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reverse electron flow

Discussion in 'Mitochondrial Rx' started by Josh (Paleo Osteo), Jan 30, 2015.

  1. i think i had this wrong to begin with, where i thought that it was only when the mitochondria was overwhelmed at cytochrome 1 electrons "backed up" and flowed backwards, reducing charge creating heaps of ROS

    in a recent thread here on t2d it was mentioned that feeding electrons into cytochrome two created the reverse flow, sending the flow back to cytochrome 1 where it can create appropriate ROS despite that cytochrome likely being broken in that context...

    is it the case that it does both, but when cty1 continues to be the site of input the ROS is overwhelming (ie fenton reaction) because delta psi decreases, and that it is appropriate ROS (ie superoxide) when the delta psi remains high due to fats (more electrons) and IR heat release to contain the charge by shrinking water micells around the mitochondria whilst being cold ?
  2. Jack Kruse

    Jack Kruse Administrator

    reverse electron flow can be a normal response to a redox shifted mitochondria. Many T2D have this.......to try to stimulate the missing superoxide burst.
  3. Shijin13

    Shijin13 Guest

    So if I understand, this is a "work around" in T2D and PCOS in an attempt to stimulate the Superoxide.......
  4. cantweight

    cantweight Gold

    Some times I think I should make a new account and post anonymously so I dont feel like a moron.....but.... I started reading trying to understand what y'all are talking about and i found this article and thought it was fascinating....got really good around page 5

    Shijin13 likes this.
  5. Jonathin

    Jonathin Gold Member

    Thanks for digging deeper in oxygen free radials. Thinking we understand something is often a mistake. I love this quote:

    "In physics the truth is rarely perfectly clear, and that is certainly universally the case in
    human affairs. Hence, what is not surrounded by uncertainty cannot be the truth."~ Richard P. Feynman ~
  6. yewwei.tan

    yewwei.tan Gold

    The way I approach this topic is first to ask: How much superoxide is needed for cellular signalling?

    I assume that evolution has gotten things yoked pretty tightly to seasonal effects, and when diet is matched to other circadian signals, the right amount of superoxide will be produced.

    Winter Time

    In a cold-adapted state, you typically live with an uncoupled metabolism. Proton gradients will be constantly kept lower, fasting blood glucose will be slightly elevated (90-110mg/dL), and in general delta-psi will be lower, which will not support reverse electron flow through Complex I, and therefore create less superoxide.

    Theoretically, it makes sense that given stronger magnetic and gravitational signalling effects during the winter season, along with a slightly reduced waking time, that less superoxide is needed.

    The cellular response to those winter conditions would then be to reduce delta psi, which prevents superoxide generation via reverse electron flow through Complex I.

    Winter also traditionally went hand-in-hand with more fasting and less food in general, which both tend to reduce delta psi and prevent reverse electron flow through Complex I.

    Summer Time

    In this case, food is usually more abundant, and carbohydrate consumption increases. There is typically sufficient amount of pyruvate being pushed through Complex I in the forward direction to generate enough superoxide for signalling.

    Transition Periods. And the Case of Type-2 Diabetes (T2D)

    Transition seasons are problematic, because natural magnetic and electric signalling systems are in flux, while availability for dietary signalling can be pretty varied. This is when reversing electron flow through Complex I can become useful for superoxide generation.

    We need high delta-psi for this to happen. This is coupled to high insulin activity as well

    For an explanation of insulin-to-delta-psi coupling, see my notes on Petro Dobromylskyj's 'Protons (30) Uncoupling and metabolic rate in insulin resistance' -- http://tanyewwei.com/notes/hyperlipid-20131127-protons-30

    The combination of high Free Fatty Acids (FFAs) in the blood along with a sudden increase in glycolysis (through eating carbs), will lead to a sudden burst in delta-psi, and a sudden burst in superoxide generation as well due to reverse-flow through Complex I.

    That's a good way of using a limited amount of dietary carbs to produce a lot of superoxide if you ask me :p, specifically at a time when superoxide signalling is needed.

    Sidenote: the combination of high FFAs + lots of glycosis shuts down uncoupling, which means less free IR heat being produced. This probably explains why I consistently felt colder after eating carbs while in Japan (winter time when I was there) -- http://forum.jackkruse.com/index.php?threads/take-it-slow.9428/page-33#post-148967

    The problem with T2D is that you have depressed insulin signalling capabilities, and likely experience the Crabtree effect (again Petro delivers) -- http://high-fat-nutrition.blogspot.com/2014/10/the-crabtree-effect-and-superoxide-in.html

    To quote from that blog (underlined sections are my additions):

    The Crabtree effect, the shutting down/mothballing of mitochondrial function, is an adaptation to oversupply of glycolysis derived substrates. It allows a limit to be set on the throughput of pyruvate to mitochondria and jettisons any excess as lactate.

