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Take It Slow

Discussion in 'My Optimal Journal' started by yewwei.tan, Jan 22, 2014.

  1. Christos

    Christos New Member

    "The Biology of Carbon Dioxide" was very interesting. I immediately thought about CT and free diving and its relation to CO2. In this blog, http://raypeat.com/articles/articles/co2.shtml, Ray talks about how mitochondria uncoupling increases CO2 production and the relation of CO2 for hibernation, thus linking to CT. Hows Lings response to Ray about Lings accomplishment.... "you didnt realize science was about money and prestige"... that sums up academia I suppose.
  2. yewwei.tan

    yewwei.tan Gold

    Cut my hair once. Never again :rofl:

    I'll only talk about CO2 here ;)

    First, it is safe to assume that the bulk of CO2 comes directly from metabolism, as well as exogenous sources (eg: high CO2 concentration in air, sitting in a High Bicarbonate concentration hot spring, etc ...). Contributions from any other sources (like the gut flora) are not significant.

    Sidenote: hyperventilation can cause loss of CO2. It is unknown how significant correcting a chronic problem like non-diaphragm driven breathing will be at maintain good CO2 levels.​

    Acute CT itself is a stressor which can induce increased metabolism, and through increased metabolism, increased CO2.

    The observations where O2 and CO2 solubility and thus concentration increase in serum are only in cases of actual hypothermia. There are times when this is usual (eg: trauma), but in what is termed 'CT' as practiced by regular folk, hypothermia is exactly the opposite of what occurs (body temp should increase or be maintain for benefit from cold exposure).

    No, I do not tie CT to CO2 :rofl:. Assuming that increasing CO2 is a desirable thing (this is another long discussion, but the research seems to point to the answer being "YES"), and someone wants to increase levels of CO2 available to their cells, then the real way to go about it will be to:

    (a) Metabolise a lot of sugars. RQ of glucose is 1.0 and fat is 0.7, and metabolism is where most people will get their CO2
    (b) Learn how to breathe properly. (bag breathing can be useful too)
    (c) Don't exercise excessively
    (d) Control their environment to be more CO2 rich. eg: bathing in CO2 or bicarbonate rich water, hyperbaric chamber with lots of CO2 (some have done up to 10% concentration), living in a CO2 rich air environment (which isn't polluted)

    Again, that is if you are trying to maximise CO2. Not saying that everyone should go about doing that :rofl:


    Personal Experiment

    As for me, my experiment is based off some really good results by eating as low fat as possible during the 2 weeks before heading to Melbourne. Basically something like 50-70g of protein from lean sources, and then rest of diet from mostly sugar, but fat intake was easily <15g. Eating was still done in a small window from about 7am to 12pm.

    Many benefits -- better vision, sustained energy, higher caloric intake (close to 3,000kcal), sustained body temp, etc ...

    No issues with hunger despite fasting 19hours while eating lots of carbs. Insulin sensitivity is obviously good enough at this point to have proper insulin control. And as Wooo! sez in article -- http://itsthewooo.blogspot.com/2015/11/hyperinsulinemic-blood-nutrient.html

    Conclusion: high insulin, and likely low FFA and disruptions of beta oxidation of fat induced by high insulin, are the real cause of being hungry. NOT low blood sugar.​

    In any case, with the success of the pilot experiment, it's probably time to run a longer experiment, on the order of at least 3 months with as low fat as possible. Pretty doable given my current circumstances, with only a few days whereby experimental conditions will not be maintained :whistle:

    The sudden increase in metabolic rate hints at many factors, most likely suppression of PUFA mobilisation, and acute improvements in Thyroid function. In any case, the main goal of the experiment is to deplete stored PUFAs to as low levels as possible. We shall see what results I get :coffee::coffee::coffee:

    Danny and fitness@home like this.
  3. thomas

    thomas Sun Worshipper

    Your knowledge of the different health variables is pretty incredible, you're way aheard of everyone. Can I call you master yew? (with this name, you seem like a martial artist:p)
  4. seanb4

    seanb4 New Member

    Very interesting, I'm enjoying your updates providing an alternative point of view.
  5. Jack Kruse

    Jack Kruse Administrator

    high insulin = A lot of UV light in the tissue.........that is what they are all missing. It is not biochemistry...........its physics at the fundamental core.

    rlee314 and Optimalbound like this.
  6. seanb4

    seanb4 New Member

    Hey, I can't find the post but I remember you saying you don't tollerate CT as well as people who have heritage in colder climates, that most likely is true but I read that high vitamin D is unhelpful to uncoupling. Could this be whats going on with you and a few others?

    You have a lot of sun/uv-b/tan/vit D. So maybe this makes uncoupling and thus CT harder?
  7. yewwei.tan

    yewwei.tan Gold

    If I'm objective, my cold tolerance was/is good by most standards. I had no problems wearing a T-shirt in 0-4C weather in Japan (at least for the first 4 days before holiday stress kicked in), have and probably can still manage 20 min cold winter ocean swims, can tolerate ice packs, etc ..... all with the appropriate flushing mechanism.

