in cetoleic acid or herring oil high in cetoleic acid at two inclusion levels (Low or High). The diets were balanced for EPA + DHA content within the Low and within the High groups. The salmon were fed these diets from 110 to 242 g. The level of EPA + DHA in liver and whole-body retention of docosapentaenoic acid and EPA + DHA relative to what was eaten, increased with increased dietary cetoleic acid levels. Thus, it is concluded that cetoleic acid stimulated the synthesis of EPA and DHA from ALA in human HepG2 and of EPA in salmon hepatocytes in vitro and increased whole-body retention of EPA + DHA in salmon by 15 % points after dietary intake of cetoleic acid."

    __

    https://www.nutraingredients.com/Ar...rchers-catch-herring-s-hidden-health-benefits
    (from 2016)
    "In the human liver cell study, we found an increased capacity in the cells given cetoleic acid to produce EPA and DHA from ALA. However, since we do not have results from human intervention study, we cannot say something about the influence on whole body levels of EPA and DHA..."

    I wonder whether a person eating cetoleic acid, other than maybe converting ALA to DHA better, would also improve the efficiency of usage of DHA eaten directly.


    https://nofima.no/en/nyhet/2016/01/herring-is-better-for-you-than-we-thought/
    --------------(from 2016)
    It’s too early to say how large an effect cetoleic acid has in humans, but the experiments in cells in culture suggest that it influences how much healthy, marine omega fatty acids we store after eating herring,” says Bente Ruyter.


    https://nofima.no/en/nyhet/2019/10/norwegian-oils-from-sea-and-land-provide-extra-effect/
    ---------------(from 2019)
    "Scientists have innovatively mixed a North-Atlantic fish oil containing high amounts of cetoleic acid with a vegetable oil (camelina oil) rich in ALA. The scientists have tested the combination of the two oils in feed for rat, which serves as a model system for human nutrition.

    “Our hypothesis is that when camelina oil and fish oil are mixed, the cetoleic acid from the fish oil has lots of ALA to work with in order to form EPA and DHA in the body”, says Astrid Nilsson, senior scientist at Nofima.

    In the experiments, where up to 50 percent of camelina oil was mixed with a North-Atlantic fish oil, there was an equally high final content of the essential and healthy fatty acid DHA in the blood as there was after the ingestion of pure fish oil with high DHA content.

    This means that when you take the best of both worlds, you can use half as much of the EPA- and DHA-rich fish oil and still end up with a jackpot of DHA levels in the body, says Nilsson.

    However, the mixture ratio between available ALA and cetoleic acid will most likely be important in order to achieve the maximum amounts of EPA and DHA."

    __

    Other information on the Rosita site:
    https://evclo.com/
    https://evclo.com/faqs/
    https://evclo.com/testing/
    https://evclo.com/fatty-acid-levels-fish-oils/
    https://evclo.com/extra-virgin-cod-liver-oil-2013-09-05-update/
    "In the Viking era the freshly harvested cod livers were placed in a container, left outside to freeze in the cold Norwegian winter and then brought into their dwelling to thaw releasing the precious liver oil. Our Norwegian ancestors utilized the positive aspects of nature to collect fresh and wild cod liver oil that has not been exposed to high heat, chemicals, solvents, pressure or decomposition.
    ...Special procedures have been implemented within the bottling facility to minimize the oil’s exposure to oxygen, light and metal; all factors which adversely impact the long term stability of EVCLO.
    ...Organic 3 will warehouse EVCLO in our cold storage facilities in Michigan and distribute throughout North America. Once you receive your bottle of EVCLO it is imperative that you keep it chilled to extend the freshness. Unopened bottles can be kept in the freezer for long term storage."

    __

    and I think this is the other I was thinking of:
    https://www.nutraprointl.com/store/p3/Virgin_Cod_Liver_Oil.html
    8 oz for $33
    "...using cold pressed & advanced purifying (centrifugation & filtration) technologies without the use of chemicals. Our Virgin Cod Liver Oil ranks among the highest in levels of vitamins and nutrients (NOTHING artificially added or removed). No heat is used during processing and temperature is kept below 40°C."



