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Tyw. Said Something That Makes Alot Of Sense!

Discussion in 'Diet' started by beachbum, Mar 1, 2017.

  1. beachbum

    beachbum Member

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    I have been reading and thinking ALOT of insulin, fat, sugar, starch, so on. I am confused but not . Like Tyw says many times in his posts to experiment with foods and I guess supplements too ( not sure) at least the food part. I too believe the key is stress. I believe insulin is the number one in line to control. It seems eveything I read says insulin this and that along with FFA. If insulin is messed up there goes the stress hormones that mess up the other hormones that we are trying to keep in check..right? Just my thoughts.:rolleyes:

    Now I have a question. Can you be insulin resistant and sensitive at the same time.
     
  2. Agent207

    Agent207 Member

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    Yes, sensivity varies depending on tissue.
     
  3. haidut

    haidut Member

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    The problem is that it is a chicken-and-egg issue. Why is insulin high? Usually because of cortisol and elevated FFA. Lowering insulin was already tried medically and it badly backfired. The drugs for lowering cortisol seem to reverse insulin resistance without causing much side effects. Now, cortisol may be high for other reasons like inflammation, but that brings us back to PUFA. So, it is hard to just "eat what does not cause you stress" when your health is compromised because most things will cause stress in state like that. Slowly getting rid of PUFA seems paramount, while also adding saturated fat to change the tissue balance as much as possible. Once you are in a decent SFA/PUFA ratio you can probably fast and exercise if you want to and it should not cause much stress while still leading to weight loss and improved insulin sensitivity.
     
  4. beachbum

    beachbum Member

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    I just read an art
    Very well put. Thank you. I also just read about insulin sensitivity and always thought that was a bad thing only if it is way to low or to high but I finally understand the difference between sensitivity and resistance. As from what you wrote above it looks like inflammation aka stress etc, lack of exercise and the big bad boy PUFA. Why do alot of studies say SFA also causes resistance..yes/no or am I reading it wrong. Thank you again
     
  5. haidut

    haidut Member

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    SFA can also cause resistance if you are overloaded with them but this is simply due to the Randle cycle at work - i.e. if a person is obese but with SFA in their fat tissue, there will probably be a high FFA level in the blood and low glucose oxidation. But unlike PUFA, SFA does not act as insulin receptor antagonist and does not lead to the inflammation (at least not nearly as much) that PUFA causes. Since fats also act like hormones, the endocrine effects of fat also matter. The SFA does not have the estrogenic, serotonergic or aldosterone properties that PUFA seems to have. Peat did say in a quote lingering somewhere on this forum that even if one oxidizes fully saturated fat it still puts the body in a stress-like state but it is a lot less stressful compared to PUFA burning.
    What Are Good Ways To Increase Insulin Sensitivity?
    "..."Just about everything that goes wrong involves FFA increase. If they are totally saturated fatty acids, such as from coconut oil and butter, those are less harmful, but they still tend to shift the mitochondrial cellular metabolism away from using glucose and fructose and turning on various stress related things; By lowering the carbon dioxide production I think is the main mechanism."-RP
     
  6. Ideonaut

    Ideonaut Member

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    An in-a-nutshell statement of great utility. As far as I am concerned, your brilliant contributions make this the best site on the internet. Thanks, Haidut! (As I head to the cupboard to grab some hydrogenated coconut oil.)
     
  7. beachbum

    beachbum Member

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    :+1:thumbup
     
  8. Drareg

    Drareg Member

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    If the body gets fat does it inherently know it's beyond its preferred weight?

    If it realises it's beyond its ideal weight somehow ,does it start to preferentially burn the fat to get back to the ideal weight? Get balanced,is it striving to get balanced?
    Observing French people eat has made me curious about this,the people I watch are not fat but will eat cream,cheeses etc and stop for a day or two,maybe a week,it's all feel and instinct with them.
    In obese countries we don't stop the next day after a big fat load the day before,we do nothing that merits the extra fat but just eat because we normally eat at set time,more fat gets piled on and now we have new layer that needs to get burned off compared to the previous set point.
    Does the body then begin to form new set points because the previous fat state was better than the new fatter state?