    Vit D cannot be said to be "unhelpful to uncoupling" in the context of cold stimulus. It only inhibits UCP2 (and some UCP3) activity. In this study by about 50%, '1alpha,25-dihydroxyvitamin D3 inhibits uncoupling protein 2 expression in human adipocytes' (Shi et. al., 2002) -- http://www.ncbi.nlm.nih.gov/pubmed/12223452

    UCP2 and UCP3 are, (a) Expressed mainly in non-thermogenic WAT, and (b) dependent on UCP1 activity in BAT, along with other factors like Irisin (for WAT->BAT conversion)

    UCP1 is of course, strongly activated by cold, Non-shivering thermogenesis is usually only mediated by BAT, and the studies below would indicate that all cold-induced thermoregulation is dependent on UCP1 activity as a start signal.

    - 'Only UCP1 can mediate adaptive nonshivering thermogenesis in the cold' (Golozoubova et. al., 2001) -- http://www.fasebj.org/content/15/11/2048.full
    - 'High Incidence of Metabolically Active Brown Adipose Tissue in Healthy Adult Humans' (Saito et. al., 2009) -- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699872/

    All such experiments with "Vitamin D" actually expose cells to Calcitriol, which is the active metabolite of the Cholecalciferol which we synthesise (or consume) and store. We do not know how a particular person regulates the pathways needed to activate Vitamin D, and we certainly do not know how a particular person would regulate these endogenous systems in the face of cold stress.

    Even if we get lots of Calcitriol-induced suppression of UCP2 and UCP3, the net effect on thermogenesis is unknown. eg: UCP1 activity may dominate regardless of UCP2 and UCP3 activity, or even perhaps the down-regulation of UCP2 is favourable in some fashion (eg: what if we discover UCP2 activity to be antagonistic to Irisin?).

    Whatever, there are no conclusions to be had in this regard.


    As for my own cold exposure, right now, it is nothing, and that is because:

    (a) It is not necessary for me
    (b) It may have counter-productive effects given my current PUFA depletion experiment. (There is some suggestion of cold-induced elongase activity to make new PUFAs)

    As for the PUFA depletion experiment, it is going very well. :zzz:

    - Skin and hair quality drastically improved
    - Body temperature regulation drastically improved (especially in response to extreme heat)
    - Metabolic rate drastically improved. Before I would maintain weight on about a 33 x BW_kg multiplier, so 75kg * 33 => approx 2475kcal of food a day. 1 month into the experiment, I'm not even bothering to count most days o_O, but it's easily in excess of a 40x multiplier (so at least 3,000kcal of food a day).
    - Accompanying this is a general good feeling most of the time

    Bodyweight is stable at just over 75kg for the entire month.

    Downsides come in the form of side effects from PUFA release. For example, skin elasticity and tone is better (no dry spots like before), but incidence of isolated spots of Acne has increased (which is something I always experience => indicative that it is a response to mobilised PUFA)

    Adherence was pretty good, with only 2 days out of the month having more than 8-10g of fat (kept food intake lower on those days too, so it most likely didn't affect PUFA depletion progress).

    Given the current good result, the experiment continues on :ninja:.

    [NOTE: This is not a recommendation of the PUFA depletion diet. You need to know what you're doing here (supplements are needed for maximal depletion rates), and need to know how to monitor oneself. Fast PUFA depletion also has side effects, which not every one can handle]

    Last edited: Dec 27, 2015
  8. JanSz

    JanSz Gold

    PUFA depletion diet.

    Wish you decided to share more. (Well you do share a lot). What, why, how.
    For now, I am assuming that you have found some excesses,
    eventually you are planning targeted replacement with the correct kind.

    Polyunsaturated fatty acid

    1 Types
    1.1 Methylene-interrupted polyenes
    1.1.1 Omega-3
    1.1.2 Omega-6
    1.1.3 Omega-9
    1.2 Conjugated fatty acids
    1.3 Other polyunsaturated fatty acids
  9. yewwei.tan

    yewwei.tan Gold

    @JanSz: my goal with PUFA depletion was to increase metabolic rate.

    This was based off observations both in rats and in humans (eg: William Brown -- http://jn.nutrition.org/content/16/6/511.full.pdf), that depletion of PUFAs in the body increased metabolic rate very significantly (in many cases by over 40%).

    That would also explain many of the observations that Denise Minger wrote about in her blog -- http://rawfoodsos.com/2015/10/06/in-defense-of-low-fat-a-call-for-some-evolution-of-thought-part-1/

    NOTE: she did comment about some diets which do contain PUFAs, but the key is quantity. I will comment on this later in this post.​

    Why a high metabolic rate is desired is a large topic that requires a lot of added explanation, which I will not do here. But if you believe that:

    (a) lots of ATP is required for maintenance of high energy
    (b) high rate of churning through metabolic products confers adaptability to changing redox demands (eg: to stabilise NAD+/NADH ratio)
    (c) metabolism as a fundamental force in overall intelligence from the cell level to the entire organism level -- http://www.basic.northwestern.edu/g-buehler/FRAME.HTM

    Then the higher the metabolism, the more adaptive the organism to any external stressors (which is the state of the current world).