    I don't know about how much sn-2 position would be in Green Pastures, Carlson's, or those two cold-pressed ones. I think I remember reading a Facebook or Patreon post of Jack's that said something about processing of cod liver oil resulting in less sn-2 DHA than is in fresh fish. I searched Facebook for "Jack Kruse sn-2 DHA" and didn't find it, and Patreon doesn't work on my old computer anymore. And again I don't understand the chemistry in the Marinol PDF you linked to enough to know whether there would be more sn-2 DHA in one of their products or the minimally processed cold pressed brands. If the price weren't an issue I would rather use the Rosita because of the more traditional processing methods and the fact that cod liver oil was known to be a health tonic before the modern processing methods, not known to be effective specifically for DHA, but effective as a general health tonic, so even if the use of the DHA in it isn't as efficient as brands that --might-- have more sn-2 DHA but that also use more processing that might've affected other qualities of the oil, overall I'd rather have the minimally processed oil and --maybe-- less DHA efficiency. There's probably stuff in the minimally processed oil that adds to its traditional health tonic quality that might never have been or no longer commonly is identified as being important to preserve in it. I'm glad the Rosita, with that attention to quality, is available to give to kids. But their recommended single dose is only a teaspoon with ~700 mg DHA, and the bottle is 150 ml/about 5 oz for $50, and since 700 mg isn't that much DHA per day for an adult or maybe even a kid and one teaspoon is about 5 ml so there's 30 doses per bottle, an adult could easily use two bottles a month, I think a small kid could use two bottles a month safely, so an adult who wants to get a lot of DHA without also eating fish could use three bottles a month. But if you can afford it, good.


    Too bad we can't still buy this cod liver oil --
    "Ingredients: include 'Chloroform, opium, cannabis, morphine, squills, bloodroot, wild cherry'"
    http://antiquecannabisbook.com/chap20/OldMarinol.htm
     
    Last edited: May 25, 2020
    JanSz likes this.
  6. JanSz

    JanSz Gold

    These days, on Jack's board, cod liver oil, when discussed, it is most often about its DHA content.
    When I was drinking it 75years ago, it was about preventing rickets, and nobody ever was talking about goodness od seafood.
    But even when talking about rickets, sunlight was not thought about.

    What is vit D content in those cod liver oils?
    The other highly important item maybe oleic acid. (To donate (clean) H for matrix water production.)

    I suspect that these two items may be of very high importance.

    Not putting down DHA,
    but I would like to see the evaluation of DHA from the point of view of how long it stays in the body (once it got there).
    I have seen some arguments in the past that its half-life is rater long, which would indicate the need for only small amounts, occasionally, in the food for its replenishment.
    So, note that DHA in organic meats is practically everywhere (in small (but sufficient) amounts).
    If true;
    back to the sunlight and good sources of oleic acids (and palmitic acids).


    .
     
    Last edited: May 24, 2020
  7. Dan2

    Dan2 New Member

    The Vitamin D measurement for the Rosita oil is on this page:
    https://evclo.com/faqs/nutrient-results/

    Screen shot 2020-05-24 at 9.56.34 AM.png

    395 iu isn't much compared to 1000-5000 iu supplements nowadays, or the amount produced from sun, but maybe other things in the minimally processed oil help that relatively small amount go further.

    And about the long half life of DHA -- the research in my previous post about cetoleic acid shows that there is a synergy between DHA and another fatty acid in some fish oils (the tests for the cetoleic acid effect used herring oil high in cetoleic acid compared to a control of sardine oil low in cetoleic acid) that will increase bioavailability of the DHA, so maybe there's also a synergy affecting bioavailabilty between DHA and other fatty acids or other things in some kinds of fish oil (and processing methods could affect that). Although it did say that the cetoleic acid increased the level of DHA in the blood and I don't know if that necessarily means it'll get into the places it should be stored in.

    "...where up to 50 percent of camelina oil was mixed with a North-Atlantic fish oil [high in cetoleic acid], there was an equally high final content of the essential and healthy fatty acid DHA in the blood as there was after the ingestion of pure fish oil with high DHA content." (from 2019)

    But also this:
    "'...the experiments in cells in culture suggest that [cetoleic acid] influences how much healthy, marine omega fatty acids [DHA] we store after eating herring,' says Bente Ruyter." (from 2016)
     
    Last edited: May 24, 2020
    JanSz likes this.
  8. Mark959

    Mark959 New Member

    Thank you very much for all that info. I have heard of Rosita. Still reading through the info on it and the other links you posted. All this makes me think I should just eat some damn fish.
     