    Chronic hyperglycaemia (too much glucose, as is with the case in T2D) induces the Crabtree effect and down regulates mitochondrial biogenesis, mitochondrial repair and electron transport chain function.

    In the present study the dose rate was chosen so that there was a near complete suppression of superoxide production from the ETC of the mice. Acute suppression of superoxide results in the reduced phosphorylation (reduced activation) of AMPK and increased phosphorylation of PDH, which shuts it down.

    This loss of superoxide is a short term mimic of the long term established Crabtree effect. No superoxide, no mitochondrial maintenance.

    Long term hyperglycaemic failure to generate superoxide is probably a more normal route to neurodegeneration than rotenone in most (but not all) neurodegenerate humans...

    The fall in superoxide production in diabetic tissue homogenates again pulls me back to brain function. Crabtree suppresses hyperglycaemic superoxide production, i.e. the effect is antioxidant​

    There are many, many notable points in that article, but for the sake of this discussion, I'll focus on the how to re-establish superoxide signalling when you cannot get the FFA + glycosis situation.


    At present, my answer to allow T2D patients to generate the appropriate level of superoxide is ketone generation.

    I posted in the Tensegrity #8 thread, linking to a post by Jane Plain (ItsTheWoooooo!! :p), and how MCTs have the magic 0.47 FADH:NADH ratio to stimulate insulin activity and ultimately re-establish the ability to generate superoxide -- http://forum.jackkruse.com/index.ph...sitivity-molybdenum-ubiquitin-pathways.12098/

    The full post by Wooo!! is worth reading, which focuses on how keto salts can be useful -- http://itsthewooo.blogspot.com/2014/08/keto-salts-mct-perhaps-useful-during.html#more

    Of course, inducing a natural state of ketosis through dietary and behavioural mechanisms is also a way to do that :p. We've heard that on the blog many times already :rolleyes:.

    I will add the caveat that DHA + iodine is essential, which is the topic of OSF #8 -- http://jackkruse.com/organization-structural-failure-8-ketosis-appears-fail/

    Sidenote: I am still unsure about how to approach the topic of intermittent fasting and diabetics. I have a hunch that it will be useful for the reasons given above.

    I also have a hunch that insulin-spiking using high-dose leucine and fast-acting proteins (like whey protein powders) with mild addition of carbs (say 50g) can be useful even in diabetic patients. This gets into my strategic re-feeding ideas which I mentioned in my log -- http://forum.jackkruse.com/index.php?threads/take-it-slow.9428/page-39#post-153945

    Exercise Sidenote:

    I am currently of the opinion that exercise-induced ROS signalling is matched to signalling needs of the body only for that bout of exercise. ie: In a perfectly functioning body, exercise-induced ROS production stops the moment the stimulus of exercise is over, and doesn't add to the next pool of superoxide generation beyond that.

    Of course, the stimulus of certain types of exercise like HIIT aren't lost when the exercise activity is over, which brings us to a whole other topic of how transient bursts of excess superoxide can be a hormetic stressor used to fix a broken system.

    I did a set of posts in the Tensegrity #11 thread about this topic, starting with this post -- http://forum.jackkruse.com/index.ph...omments-welcome-here.12294/page-2#post-149409


    OK. Enough morning ramblings from me :D

    Last edited: Jan 30, 2015
  7. Yew,
    awesome rundown
    Shijin13 likes this.
  8. I agree that exercise induced changes are hormetic. I have been asked to work w jack bobridge as he attempts cycling world record this year, they still perceive tbey have to train 5 times a week

    You can tinker w a datsun engine 5x a week to make the best of what you have but youre better to save for a ferrari :p
  9. ssj3

    ssj3 Silver

    But does the constant drive for year round performance create a mismatch or does it alter the cellular environment to handle it?
  10. Shijin13

    Shijin13 Guest

    @yewwei.tan Awesome sauce! Yes! I still have difficulty transitioning from Sumer to Winter. Fall's a Bitch. Winter to Spring - not so much any more.
  11. yewwei.tan

    yewwei.tan Gold

    I actually don't know the answer to this :rolleyes:

    From a purely energetic perspective, and assuming a high level of aerobic efficiency, any activity below anaerobic threshold would produce a constant amount of ROS in proportion the to amount of succinate pushed through Complex II. My personal opinion is that the system is always a little bit leaky, and that you reach a threshold where you get both excess strain on collagen tissues and excess ROS production above and beyond signalling demands.