    The tradeoff is increased nutrient needs, which is something I will briefly touch on later in this post.


    I will quote some of claims of the the negative effects of PUFA from Giorgi (haidut) -- https://www.raypeatforum.com/forum/viewtopic.php?t=6666#p80643

    1. PUFA inhibit pyruvate dehydrogenase (PD) - the enzyme responsible for the proper processing of carbs. Saturated fat activate PD. Things that inhibit PD will cause increased aerobic glycolisys (more lactate, less CO2) and will slow down oxidative metabolism. Things that enhance PD will generally do the opposite. While there is some small disagreement on the topic, MOST studies agree that PD is greatly suppressed in tumor tissue and greatly enhanced in healthy organisms.

    2. PUFA enhance pyruvate dehydrogenase kinase (PDK) and saturated fat inhibits it. This is the enzyme reponsible for inhibiting PD above. Again, PDK is overexpressed in tumor tissue and suppressed in healthy one.

    5. PUFA inhibit 5-alpha reductase, saturated fat enhance it. This is the enzyme responsible not only for converting T into DHT but also for converting pregnenolone into various other beneficial steroids. Thus, drugs like Finasteride not only make you impotent through decreased DHT, but also make you zombified due to inhibiting the conversion of pregnenolone into allopregnanolone. Suicidal depression and permanent impotence are known side effects of 5-alpha reductase inhibitors. Peat has said that testosterone (T) is almost as dangerous as estrogen, and the studies agree on it. Competitive, long term athletes like soccer players, basketball players, NFL players, etc have abnormally high rates of ALS and the latest research has tied it to abnormal testosterone metabolism (I think it was the fluctuations between very high and very low seen in athletes due to sporting events).​

    There are many other reasons to avoid PUFAs of all forms, but it can be argued that the main problems occur at the mitochondrial and immune system level. For a mitochondrial effect primer, Petro @ Hyperlipid is a good read (he is of course, very anti PUFA):

    - http://high-fat-nutrition.blogspot.com/2015/10/protons-and-ultra-low-fat-once-more.html
    - http://high-fat-nutrition.blogspot.com/2012/11/protons-physiological-insulin.html
    - http://high-fat-nutrition.blogspot.com/2012/08/protons-fadh2nadh-ratios-and-mufa.html

    The claims of "immune suppressive" effects of n-6 and n-3 PUFAs are also likely true. This applies to DHA as well, and I outline some mechanics in my (still incomplete) article -- http://tanyewwei.com/blog/dha/#isoprostanes-and-neuroprostanes:be30353b6977b7107e48806b5457b119

    There are claims of "gut resilience" in a low PUFA state. The only studies are done on rats, but "PUFA deficient" rats basically suffered less intestinal permeability to endotoxin (lipopolysaccharide), and could recover from bigger shocks: 'Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability' (Li et. al., 1990) -- http://www.ncbi.nlm.nih.gov/pubmed/2188748

    Whether or not these gut barrier protective benefits extend to humans is unknown, but given my history of gut issues, it is worth a shot given the low risk of a properly constructed PUFA depletion diet.



    As far as dietary intake goes, the fastest rate of PUFA depletion is going to be as close to zero fat, and hence close to zero PUFA, regardless of source.

    This is not strictly necessary, since any fat intake (PUFA include) which is below the level at which the body uses PUFAs will lead to depletion.

    "Depletion" isn't a good word, because it implies that PUFAs are inherently "bad for you". It refers to a reduction in body levels of PUFA to a level whereby need is exactly matched by synthesis through endogenous pathways. I referenced an in vitro study in my DHA article, showing that adipocytes can make ALL fatty acids from carbs -- http://tanyewwei.com/blog/dha/#side...-fatty-acids:be30353b6977b7107e48806b5457b119

    De novo lipogenesis (DNL) can actually make the precursors for even DHA, all in physiologically significant amounts, and therefore DHA is possibly not even essential to be obtained from the diet. Whether or not these processes occur to such a significant in vivo is actually pretty likely (see the Masai study in my article, whereby low intakes of DHA were met with higher endogenous DHA synthesis)

    Regardless, I will define the "PUFA deficient state" as one whereby most (if not all) functional needs for PUFA in the body is met through endogenous synthesis, and is therefore tightly regulated to only produce the needed amounts. Observationally, this produces a high energy flux in the organism, along with a lot of metabolic by-products (ATP and CO2), yet showing large uncoupling capacity of mitochondria to deal with thermogenic needs or substrate excess.