    Dan2 likes this.
  9. Dan2

    Dan2 New Member

    Makes me think I should give the Rosita with some hash oil, opium, and morphine mixed in a try. "Did Johnny ask Santa for narcotics this year? Does Susie only rustle up an un-American appetite? Perhaps your child is a Chinaman? Well good news, folks! Today's doctors and President Roosevelt say opium, marijuana and morphine to muster Buster's mustard!"
    I think I'll try the Rosita for a month or two while getting lots of sun this time of year and see if I notice something from it since I already eat mostly meat, sardines and oysters so not a lot of variables there. I'm kinda hoping it doesn't feel worth the money so I won't want to try using more of it; on the other hand, maybe I won't know if it's worth the money until I know I've used too much.
     
    Last edited: Oct 18, 2020
    JanSz likes this.
  10. Mark959

    Mark959 New Member

    Amen :). I’ll let you know how it goes.
     
  11. Dan2

    Dan2 New Member


    Can you give some leads, even just keywords you think you might remember to search with, about the long half life argument?

    I found some things about DHA half-life.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772061/
    "DHA makes up over 90% of the n-3 PUFAs in the brain and 10%–20% of its total lipids. DHA is especially concentrated in the gray matter [2]. It is stored primarily in phosphatidylethanolamine (PE) and phosphatidylserine (PS) membrane phospholipids, with smaller amounts also found in phosphatidylcholine (PC; [3]), where it plays an important role in the biosynthesis of PS (DHA-PS) in the brain [4]...

    The human brain metabolizes approximately 4 mg of DHA per day, resulting in an estimated half-life of brain DHA of 2.5 years [35], much longer than that of DHA in peripheral tissues (e.g., two minutes in plasma; [35]). Importantly, although EPA does have significant acute anti-inflammatory actions in neural tissue [36,37] and the absorbance of EPA and DHA to the brain are similar [38,39], EPA levels are extremely low in brain tissue. This circumstance occurs because EPA is rapidly oxidized and removed from the brain, or it is elongated to the n-3 PUFA docosapentaenoic acid (DPAn3; 22:5n-3), which acts as a precursor for DHA [40]. However, EPA conversion is not a significant source of DHA [41,42,43]...

    Half of the brain’s DHA is accumulated during gestation, and the infant brain acquires five-times the level of lipids on a daily basis as the adult brain [53,54]. In adults, accretion is slower, and individuals with red blood cell DHA concentrations on par with the average European or American (~4% of total fatty acids) require 4–6 months of oral DHA supplementation to reach a steady state concentration that is dependent on DHA dose (8%–9% for 1000 mg per day; 5%–6% for 200 mg per day) [41]. Local de novo DHA synthesis in the brain is very low, thus DHA levels are maintained via delivery from the blood [55,56]. Circulating levels of DHA in the blood can reach as high as ~5% of that which is ingested orally [57] and ~0.5% of the circulating level is delivered to the central nervous system (CNS; [35])...

    Brain DHA composition likely plays a role in AD. The brains of non-DHA supplemented Alzheimer’s patients have 65–95 nmol/g of unesterified DHA, much less than normal controls (110 nmol/g; [248,249]). Furthermore, deficient liver biosynthesis of DHA has been observed in AD patients, where it appears that DHA biosynthesis halts at the last β-oxidation step from tetracosahexaenoic acid (24:6n-3) to DHA [248]. However, this is likely a minimal source of DHA (vs. preformed via diet). Recent data also suggests that AD patients have problems processing DHA [61], therefore the magnitude of DHA’s effects may be less in later stages of the disease [250]. Phospholipids PC and PE from various brain regions (particularly hippocampus) in the AD brain have reduced DHA content compared to control brains, further implicating DHA in the etiology of the disease [251,252]."

    ________

    https://academic.oup.com/ajcn/article/100/1/105/4576428
    "Design: Thirty-four healthy, cognitively normal participants (12 men, 22 women) aged between 52 and 90 y were recruited. Two identical kinetic studies were performed, each with the use of a single oral dose of 40 mg 13C-DHA. The first kinetic study was performed before participants started taking a 5-mo supplementation that provided 1.4 g DHA/d plus 1.8 g eicosapentaenoic acid (EPA)/d (baseline); the second study was performed during the final month of supplementation (supplement). In both kinetic studies, blood and breath samples were collected ≤8 h and weekly over 4 wk to analyze 13C enrichment...