    Short-term that is a hormetic stressor that leads to adaptations which I think are beneficial (higher autophagy rates and higher ROS scavenging rates), and long-term it's obviously not good. But if you stay below that damage threshold, I'd think that year-round activity of this sort seems fine.

    How to determine that threshold is a whole different story to which I have zero answers to. You're trying to get within striking distance of a moving target that likely has a history of flaws (injuries or neuro-muscular inefficiencies).


    Training that leads to hypertrophy I think is mediated by energy-mass equivalence. If you can provide enough energy to all tissues in the body without compromising the brain, then I don't think this is a seasonal effect per se. You could probably argue that you are "allowed to get bigger" in winter time.


    Training of CNS efficiency I think is tightly regulated by the CNS if you pay attention to the feedback loops from the CNS. This is where I think HRV and RPEs become useful, and sticking to those leading indicators of CNS fatigue will allow you to basically train ad-infinitum below the CNS efficiency threshold.

    You know, I'm starting to think that a more structured approach to utilising late season carbs is warranted during transition phases. I want to write more about this soon o_O

  12. Shijin13

    Shijin13 Guest

    Awesome.... love where you're taking us with y our musings Yew. This fall while rough was interesting. I had ZERO Desire for the late season carbs. sweet potatoes and squash held no appeal. I wonder for those of us with PCOS, T2D and other mitochondrial disorders actually begin to see a reversal when they strictly adhere to circadian cycles over time. my own experience tells me that this occurs.

    after being sick for almost two weeks - now that I'm recovering and sleeping (Even with ABX and predinsone) I've found once sleep returned BOOM I'm waking up at 530-6am no alarm clock required. Sleep is so important to healing and disease reversal. Its amazing how the smallest amount of inflammation can throw off the entire system including sleep even when you're strict about the circadian signals.

    I think @cantweight has some valuable insight here given her current biohack..... we don't need carbs in winter. the challenge is figuring out how to properly fuel the body when its in the transition when we're not optimal.

    I will say suddenly I want spinach salads with warm bacon balsamic vinaigrette topped with seafood. I think the returning to longer light cycles here in the Northern Hemisphere have triggered something in me for those early crops like spinach, brussel sprouts, cabbage, collards, broccoli and cauliflower..... so I'm going with it. Fruit has yet to trip my triggers at this point...
  13. cantweight

    cantweight Gold

    I tried a carb refeed....it went over like a fart in church.
  14. yewwei.tan

    yewwei.tan Gold

    I'm not necessarily focusing on the carbs per se when I talk about a refeed. Experiments on myself have also proven in me at least, that insulin is the main factor, regardless of carb intake.

    As stated in my first post in this thread, boosting insulin signalling is basically saying that you've raised delta-psi across cell membranes.

    Personally, I would love to do this (pretty extreme) experiment with someone who is not Leptin Sensitive (EDIT: "not Leptin Sensitive" doesn't mean someone who is really sick like a T2D, I'm talking something like 20-30lbs overweight, just starting to see negative health symptoms):
    • 10g Leucine + 30g whey together with dinner, which is eaten during the period of highest protein synthesis (last 2 hours of daylight). This will create a 2-3 hour insulin spike, which is adequate time for enhanced cellular signalling to have a significant effect
    • Ideally some HIIT before dinner if tolerated, but not needed
    • High dose bitter melon extract (at least 1g of bitters)
    • body-in-water cold thermogenesis after dinner
    • Ideally done during summer time (because I think rates of protein synthesis are higher, and people's Vit D is usually better), though I think the season doesn't matter hugely because the effects are transient.

    I'm speculating on the mechanism being increase delta-psi, more uncondensed protein polymers, increased cellular signalling, with the combination of timing during increased autophagic rates, to basically give the body a window to read and react very well to what it needs to do. Again, this assumes the building blocks like DHA are already in place.

    Sidenote: the 10g leucine is what is going to give that insulin spike without needing any carbs. TBH, this tastes really really bad o_O, which is yet another barrier to getting this experiment done ..... I actually like "natural foul-tasting" stuff like rotten fish or stinky-tofu, but this is just an artificial coat of yuck on your tongue. Same thing with stuff like keto salts :confused: (which can be added to this experimental protocol, likely to good effect)​

    There is also very clear effect of re-feeds on cell water. The clearest indicator that a re-feed went well among those who are already Leptin Sensitive is a huge increase in thirst. This is basically the same symptom you find with CT, which is why I speculate that the main driving effect is sudden uncoupling of the metabolism to liberate a lot of free heat.