    Practically speaking, rat studies will show that a diet that is 15% Saturated fat (no PUFA, Saturated fat in the form of hydrogenated coconut oil), will still lead to PUFA depletion -- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216405/ . It is mainly PUFA avoidance, and not fat avoidance, that leads to PUFA depletion.

    15% is still a low fat intake, and I think some of the practices that Minger cited show good result up to a 20% fat intake. It is still a low fat diet, and we can discuss the merits of fat vs carbs separately (This will require another 20,000+ word article). Minger's article does suggest a threshold at 10% fat intake though, below which insulin sensitivity is "magically maximised". There is no proof either way, and experimentation is needed.

    Rate of PUFA depletion is an issue to consider. A near fat-free diet will lead to fastest rates of depletion, and also the most side effects from those circulating PUFAs. Everything from prostaglandin production, to liver stress, to mitochondrial Complex 1 inhibition, can result from having lots of free flowing PUFAs. Slower rates of depletion by simple removal of dietary PUFAs and MUFAs, while keeping some saturated fat intake, is the usual recommended path for anyone looking to achieve this goal.

    Technically speaking, if one is using up a large portion of dietary PUFAs before they can be stored, which will be the case in a caloric deficiency, then some low level of intake will not harm an already healthy metabolism. This may explain some of the studies that Minger discussed, whereby sometimes up to 20g of PUFA were included (while maintaining a low overall fat intake).

    Some claim that PUFA depletion is based measured by serum levels of n-9 Mead Acid. I have yet to look into this aspect, so no comment on it for now. I just use caloric intake and body temperature as a proxy for metabolic rate.


    I chose arbitrary to go for maximal rates of PUFA depletion, while monitoring varies meridians and nutrient needs. My liver and adrenals were working well prior to the experiment, so I expected to be able to handle any additional PUFA stress.

    As for nutrient needs, the most common nutritional increases come from: Vitamin B1 and B6

    Personally, what I experienced:

    - I started testing coherent for approximately 100mg of B1 and 200-300mg of B6 a day.
    - I tested for B7 about twice a week at a 10mg dose each.
    - I did not test for the commonly needed Vitamin B2.
    - Methylation support requirements went down drastically. (Manganese, Molybdenum, 5MTHF, Lithium Orotate)
    - Niacinamide anywhere from 500mg - 1500mg a day with meals
    - K2 MK4 requirements dropped to around 5mg a day (used to be 15-20mg a day)
    - Vit C, Magnesium, Zinc, and bunch of other minerals stopped testing at all (not needed)
    - Nicotine completely stopped testing coherent (prior to this, I would test ON for up to 40mg a day)
    - Protein needs and appetite went down dramatically (no meat at all except for one Christmas lunch :rofl:). Probably about 30-40g a day on average from plant sources
    - Liver meridians are much much clearer. This intervention has clearly relieved a lot of my prior liver stress (which comes back on every time I eat too much fat or protein)
    - Any form of Adrenal support herbs don't test for me anymore. Adrenal meridians have been clear all month.
    - Thyroid meridians all clear.
    - Muscle Trigger point incidence down. Flexibility and stretch-relax response much better (especially around the region of my right hip and sacral -- the thing most affected by an old L3-L4 herniation). Better muscular recovery from all of stretching, endurance, and higher tension stimulus.

    Many more ..... :p

    - The one set of meridians that test ON and OFF are lymphatic and immune system related stuff. I would guess that the immune system is trying to shake off liberated PUFAs, and is being a little over-active as a result, but I won't speculated on mechanisms. Key thing is to monitor and deal with new issues as they arise.

    In terms of dietary intake, it's basically nothing but carb sources, with whatever incidental protein comes with them. Main sources include rice, dried fruit, more rice, more fruit, more rice, random condiments, more rice, juice, riz, soft drinks, random marshmellows and gummy worms when I feel like it.
    pusheen-rice.png pusheen-rice.png pusheen-rice.png

    Probably anywhere from 600-900g of carbs depending on the day. I just adjust intake to whatever I feel like eating. Weight and waist measurements have been stable all month, so there isn't any excess storage going on. Visually speaking, I look just as lean as I usually do.

    Various experimentation has led me to eat in a small window of around 4 hours, usually 8am to 12pm. No negative side effects from the large meals.

    Random Sidenote: I did a single ketone test just for fun, after having eaten 3000+kcal of the aforementioned diet the previous day before 12pm, then took blood ketones the next day at around 6am. Meter registered 0.6mM, which is basically low-level keto :whistle:. Blood glucose back down to 4.2mM, so good luck figuring out what is happening here :ninja:. I didn't do another test since it wasn't useful anyway.​

    Shijin13, Optimalbound and seanb4 like this.
  10. JanSz

    JanSz Gold

    Can't wait for that. Please hurry.

  11. JanSz

    JanSz Gold

    Very interesting research.
    Hope that all will work for you as expected.
    Thank you for sharing.
    To figure out my Fatty Acids I use blood testing.
    You are using Biotensor Rod
    to figure out your coherence of meridians, when good you are assuming good fatty acids.
    Thank you for the details you posted on posts #965, #984.