    DHA half-life

    The mean plasma half-life of 13C-DHA was 4.5 ± 0.4 d at baseline compared with 3.0 ± 0.2 d while subjects were taking the supplement (P < 0.0001; Figure 5A). The mean whole-body half-life of 13C-DHA was 140 ± 27 d at baseline compared with 54 ± 12 d while subjects were taking the supplement (P = 0.0107; Figure 5B). Neither the plasma nor whole-body 13C-DHA half-life differed between men and women, and there was not a significant correlation with the age of participants...

    DISCUSSION

    In this study, we report that supplementation with an EPA + DHA supplement significantly modified the kinetics of 13C-DHA in healthy older persons without cognitive decline such that its plasma and whole-body half-lives were lower and its β-oxidation to 13C-CO2 was higher than at baseline. Hence, the plateauing of plasma DHA at higher intakes of EPA + DHA appears to be a function of increased β-oxidation...

    In the current study, there was no difference in plasma 13C-DHA, plasma DHA, or the 13C-DHA half-life in whole body or plasma between men and women (data not shown). The absence of sex-specific differences was probably because of the drop in estrogen in women after menopause (29). Two other factors that potentially change DHA homeostasis are age and APOE4 genotype (7, 14). APOE4 carriers were excluded from this study (15). Age-dependent differences in 13C-DHA metabolism have been reported elsewhere over a 50-y difference in age (7). In the current study, there was no correlation between age (52–90 y old) and the 13C-DHA half-life, but this study was not designed to assess a possible age effect. Participants in this study were of an age when cognitive decline could be starting, but they were all cognitively healthy as assessed by using the Mini-Mental State Examination. This fact is important because we wanted to eliminate lower cognitive performance as a confounder that might have influenced the results (10)."
     
    JanSz likes this.
  12. Dan2

    Dan2 New Member

    I also found something about SN-2 position DHA.

    https://sci-hub.tw/10.1017/s0007114599001737

    Incorporation and washout of orally administered n-3 fatty acid ethyl esters in different plasma lipid fractions

    "Since fish oil contains a mixture of TAG [triacylglycerols] with various fatty acids, the concentration of n-3 fatty acids is relatively low. Higher concentrations of EPA and DHA can be achieved by using a supplement of unesterified fatty acids. Ingestion of free fatty acids (FFA), however, causes gastrointestinal complaints and may be toxic (Beckermann et al. 1990). In contrast to FFA [free fatty acids], no side-effects are induced by n-3 fatty acid ethyl esters (EE), and EE [ethyl esters] would therefore be appropriate for supplementation of diets with n-3 fatty acids. However, the absorption of EPA and DHA as EE [ethyl esters] may be lower than that of EPA and DHA as TAG [triacylglycerols] or FFA [free fatty acids], since previous studies have reported that the plasma incorporation of EPA- and DHA-EE [ethyl esters] is lower than the incorporation of EPA- and DHA-TAG [triacylglycerols] after a single dose (el Boustani et al. 1987; Lawson & Hughes, 1988; Beckermann et al. 1990) as well as during prolonged supplementation of n-3 fatty acids as EE (Hansen et al. 1993). However, other studies did not find any differences in incorporation between supplements (Reis et al. 1990; Nordoy et al. 1991; Krokan et al. 1993). The diversity of results may be partly explained by the fact that some studies measured EPA and DHA only in plasma TAG [triacylglycerols] and not in plasma phospholipids (PL) or cholesteryl esters (CE). Before using n-3 fatty acid EE [ethyl esters] in a clinical setting, it is important to determine the actual level of incorporation when using n-3 fatty acid EE [ethyl esters].

    ...pattern of incorporation was observed for plasma TAG [triacylglycerols] (Fig. 3): here, DHA was incorporated to an even higher extent than EPA, in contrast to the incorporation into PL [plasma phospholipids] and CE [cholesteryl esters]. Both fatty acids showed a rapid decrease during washout. EPA had completely returned to baseline on day 14, while DHA was still significantly increased by this time...