    One thing that I still need to reconcile is how transient hard-and-fast insulin spikes seem to increase uncoupling, regardless of how much carbs are eaten, when I'd expect the glycosis + high FFA combo to kill uncoupling rates.

    You need leptin to signal well for these cascades to happen optimally, and the mechanisms are described in the Intermittent Fasting blog post -- http://jackkruse.com/intermittent-fasting-and-leptin/ . Still, I suspect that forcing an insulin spike can overcome this leptin insensitivity transiently, even in those who are Leptin Resistant.

    The experiment above is basically a test to:
    • Force as much autophagy as possible within the period of increased protein synthesis
    • While selectively uncondensing the appropriate (anything not fat) cells for a short period of 2-3 hours, to get them to sense the environment and respond accordingly (assumes the raw materials to respond are in place -- Epi-Paleo diet is assumed)
    • Force as much uncoupling through the CT + bitter melon combo to cause as much fat cell apoptosis as possible (fundamental way to improve leptin sensitivity)
    Addition of fast-acting carbs will likely be helpful during this experiment regardless of the season. The effects are intended to be transient, and the added boost to delta-psi and superoxide production can be helping for autophagy. The emphasis on fast-acting carbs is very important, we're talking something like 30-50g of pure dextrose powder here.


    I think the only way that I will get my experiment done is to sell it as a weight loss tool -- it will cause some serious fat loss. Time to talk to Mum and see if I can get her on board :p

    Last edited: Feb 3, 2015
    FutureVision and Danco3636 like this.
  15. Da-mo

    Da-mo Gold

    I was pretty much doing this experiment before Xmas but without the carbs. Basically a Leptin reset diet - no carbs at dinner around 5 or 6pm and straight into the cold tub with ice at 10-12degC. Sleep quality was off the planet and body fat % dropped as low as I've ever managed to get it. I'd like to do it again but this time add a workout pre-dinner.
    Also found the experiments done by Eric fascinating http://forum.jackkruse.com/index.ph...increases-adiponectin-by-62.8672/#post-150244 especially the part about nutrient partitioning and glycogen super-compensation. I'd like to try that too - but without the junk food.
    Shijin13 likes this.
  16. ssj3

    ssj3 Silver

    I not quite sure what is trying to be achieved here... but here are some notes I have:

    Protein Synthesis

    -3 pathways to stimulate mTor... mechanical stress (Erk/MAPK), leucine (PI3K), and growth factors (i.e. IGF, Insulin - hVps34 and MAP4K3).

    - mTor signalling is also dependent on cell volume.

    - Glutamine is necessary for cellular leucine uptake to activate mTOR

    - Glutamine induced cell volumisation is necessary to turn on mTOR and protein synthesis. Cellular glutamine influx and rapid efflux is coupled to leucine uptake and mTOR activation.

    -System L transporters are responsible for the influx of leucine and the other BCAAs in exchange for the efflux of other amino acids. Systems A transporters - glutamine is coupled to sodium uptake.

    - Glycine is taken up by the system A transporters. Glycine can potentially increase cell volume during leucine uptake.

    - insulin also indirectly activates leucine uptake and increases cell volumisation via glucose and amino acid uptake.

    - So to max out protein synthesis a combination of 5g Leuince, 10-15g Glutamine and 5g Glycine with fast acting hydrolates. Fast acting carbs to support also.

    I also wouldn’t be taking in a bolus of simple sugars like dextrose since they have a high osmolality which will delay gastric emptying into the small intestine… unless of course you want stomach cramps or hypoglycaemia. You could look into highly branched cyclic dextrins which will give a quick but also sustained release of glucose.

    And I have a note that IL-6 coordinates the insulin-potentiating and fat-burning effects of exercise. Very “leptin-like” in character, IL-6 functions as a sort of muscle “fuel gage”, also increases insulin sensitivity, lipolysis, and fat oxidation.
  17. yewwei.tan

    yewwei.tan Gold

    I not 100% on what exact mechanisms I'm trying to tap into either :p. All I know is that there is a certain threshold of insulin whereby lots of stuff happens, and it which is useful if used transiently (kept high for 2-3hours). Obviously it's great for weight loss in those who are leptin sensitive, and I'm just trying to tease out a framework which can be used on an intermittent basis to achieve other health outcomes.