    Wonder if you would be willing to test your Fatty Acids using blood,
    so I and possibly others could better follow your progress.

    You are going with idea that:
    De novo lipogenesis (DNL) can actually make the precursors for even DHA,
    all in physiologically significant amounts,
    and therefore DHA is possibly not even essential to be obtained from the diet.
    That is bold.
    I would not do that without reliable and rather frequent blood fatty acids testing.
    You are starting this hack fully loaded with numerous fats.
    You have mentioned elsewhere thay half life of brain DHA is over 2 years.
    I guess that you will have to do this hack for more than 2 years to draw conclussions.

    Then is that (hardly appealing) diet of rice + sugar.

    Yehuda found that to have a shot at achieving (long term) good fatty acids profile diet should contain 4:1 ratio of LA/ALA
    After that one need numerous micronutrients to facilitate further conversions.
    I check that with Spectracell Micronutrient testing.
    Then one have to hope that all works as expected, and tweak as need after each test.
    You are mentioning numerous micronutrients and start it with words:
    "- I started testing coherent for approximately......"
    How is that testing done?
    I assume you are doing all this with your Biotensor Rod?


    In terms of dietary intake, it's basically nothing but carb sources, with whatever incidental protein comes with them. Main sources include rice, dried fruit, more rice, more fruit, more rice, random condiments, more rice, juice, riz, soft drinks, random marshmellows and gummy worms when I feel like it.


    Last edited: Dec 29, 2015
    seanb4 likes this.
  12. yewwei.tan

    yewwei.tan Gold

    @JanSz: Addressing some issues:

    DHA being possibly unessential from diet

    There needs to be a definition of "essential". I cite studies in my article clearly showing that even some vegans who eat no DHA can achieve the same level of blood DHA concentration as fish eaters. Why? Because it is most likely endogenously regulated to a fair degree.

    "Need for DHA" needs to be defined. I cited studies showing DHA turnover to be 3.8 ± 1.7 mg/day, and likely with 5g of total DHA in the brain at most.

    I cannot give exact figures for retinal DHA turnover (because there isn't any research). My only estimate was that there may be 44mg of DHA in the entire retina. Daily turnover rate is unknown -- http://tanyewwei.com/blog/dha/#total-retina-dha-flux-unknown:be30353b6977b7107e48806b5457b119

    We can say that all of the brain needs can be met through endogenous synthesis alone, provided that endogenous systems are working properly.

    DHA mechanics in the brain are not well understood. Even with normal aging:
    - DHA likely increases in the hippocampus -- http://link.springer.com/article/10.1007/s11745-015-4030-z
    - while it likely decreases in the cerebellum -- http://www.ncbi.nlm.nih.gov/pubmed/12512956

    That's not even considered disease. What we see in some disease states like Alzheimer's is an accumulation of both DHA and (very harmful) DHA breakdown products. It is obviously not DHA that is the important player here -- there is some level of background inflammation, which causes a large breakdown of DHA, and increases the turnover rate for DHA. But we can also say that adding more DHA is literally adding more potentially unstable material to be broken down. Obviously, the brain depends on some essential levels of DHA for proper function, and has no choice but to supply DHA to a broken system.

    Regardless, between the low DHA flux in the brain, and the very very tight endogenous control of DHA in and out of the brain, we can definitely say that excessive DHA intake is not good for the brain.

    Whether or not DHA can be met by endogenous production will depend on the person. I will not rule out the possibility of not needing any DHA whatsoever (which will also explain the health of some vegans), but I will also say that eating say 500-1,000mg of DHA a week is likely not harmful.

    We can discuss whether DHA is needed in other tissues besides the central nervous system. I am of he opinion that it is definitely not required in any significant amount in any organ system. Probably the only system that would benefit from a little more DHA is the heart.

    The previous statement is a claim that I make based upon un-published sections of my article, and requires thousands of words to fully explain :rofl:. However, I can say that in nature, we will find DHA specifically in tissues which require High rate of switching between action and resting potential. This means high Ca2+ flux in and out of the cell (based on Gilbert Ling's work). Neurons require these sorts of operating conditions, as do very high rate-coding muscle fibers in animals like hummingbirds and rattlesnakes, and those are the tissues where we find DHA. "Less busy" tissues have no need for DHA (and this describes all the cells in our body except nervous system and cardiac muscle).

    The exact mechanics need to be elucidated (in a couple more thousand words :zzz:), but I am convinced that the clues lie in what DHA is observed to do in cell membranes and lipid rafts -- it tends to repel cholesterol and certain proteins. Whatever it is doing, it is "pushing certain things away from it", probably by virtue of the electromagnetic properties of the double bonds, and that has the net effect of getting the repelled substances to where they need to go at high rates (also explaining why DHA is useful in tissues requiring fast-action-potential).

    Sidenote: I think that DHA is the best at it's job since it has the most number of double bonds possible. I also think that you can do the same job, less efficiently, with molecules containing 4 double bonds.