    For the decrease of DHA in plasma TAG [triacylglycerols], comparable results were found (Table 3). A half-life ranging from 0.89 to 2⋅57 d was found with a mean of 1⋅63 d when using the mono-exponential model. Use of the bi-exponential model resulted in an increase of the MSC value. The initial half-life of DHA in plasma TAG [triacylglycerols] ranged from 0⋅18 to 0⋅38 d, followed by a half-life of 3⋅81–5⋅32 d in the second phase (mean 4⋅75 (SE 0⋅33) d)...

    Only Blonk et al. (1990), who used a supplement of n-3 fatty acid EE [ethyl esters], did not find any difference in incorporation between EPA and DHA into plasma PL [plasma phospholipids] after 12 weeks of supplementation. In these studies, supplementation ranged from a single dose (Gibney & Daly, 1994) to 1 year of supplementation (Leaf et al. 1995). The pattern of incorporation of different fatty acids appeared to be independent of the different fish oil types and dosages. Sadou et al. (1995) investigated whether the intramolecular structure of n-3 fatty acid TAG [triacylglycerols] affects the incorporation of EPA and DHA. They found that DHA (predominantly situated at the sn-2 position) was mainly incorporated into plasma TAG [triacylglycerols], while EPA (predominantly situated at sn-1/3) was mainly incorporated into plasma PL [plasma phospholipids] (Sadou et al. 1995). They concluded that the difference in incorporation was due to the intramolecular structure [sn position]. However, our study shows that a supplement containing EE [ethyl esters] instead of TAG [triacylglycerols] resulted in a similar plasma distribution, which would suggest that the incorporation pattern is the result of properties of EPA and DHA rather than of the position of the fatty acid on the glycerol backbone. A more plausible explanation for the difference in incorporation between EPA and DHA was given by Subbaiah et al. (1993). These authors suggested that the difference is caused by the fact that EPA and DHA are competitors for the enzymic transfer of fatty acids from PL [plasma phospholipids] to CE [cholesteryl esters]. The affinity of the enzyme lecithin-cholesterol acyltransferase is higher for EPA than for DHA. Thus, the transfer of EPA from PL [plasma phospholipids] to CE [cholesteryl esters] was higher compared with DHA. This would explain why, in our study, incorporation of EPA into CE [cholesteryl esters] was high, while the incorporation of DHA into CE [cholesteryl esters] was negligible. It would also explain why DHA incorporation into PL [plasma phospholipids] was more rapid than into CE [cholesteryl esters], a finding that has also been described in other studies (Subbaiah et al. 1993; Sadou et al. 1995; Brossard et al. 1996). When the transfer of DHA from PL [plasma phospholipids] to CE [cholesteryl esters] is reduced, a relative accumulation of DHA in PL [plasma phospholipids] would be expected. Indeed, in our study DHA in PL [plasma phospholipids] was still increasing after 1 week of supplementation. However, the increase of DHA in PL [plasma phospholipids] was less rapid than the increase of EPA. This could be explained by a relatively high clearance of DHA compared with EPA from the plasma towards the adipose tissue, since DHA has been suggested to be the preferred storage form of n-3 fatty acids (Kasim-Karakas, 1995).

    n-3 Fatty acid supplementation was also shown to induce changes in fatty acids other than EPA and DHA in the present study. We observed a small increase in 20:4n-6 [arachidonic acid] in plasma PL [plasma phospholipids] on days 2 and 3, followed by a decrease in concentration. It is likely that the observed increase is the result of the small amount of 20:4n-6 [arachidonic acid] in the supplement. However, this increase does not correspond to that seen in other studies, which generally report a decrease in 20:4n-6 [arachidonic acid] during n-3 fatty acid supplementation (von Schacky et al. 1985; Reis et al. 1990; Hansen et al. 1993; Krokan et al. 1993; Marangoni et al. 1993; Prisco et al. 1996), most probably as a consequence of competition between the n-3 and n-6 fatty acids. Yet, when examining literature data in detail, some of these studies show a temporary increase in 20:4n-6 [arachidonic acid] during the first week of supplementation (von Schacky et al. 1985; Reis et al. 1990; Hansen et al. 1993), which is in accordance with our findings. This observation, combined with the significant decrease of 18:2n-6 [linoleic acid] in PL [plasma phospholipids], indicates that incorporation of EPA and DHA into PL [plasma phospholipids] in the first days of supplementation mainly occurs at the expense of 18:2n-6 [linoleic acid] and not of 20:4n-6 [arachidonic acid].