    Personally, I'm trying to find out what is the practical minimum dose of consumables needed to achieve those effects. Then I hope to look at the observed effects to try and deduce plausible mechanisms from what is observed to be true, and then hopefully formally something that can be used for sick populations.

    With that said, thanks for the leads :D. I'll definitely be taking those mechanisms into account during my readings and musings.


    Good point on the combo for maximal insulin spiking. That's useful in quantifying the minimal food intake to spike insulin (if you call amino acids "food" ;))

    I've personally done something like 60-100g whey protein together with my 10g dose of leucine, which at the high end, gives a dose of 21g leucine, 19g of glutamic acid (requires enzyme reduction to glutamine), and 2g Glycine.

    Sidenote: my personal experiments were mostly done using this WPI -- https://professionalwhey.com.au/product/nz-whey-protein-isolate/

    Though I did try this hydrolysed WPI as well -- https://professionalwhey.com.au/product/hydrolysed-wpi/ , which would theoretically get into the bloodstream faster. It tastes like crap though :confused:


    Good point on dextrose regarding gastric emptying :D. I think I've confounded this by dramatically increasing my water intake during such re-feeds in preparation for the increased thirst that I know I'll experience.

    I've definitely drank an additional 1L to 1.5L of water during such re-feeds. Plus I would take the leucine + whey + dextrose combo first thing in the meal on a relatively empty stomach (last meal at least 4 hours prior), along with the water, which I would think counteracts any osmolatily increase from the dextrose, as well as prevent any other food from slowing uptake of said dextrose.

  18. Jack Kruse

    Jack Kruse Administrator

  19. ssj3

    ssj3 Silver

    Well personally I don't like the idea of going down this path to achieve fat loss. There are so many more important things to consider... get your environment right, build better habits, get lifestyle in check, etc.

    Only then can I see the need to flood the body with designer products like this if you are trying to max out muscle growth, trying to achieve a freakishly low body fat % (and already low) and are frequently taking a beating with some high volume programming. Eat real food and lots of it.... I see a consistent theme that concerns me through a lot of these threads to try to survive while eating less. Calories may not matter per se but I don't think that means to not flood the body with as much quality seasonal food as possible. Then as the seasons change you will be able to reap the benefits of natural changes in intake.

    BTW... I think that the dextrose will slow gastric emptying of everything else you take with it like the whey.

    Here are some cites that will hopefully help you:

    Terzis G, Georgiadis G, Stratakos G, Vogiatzis I, Kavouras S, Manta P, et al. Resistance exercise-induced increase in muscle mass correlates with p70S6 kinase phosphorylation in human subjects. Eur J Appl Physiol 2008;102:145-52.
    Chesley A, MacDougall JD, Tarnopolsky MA, Atkinson SA, Smith K. Changes in human muscle protein synthesis after resistance exercise. J Appl Physiol 1992;73:1383-8.
    Phillips SM, Tipton KD, Aarsland A, Wolf SE, Wolfe RR. Mixed muscle protein synthesis and breakdown after resistance exercise in humans. Am J Physiol 1997;273:E99-107.
    Tipton KD, Ferrando AA, Phillips SM, Doyle D, Jr., Wolfe RR. Postexercise net protein synthesis in human muscle from orally administered amino acids. Am J Physiol 1999;276:E628-E634.
    Baar K. The signaling underlying FITness. Appl Physiol Nutr Metab 2009;34:411-9.
    Baar K, Esser K. Phosphorylation of p70(S6k) correlates with increased skeletal muscle mass following resistance exercise. Am J Physiol 1999;276:C120-C127.
    Schliess F, Richter L, vom DS, Haussinger D. Cell hydration and mTOR-dependent signalling. Acta Physiol (Oxf) 2006;187:223-9.
    Fumarola C, La MS, Guidotti GG. Amino acid signaling through the mammalian target of rapamycin (mTOR) pathway: Role of glutamine and of cell shrinkage. J Cell Physiol 2005;204:155-65.
    Nicklin P, Bergman P, Zhang B, Triantafellow E, Wang H, Nyfeler B, et al. Bidirectional transport of amino acids regulates mTOR and autophagy. Cell 2009;136:521-34.
    Drummond MJ, Glynn EL, Fry CS, Timmerman KL, Volpi E, Rasmussen BB. An increase in essential amino acid availability upregulates amino acid transporter expression in human skeletal muscle. Am J Physiol Endocrinol Metab 2010;298:E1011-E1018.
    Heublein S, Kazi S, Ogmundsdottir MH, Attwood EV, Kala S, Boyd CA, et al. Proton-assisted amino-acid transporters are conserved regulators of proliferation and amino-acid-dependent mTORC1 activation. Oncogene 2010;29:4068-79.
    Hundal HS, Taylor PM. Amino acid transceptors: gate keepers of nutrient exchange and regulators of nutrient signaling. Am J Physiol Endocrinol Metab 2009;296:E603-E613.
    Hyde R, Taylor PM, Hundal HS. Amino acid transporters: roles in amino acid sensing and signalling in animal cells. Biochem J 2003;373:1-18.
    Zhong Z, Wheeler MD, Li X, Froh M, Schemmer P, Yin M, et al. L-Glycine: a novel antiinflammatory, immunomodulatory, and cytoprotective agent. Curr Opin Clin Nutr Metab Care 2003;6:229-40.
    Hyde R, Peyrollier K, Hundal HS. Insulin promotes the cell surface recruitment of the SAT2/ATA2 system A amino acid transporter from an endosomal compartment in skeletal muscle cells. J Biol Chem 2002;277:13628-34.
    Takii H, Takii NY, Kometani T, Nishimura T, Nakae T, Kuriki T, et al. Fluids containing a highly branched cyclic dextrin influence the gastric emptying rate. Int J Sports Med 2005;26:314-9
  20. yewwei.tan