    Final quote from my article:

    One thing that we do know is that DHA is probably not directly involved in any reaction (where charge transfer happens). It is so volatile to begin with, and if it were the site of energy transfer, so much of it would get degraded so quick that it's utility would be nil.​

    Observationally speaking, DHA is functionally used in phospholipid form, and in that form is highly, highly susceptible to oxidation. Again, the body obviously has to regulate the environment in which DHA is found very, very, very tightly. Eating more DHA is going to put more strain on those regulatory pathways.

    Excess is definitely bad, but "excess" is going to be vastly different for different people. If you are truly DHA deficient, then eating some to be stored for later use is probably good. If you are like me, and have had more than enough for too long, then avoidance is good. Therefore in my PUFA depletion protocol though, it is essential to remove all PUFAs, DHA included.

    As usual, I will coherence test for DHA to determine when I should eat it. It's been testing OFF for the last 4 months :zzz:. I'll wait until it goes back ON to add it back. And yes, the methodology is the biotensor rod, which I am really not going to talk about, because I have no mechanical explanation for how this works at all. All I know is that the results have been too accurate and reliable to ignore :ninja:

    I am really not concerned about testing for blood lipids. It is financially expensive, not easily accessible, and doesn't provide useful information in my context. Also note that I am 75kg while carrying around about 10kg of lipid mass (based on a DEXA scan), meaning that both blood and tissue levels of lipids are going to vary very wildly with any sort of dietary intervention since I'm not carrying around much fat stores to begin with. (Still about as lean as the pictures here -- https://forum.jackkruse.com/index.php?threads/take-it-slow.9428/page-48#post-174319)

    Sidenote: I find the blanket recommendation of the 4:1 ratio of n-6:n-3 not very useful. Clearly the absolute amounts of PUFAs matter a lot. eg: say you take someone who has 15% of blood lipids as n-6. PUFA depleting that to 5% (which is a realistic figure given the William Brown experiment) would improve the ratio dramatically without any change in n-3 levels. Also, this is a blood marker. The PUFA depletion experiments show tremendous variation between serum and tissues levels of PUFAs based on varying conditions. Anything from "get stressed => release more fats (and thus PUFAs)" to "just ate some nuts => more PUFAs transiently in blood", can skew a serum ratio dramatically just over the course of a few hours.

    I am much more concerned about the actual performance of specific organ systems. Is my brain energy point doing well? Is eyesight up to par? Can I handle digestive stresses? I can deal with emotional stressors? Is sleep good? etc ..... The answer to all of those has been 'YES' on this intervention, and consistent monitoring using my own methodologies has proven to be reliable and granular enough for me to make all the needed adjustments.


    And yes, such a dietary intervention is designed by myself, for myself, with no recommendations made to anyone else :alien:. I shall enjoy my rice.

  13. JanSz

    JanSz Gold

    You are into very important research.
    I was waiting for long time for research on fatty acids (that would sound convincing to me).
    It is unfortunate (for me) that the tests and guidance that you are using are not available to me.
    Obviously it will be nice if what you are doing will support your good health.
    If you are successful, how are you going to convey your knowledge to others?

    You said:
    I chose arbitrary to go for maximal rates of PUFA depletion,
    while monitoring varies meridians and nutrient needs.
    If I had similar plan,
    I would say:
    I chose arbitrary to go for optimal levels of fatty acids,
    while monitoring fatty acids and micro-nutrients levels (in the blood).
    I will follow xyz as optimal levels because of abc.

    Most people on this site eat lots of seafood.
    Some people posted their Fatty Acid analysis.
    Only half of them have them about right (no need for adjusting).
    The other half have excessive EPA and depressed AA (fish or fish oils are not working for them).
    You have a 50% chance to be in either group.
    Are you sure that meridian testing will give you detailed enough information?

  14. yewwei.tan

    yewwei.tan Gold

    I'm not concerned with conveying knowledge to other people ;). If people want to read and apply what I write for themselves, then that's alright. If people ignore me, that's also alright.

    "Optimal Levels" of fatty acids will vary according to the person and their environment.

    Having high PUFAs in blood and tissue is a great way to become insulin resistant, suppress hormone production, suppress immune function, slow down cell turnover, and drastically reduce metabolic rate and nutrient needs (just to name a few effects). This is a survival advantage for the many animals who rely on such adaptations to go through hibernating periods. The same mechanics applied (though to a lesser degree) to humans in pre-electric times to help them get through low light environments.

    The opposite effect is true with PUFA depletion. Hormone production and sensitivity of all forms increases, cell turnover increases, nutrient needs increase, adaptability to various stressors increases, etc .....

    Sidenote: if you follow Guenter Albretch-Bueller's cell intelligence and 'Anarchy of the Genome' works, which show that metabolism is what cells use to generate the light signals to communicate with each other, then high metabolism is the "adaptive state" whereby groups of cells relay local and global environmental information to each other, and select (and modify) the genes needed to deal with that environment.