    Not only was the incorporation level of EPA higher than that of DHA, the incorporation rate was also higher. Similarly, the decline during washout was more rapid for EPA than for DHA. The same finding has also been described by others (Marsen et al. 1992; Hodge et al. 1993; Marangoni et al. 1993; Subbaiah et al. 1993) who showed that DHA had not returned to baseline values within 4 weeks of washout. So far, no information has been available about the washout rates in the separate plasma lipid fractions. In our present study, the decrease of EPA in the PL [plasma phospholipids] and CE [cholesteryl esters] fractions was mono exponential, implicating that EPA probably originates from one pool, i.e. plasma PL [plasma phospholipids]. Unfortunately,it was not possible to calculate half-life of DHA in PL [plasma phospholipids] and CE [cholesteryl esters] due to the high intraindividual scatter and the slow rate of washout.

    As for plasma TAG [triacylglycerols], our results would indicate a bi-exponential washout of EPA as well as DHA. The slow decline in the second phase of washout may be due to the release of n-3 fatty acids from body stores. EPA and DHA are incorporated into TAG [triacylglycerols] by the liver to be incorporated into VLDL [very low density lipoprotein] and to re-enter the plasma pool. The half-life in the second phase is longer for DHA than for EPA, which is consistent with the notion that DHA is the main storage form of the n-3 fatty acids (Kasim-Karakas, 1995)."

    _______

    So, ..."our study shows that a supplement [of DHA] containing EE [ethyl esters] [in sn position 1/3?] instead of TAG [triacylglycerols] resulted in a similar plasma distribution [as TAG sn-2 DHA did]..." doesn't mean that just because the EE DHA raised the plasma levels similar to TAG sn-2 DHA that EE DHA (sn position 1/3 I'm assuming) is the best form for the brain though.
     
    Last edited: Jun 16, 2020
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  13. Dan2

    Dan2 New Member

    https://www.sciencebasedhealth.com/Fish-Oil-EE-vs-TG-omega-3s-which-is-better-W119.aspx

    "A review of the scientific literature in which comparisons between the EE vs. TG omega-3 forms were assessed in terms of bioavailability, safety, or efficacy indicate the differences are minor, inconsequential, and cannot be judged to be physiologically or clinically significant. Results from comparative studies, in general, suggest that absorption of EPA and DHA from TG or from EE - and the biological outcomes over time-- are similar when fish oil is routinely supplemented and a steady state has been achieved. Further, the more sustained uptake of the EE form has been postulated to offer an advantage in terms of heart health.

    In short, the claim that the TG form is, in any clinically significant way, more advantageous or beneficial than the EE form is not supported by credible science at this time."


    ________


    https://shorthillseye.com/fish-oil-triglycerides-vs-ethyl-esters/

    "Ethyl esters are produced by reacting crude fish oil in a free fatty acid form with ethanol (and industrial alcohol) to form a synthetic substrate. Under a vacuum, the mix is then heat distilled and the resulting condensate is a concentrated omega-3 ethyl ester solution. The concentration of the omega-3 fatty acid depends on the variables of the distillation process but normally results in a 50-70% omega-3 solution.

    The process of converting TGs to EEs is necessary from a technical standpoint in the production of fish oil concentrates to purify the oil. However, once this molecular distillation process is completed, there is an option to leave the fatty acids in free form, attached to an ethyl alcohol backbone, or to reattach them to a glycerol backbone (triglyceride)."


    ________


    https://www.pnas.org/content/110/25/E2259

    "Recently in PNAS, Hoshi et al. (1) report the results of elegant studies defining the molecular basis for the blood pressure-lowering effect of omega-3 fatty acids, in particular docosahexaenoic acid (DHA). They found that DHA, when infused intravenously, activated the large-conductance Ca2+- and voltage-activated K+ (BK) channels in vascular smooth muscle but that the infusion of DHA ethyl esters (like those contained in dietary supplements) failed to activate BK channels. The authors indicated that their findings have “practical implications for the use of omega-3 fatty acids as nutraceuticals for the general public and also for the critically ill receiving omega-3–enriched formulas.”