    yewwei.tan Gold

    Gotcha, time to clarify motivations then .... :p

    The use of processed agents are for the purpose of experiments, that I hope to use to figure the empirical effects of transient high insulin spikes. My first post in this thread, hinted at the fact that I think forcible manipulation of insulin could be a way to improve cellular signalling, which would lead to better health outcomes -- http://forum.jackkruse.com/index.php?threads/reverse-electron-flow.12744/#post-154437

    To be clear, these are experiments, and I am not recommending that anyone do them yet (I am performing some of these on myself, and for that readers can follow my log :D).

    Fat loss is a side effect IMO :cool:. I still think the underlying mechanism is a sudden rise in the rate of uncoupling, and anything that raises uncoupling rate I want to see if I can safely utilise to get rid of excess proton stores. Excess protons is a problem that many people have, and getting to an easy-to-use mechanism to get rid of those excess proton stores is the goal.

    Fat loss in the form of fat cell apoptosis is also a fundamental way to improve Leptin Sensitivity. Cold Thermogenesis does this, and the basic mechanism is stimulation of metabolic uncoupling. Well-timed insulin spikes during periods of high protein synthesis may be another way to get this effect.

    Also, anything that stimulates loss in mass must also necessarily be affecting energy somehow. So the natural train of thought is: "Do transient insulin spikes lead to better cellular signalling and therefore improve cellular energetics, therefore causing loss of mass? o_O", and "Does the transient nature of these spikes limit any potential for harm?"

    Those questions need to be considered separately for people in different states of health of course.

    The motivation here can kinda be described as getting better body composition, but I think that's a side effect of getting better cellular energetics. The goal is definitely still to increase energy within the body, usually with the effect of losing mass. I definitely do not view this as a way to strategically concentrate energy to muscles :eek:

    Practically speaking, I'm hoping something like 30g whey + some honey + some fruit + some milk blended up into a shake achieves the desired effect.

    Empirically speaking, protocols like Carb Back-loading, which utilise the same mechanisms, work tremendously well as a weight loss strategy in Leptin Sensitive people. Reconciling this carb-heavy approach with the cellular energetics angle requires some experimentation (hence the use of insulin-spiking proteins to achieve the effects of high insulin without carbs)


    The frequency of such insulin spiking has not yet been discussed properly. The seasonal considerations have also not yet been discussed properly. That's because I'm still not yet sure enough of mechanisms to discuss that :confused: (though I have my guesses)


    There is no suggestion to limit total food intake. The experiment is simply to create insulin spikes using particular insulin-stimulating foods at a particular time of the day.

    In my personal case, and the case of one of my good buddies (not on the forum :rolleyes:), I'm seeing the ability to maintain food intake quantity while losing weight using this strategy. If I can work out a mechanistic explanation for that, it would be a great way to get more high quality food while improving cellular energetics.


    The dextrose was just raised as a hypothetical carb source for experimentation purposes. As you point out, it's probably not a good substance even for that purpose :confused:.


    Hope that clears some things up :D


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