    One can even speculate that the endotoxin resistance seen in high metabolic states is part of the repertoire of adaptations needed for fast assimilation of viral genetic components through the gut -- inevitably, there will be endotoxin exposure, and the immune system needs to be on point to deal with whatever that comes past the body's barriers, all while selecting any useful material from the environment.​

    I can comment slightly about why I think the "rate of living" hypothesis is not correct, and how cell turnover needs to be qualified according to the context. Trying to keep ubiquitination and apoptosis low is not a winning strategy for many cells, and the conditions for the cells that should not turnover, like cardiac and brain tissue, require a high metabolism (Brain tissue metabolism can be definition never be low, and even in prolonged fasting, there are huge adaptations to maintain the high energy state of the brain).

    On the other hand, if your skin cells and intestinal cells are not turning over every 1-3 days, you are in for big trouble. Even peripheral nervous system tissue is probably something that we want to be able to turnover at appropriate intervals. This applies to everything from wound healing to movement quality to gut functions (gut is heavily innervated, and needs to modify those networks accordingly). Obviously the collagen matrix and connective tissues need to be re-built on a daily basis, lest major degradation in movement occurs. Even the liver needs to turnover all it's cells every few months.

    Sidenote: given that groups of cells are more capable of responding to stimuli than single cells, and that the communication is through light (specifically 600-1200nm Red and IR wavelengths), we have a plausible way of studying organ and organism level intelligence when it comes to making decisions for organs and for the organism.

    To take some excerpts from a work-in-progress unpublished article of mine:

    What organisms need is top-down control with reliable workers, and accurate bottom-up feedback / communication mechanisms

    A cell can:

    * Take in signals from anywhere where it has both contact and a contract with
    * Decide whether to accept or reject those signals (at its boundary / membrane)
    * Send signals to anywhere it has both contact and a contract with

    eg: A "receptor" may be a contract to:

    - accept a particular signalling molecule at the membrane
    - which then performs charge donation / subtraction
    - with one or more specific quantas of energy
    - in a specific order
    - deal with the (now unneeded) molecule in some deterministic fashion to relay information back to the sender

    A robust cell is one that has the energy and intelligence to only accept the signals that are needed, while being able to defend against high-energy insults (like a cellphone signal), all while maintaining the conditions needed to modulate between resting and action potentials (only doing the work needed of it).​
    In other words, there is a sort of top-down control that determines exactly what to do next, when a "worker" cell suddenly becomes defective (eg: enough of the mitochondrial Cytochrome C Oxidase in the cell stops working due to Nitric Oxide binding). There is likely the power to replace the cell perfectly (no defects), or choose not to replace it at all (maybe there aren't enough resources), or any number of options. A system that is provided with the appropriate energy will be able to make good decisions.

    We have no way of quantifying this, but all the evidence points to the fact that such higher level coordination must exist, and that it doesn't require a brain (collections of cells will suffice).

    Metabolism of specific systems then becomes a big deal, and PUFAs play a big part in signalling the metabolic environment. (There are other factors of course, and I will not downplay the ability of certain frequencies of EMF to royally screw everything up)

    Sidenote of a Sidenote :p: I have discussed this question with @Josh (Paleo Osteo) before ... when you look at the way a "healthy death" occurs, are we seeing a suddenly deterioration of low-level cell components, or are we seeing a failure of a higher level control system?

    We know the stories of the healthy old person, with no ostensible health issues, who suddenly sees a big deterioration one day, and is suddenly dead in their sleep a month later. Somewhat similar to case of Lemmy Kilmister, who really only saw major health issues in the last 3 years of his crazy crazy life, and then suddenly died of a very quickly developing cancer.

    The question is, what is failing here? Is it,
    (a) the sub-cellular components -- like the mitochondria, or the nuclear DNA of individual cells?
    (b) some higher level control mechanism that suddenly decides to call it a day?

    I will bet that:
    - Failure of (a) will precipitate (b), and that this is the most common case in the modern world
    - (b) will happen no many how well (a) is taken care of -- all organisms are programmed to die at some point
    - (b) will maintain (a) so long as (a) is functioning above a particular energetic threshold

    ie: Ensuring a high metabolic rate by optimising (a) seems to be the key factor in healthy aging populations. Whether or not you gain this metabolic advantage through having genetically advantaged non-leaky mitochondria, or if you manage to chronically provide mitochondria with enough energy, the effect is probably going to be the same.​

    It is clear that PUFAs modulate metabolism to a large degree. Why exactly they do this, I do not know. I just list the observations to as granular a level as possible, and then try to make replicable changes to myself to produce the conditions that I want.

    Given my tropical environment and need to respond to the many stimuli of the modern world, I will opt to experiment with the route of highest metabolism for now, and reducing tissue PUFA levels seem to be a good procedure with lots of precedent successful result.

    I would contend that most people in this stressful world face the problem of a lack of system adaptability, and will benefit from a higher metabolism.