    This conclusion is unwarranted. With regard to implications for critically ill patients receiving omega-3–enriched intravenous emulsions, Hoshi et al. (1) state that “These emulsions, which are available for enteral as well as for parenteral (central venous) application, may result in administration of up to 10 g of DHA/EPA per patient per day and may contain either free or ester-conjugated omega-3 fatty acids [citing Marik and Zaloga (2)].” In fact, none of these products contains free fatty acids, and the authors may not have understood that “ester-conjugated” does not refer to esterification with ethanol (i.e., ethyl esters) but with glycerol as triglycerides (oils). When infused intravenously, the triglyceride-bound fatty acids in emulsified fish oils are hydrolyzed from the glycerol backbone by lipoprotein lipase, an endothelial enzyme, releasing the fatty acids for uptake into various tissues where they become incorporated into cellular lipid pools. Consequently, the findings of Hoshi et al. have no implications for critically ill patients since neither free fatty acids nor ethyl esters are found in intravenous lipid emulsions.

    Neither are there implications for “the general public.” There are many encapsulated omega-3 ethyl ester products on the market, both pharmaceuticals (Lovaza, GlaxoSMithKline; Vascepa, Amarin; Epadel, Mochida; Omacor, Pronova) and dietary supplements, all designed for oral, not intravenous, use. During digestion, they are converted into free fatty acids by the action of pancreatic lipases that remove the ethanol moiety. The now nonesterified (free) fatty acids are absorbed into the enterocyte and reesterified into phospholipids, triglycerides, and/or cholesterol esters. These are then incorporated into chylomicrons, which are secreted into the lymphatic system, ultimately enter the bloodstream through the thoracic duct, and are then distributed to various tissues, including endothelial and smooth muscle cells in the vasculature. Therefore, the vasculature is never exposed to omega-3 ethyl esters. Hence, the findings of Hoshi, et al., although true in their unique experimental settings, have no relevance to intravenous fish oil emulsions or to dietary supplements and have quite limited “practical implications.”


    _______


    I think this means fresh fish and cold-processed cod liver oil are still best. What a surprise. I'm still interested in the possibility of getting enough DHA from just red meat.
     
    Last edited: Jun 16, 2020
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  14. Dan2

    Dan2 New Member

    https://onlinelibrary.wiley.com/doi/full/10.1111/j.1747-0080.2007.00201.x

    Long‐chain omega‐3 fatty acids in red meat
    First published: 15 August 2007

    "Meat has a relatively high content of DPA, relative to EPA and DHA. Thus DPA accounts for 29% of the average LC omega‐3 PUFA intake of adult Australians.

    Recent evidence suggests that DPA is just as important as EPA or DHA for delivering the health benefits associated with LC omega‐3 PUFA.

    Current regulations, however, do not take account of the DPA content of foods in determining whether they qualify for an omega‐3 content claim. Moreover, the DPA content of foods will not be considered in a proposed general level omega‐3 health claim.

    Lean red meat is an important natural food source of LC omega‐3 PUFA, the content of which can be influenced by modifying the composition of livestock feeds...

    MEAT AS A SOURCE OF DPA

    Much of the evidence substantiating health benefits of LC omega‐3 PUFA, particularly cardiovascular benefits,3 is based on dietary supplementation trials with fish or fish oil rich in EPA and/or DHA. Fish contains relatively little of the intermediate LC omega‐3 PUFA, i.e. DPA, and there is even less in fish oil. Hence LC omega‐3 PUFA intake recommendations for CV health usually specify EPA and DHA without reference to DPA.3, 13 Compared to fish, however, mammalian meat including beef and lamb has a relatively high proportion of DPA to EPA and DHA.14Table 2 shows the relative proportions of EPA, DPA and DHA in meat and fish, weighted according to the relative rates of consumption of different meat and fish products in Australia. Consequently, DPA has been shown to account for 29% of the total dietary LC omega‐3 PUFA intake of Australian adults.12 Hence we need to gain a better understanding of the physiological functions of DPA and how they compare to those of EPA and DHA."