    The meridian testing seems to be very accurate in practice. Changes in energy flows between components seem to underlie all disease states. I can only speak for myself, but Josh Ferber (who taught me the skill set) has seen much success with the methodology with a large set of clients.

    As for mechanics, it is obviously light mediated, but I do not know how, nor do I really care to investigate how. Dietrich Klinghardt would suggest that it is light polarisation from both organs and meridians that is the metric for health (video below). Perhaps it is what I am detecting using the biotensor, but I do not know. So long as it is reproducible and practically valid, I shall keep it as a tool in the toolbox.

    Of course, basic subjective and objective assessments continue as well. Perceived energy levels, ability to complete challenging mental tasks, motivation to do work, etc ... all will give me enough hints to say if something I am doing is not working.

    Again, my philosophy is always going to be: If it is harmful, don't do it. But if it is not harmful, experiment aggressively. In that regard, until the PUFA depletion diet shows negative side effects (which will be detected early using my testing methodologies), I will freely experiment with it.

    Finally, the discussion of EPA, AA, and basically all fatty acids, needs to one of "regulation", not "excess". What is important is the functional use of PUFAs. ie: When they are stored as Triglycerides in adipose tissue, they are functional to a much lesser degree. (note that we have no idea to what extent adipose tissue signalling is affected by stored fatty acids, though it is likely that it is not a significant effect). When do these stored fatty acids get mobilised? What decides when to bind them to the appropriate carriers (like LysoPC)? etc ... All of these are endogenously modified processes which can make one person more able to tolerate a ton of seafood, and another to do horribly on it.

    Is seafood necessary? No answer there. Need will vary. The answer for me in the last 4-5 months has been resoundingly "NO", and I shall see if and when the light switches back to 'YES' again. (This is referring to optimal function BTW, not just essentiality -- I have been more performant without the seafood than with it, and it stems from my liver issues)

    Last edited: Dec 30, 2015
    rlee314, Torrid, Shijin13 and 7 others like this.
  15. ^ LIKE x1000
    Lahelada likes this.
  16. i believe his name is dietrich klinghardt tho
  17. Inger

    Inger Silver

    A few thoughts I got from it,
    maybe that is why Jack puts crustaceans and oysters/mussels/other shellfood on the top of his food pyramid, they do not have much fat content? But lots of minerals and other nutrients?
    If eating fatty seafood only that would give us too much PUFAs? Which maybe would work if we lived in real cold and had it raw only?
    I wonder if the amount of processing the PUFAs also matter in "our need to clear them". Cooking for sure changes PUFAs and any other fat too to some extent....
    I sure feel better when eating the fats raw...... I also do well on high seafood but I do most of it raw.
    Maybe it also is because of where I live?

    if your main calories comes from white rice etc. how do you get other minerals and nutrients that you need? Is that why you need to supplement?
    Seems kinda counter-intuitive to me...
    but maybe you do just temporarily? I would not like to be dependent of any supplements.....

    Hope you write follow ups frequently :)
    I have to smile about that you seems to try out new stuff often :) it is great, that is how we learn! Just if we change too many things too often we might have a hard time to know what really worked and how
    I hope you continue with this experiment long enough before you change something so you see the long term effects, I am curious :) :) :)
    Jonathin, Danny and seanb4 like this.
  18. Danny

    Danny New Member

    Yew... great insight! "more performant w/o seafood, and it stems from my liver issues" ... I read what you said about liver function and DHA assimilation. Do you function better when in ketosis vs. not? I am nowhere near as methodical as you... I have determined however, that I seem to function at a higher level when I eat raw seafood than cooked. I have liver/gallbladder issues as well.

    Last edited: Jan 2, 2016
  19. Danny

    Danny New Member

    I definitely function at a higher level when eating raw fats and raw seafood as well. do you prepare your own high seafood? I've had high red meat, but never seafood.

  20. Inger

    Inger Silver

    Danny, no..lol I eat a diet high in seafood, not high-seafood ;) I have not tried that yet... except of some oldish fish heads in my smoothie that smelled bad already, uh!
    Did not get any issues from them tho.. felt as good as always, weirdly!

    I was think about Yews diet prior to his new hack and it was high in canned seafood iirc...
    Which IMHO is not really natural foods for us. I use canned seafood for emergency only... It work for that but I can not imagine to live off them. No canned foods actually.
    I always prefer fresh foods... and better, raw. With fresh I do not mean it cant be aged tho.. but it has to be raw aged, with enzymes intact and bacteria and what else is in there ;)

    I also wonder if there is not a natural "fat depletion" if we eat what nature offers in season. I know seafood and meat are way less fatty in certain seasons.... means we would get months of way less fat and more protein if we lived off nature seasonally what surrounds us.
    Jack also says.. summer is not a high fat season... and I agree. For people north it would mean not many carbs as they are scarce here even in summer, but way higher protein.
    I feel great on that kind of a diet in summer I have to say.

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