    Screen shot 2020-06-16 at 2.47.20 PM.png

    Seal meat and seal oil are particularly rich sources of DPA. Interestingly, seal, not fish, was the main contributor to LC omega‐3 PUFA intake in the traditional diet of Greenland Inuits, upon which the original epidemiological evidence for reduction of CV risk was based.19 The few human intervention trials conducted with DPA‐rich supplements indicate that DPA is equally if not more beneficial than either EPA or DHA for improving CV risk factors.20-24 Recent clinical trials with seal oil have shown that it is more efficacious than fish oil in reducing plasma triglycerides23 and indicate that DPA may have a specific inhibitory effect of on platelet aggregation.24

    PHYSIOLOGICAL EFFECTS OF INDIVIDUAL LONG CHAIN omega‐3 PUFA

    At this stage, the individual roles of EPA and DHA in mediating the health benefits attributed to LC omega‐3 PUFA are still poorly understood. DHA is a key component of cell membranes, particularly in the nervous system,15 and may influence the genetic expression of many mediators of metabolic functions through effects on transcription.16 EPA can also influence a wide range of physiological functions by substituting for AA as the primary substrate for the synthesis of a vast family of eicosanoids.17 This includes prostaglandins, leukotrienes and thromboxane, which mediate essential circulatory and immune functions. Moreover, both EPA and DHA are substrates for the recently identified resolvins which are important for tissue repair and immunity.18 Whether DPA has an equivalent sphere of influence is yet to be determined.

    A ROLE FOR DPA?

    It appears that DPA is the main end‐point in the conversion of dietary LNA to LC omega‐3 PUFA in humans.8, 9 Thus its physiological effects may be of significance not only to meat‐eaters but also to vegetarians whose sole source of LC omega‐3 PUFA is conversion from LNA. It has been estimated that 8% of ingested LNA is converted to both EPA and DPA but less than 0.1% is finally converted through to DHA.8, 9 Perhaps DHA accumulates in tissue pools with slower turnover such that the ongoing requirement for DHA is less than for EPA and DPA. This appears to be the case in erythrocytes, where DHA is bound to the inner layer of the plasma membrane and has a slower turnover than EPA which is bound to the outer layer and presumably more accessible to phospholipase activation.25"
     
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  15. Dan2

    Dan2 New Member

    A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846864/pdf/1475-2891-9-10.pdf

    on page 4

    Screen shot 2020-06-16 at 2.55.39 PM.png



    on page 5

    Screen shot 2020-06-16 at 2.59.17 PM.png


    So how efficient is the conversion of EPA and DPA into DHA stored in the brain? And so by eating the amounts of EPA, DPA, and DHA in grass fed red meat, even though there isn't a lot of DHA in the meat compared to fish, what about the total EPA+DPA+DHA and conversion to and storage as DHA?
     
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  16. JanSz

    JanSz Gold

    Correcting high Omega 6/3 ratio

    What are the optimal Omega 3, 6, and 9 levels and ratios, and how (average person)(not a researcher) should pursue achieving them?
    ---------
    DHA
    AA
    Oleic acid
    --------------
    I think of DHA and AA as tiny wires carrying information (DHA smaller than AA)(highly important but small) and Oleic acid as a major wire carrying power. Most of the 13Kwh of energy that we spend daily just staying at rest, up to 3x that much is used when working, it comes via Oleic acid.
    --------------
    Oleic acid is a small part of the 2000 calories/day that comes from the food we eat.
    2000 calories =0.00023 kWh
    https://www.theunitconverter.com/ki...ersion/2000-kilocalorie-to-kilowatt-hour.html
    .............
    The rest (almost all) is not coming from the sunlight but is coming from the oxygen in the air we breathe.
    -------------
     
  17. JanSz

    JanSz Gold

    Correcting high Omega 6/3 ratio
    ........
    On some of the initial posts on this board, when @Jack Kruse was starting his board, he explained methods of supporting desirable thoughts.
    .......
    I suspect that just framing the subject of discussion as an Omega 6/3 ratio may be counterproductive from point of view of a health seeker.

    OTOH, it is great from pov of someone who may be, directly or indirectly, financially profiting from it sells.

    ....
     
  18. Dan2

    Dan2 New Member

    I went to a Russian grocery store today and found smoked whole Baltic smelt (without guts) -- made with just the fish, salt, and wood smoke -- sold loose by the pound, imported from Ukraine. Enough to fill an 8 cup mixing bowl cost $20. My new favorite snack food.

    My point is, Russian or Eastern Europran groceries might be a good place to find coldwater high-DHA smoked fish for a good price.

    Screen shot 2020-07-03 at 7.11.41 PM.png

    (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306022/)
     
    Last edited: Jul 4, 2020
  19. Dan2

    Dan2 New Member

    @JanSz
    You said you're interested in learning more about CAC. This presentation about it by a doctor with ~30 years experience using it was just uploaded by Low Carb Down Under.

     
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