    While this is going on it has a glitch relative to glucose,it knows it has to burn fat to be in the balanced state again so as time passes and you get fatter the ratio of glucose burning to fat changes,more fat the more desperate the body gets to burn it so ups the focus on fat metabolism.
    At the start the ratio was lower and all you needed to do was check fat for a few days.


    Their are a lot of underlying patterns that build over time in the human organism,the environment layers them on, is it possible that the organism knows a better state,balanced state or ideal state?
    We don't like aging,we look our best at certain body fat percentages,all this can be influenced by culture and ego but I think the body knows it shouldn't be getting into these states,consciousness knows better maybe?
     
  9. tyw

    tyw Member

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    Context always matters o_O

    Insulin is just a signalling molecule, and is a part of an integrated system of endogenous regulation. There cannot be a discussion about insulin without a discussion of the existing context, existing constraints, existing demands, and desired end state.

    There must also be an understanding of what exactly insulin does. I've linked to Chris Masterjohn's podcast about Insulin Resistance before, and here it is again -- https://chrismasterjohnphd.com/2016/08/24/insulin-resistance-isnt-all-about-carbs-and-insulin/

    Regarding the points of @haidut

    Completely False. Insulin is high because you eat something. Eating any food at all will raise insulin levels. Sure, fatty foods do not require nearly as much of an insulin response as high carb foods, but insulin goes up way above fasting levels with any food intake whatsoever -- *The Scribble Pad*: Dietary fat is insulinogenic. Sorry, guys.

    Again, context matters. Give somebody nothing to eat for 2 days. Cortisol is high, FFA is high, insulin is at rock-bottom levels .... similarly, put someone on a diet that is 80% calories by fat (the classic ketogenic diet), feed them to eucaloric sufficiency, and systemic insulin release is going to be very low.

    Sure, you take an obese diabetic eating a 30% carb, 50% fat diet, and their insulin regulation is screwed. No amount of cortisol reducing interventions is going to trump the body's need to secrete insulin like hell to deal with those carbohydrates.

    Or how about take an obese person, put them on a ketogenic diet, induce physiologic insulin resistance, which thereby prevents net ingress of calories into fatty tissue, thereby causing easy loss of that fatty tissue. ie: When trying to lose weight, it is a good thing to be insulin resistant in fat tissue. Insulin is a signal to "put energy into the cell". Why do you want to put energy into fat cells when trying to lose fat? Context is Everything.


    False. Cortisol is high because the body is demanding more energy than existing transient supplies can handle. ie: stress (credit to PaleoOsteo) -- Stress is defined as any time when the needs of the body outweigh its resources.

    Exercise hard for an hour, cortisol rises to meet energetic demand. The rest of the catecholamines should also be included in this mix, and all signal the body to use all fuels -- carbs, fat, and if needed, amino acids from protein breakdown.

    Once the stressor is gone, and demands are back to baseline, the body no longer needs to signal extra energy, and things go back to normal.

    PUFA should barely even enter the discussion ..... or put differently, let's assume that you have someone who is perfectly PUFA depleted. Then, put them through those crazy tough mudder challenges where they exercise for hours on end. Their cortisol will be through the roof, PUFA or not ..... Energetic stress drives cortisol and catecholamine signalling, not presence of PUFA.

    Note of course, that these increased energetic demands also applies to daily nonsense like being stuck in traffic, an argument with the spouse, a shitty day at work, etc, etc .... Humans have this ability to see into the future, and worry about imminent threats, which can be just as much a stressor as the real threat. (ref: Robert Sapolsky's work)


    Context please. I have provided evidence time and time again that beta oxidation of SFA blunts Insulin's function on a cell, whereas, beta oxidation of PUFA doesn't.

    The mechanics, plus actually clinical evidence for PUFA not disrupting carbohydrate metabolism, whereas SFA does, has been discussed in this thread -- How The Sugar Industry Shifted Blame To Fat

    I have also shown ample evidence that PUFA is going to be mobilised and used as energy more easily than SFA. (and note that PUFA used for energy is completely benign ... you take a fatty acid, and then turn it into nothing but NADH and FADH2) -- Need Thyroid Med HELP!

    Again, what is the context? Feed a low-PUFA, SFA-dominated, ketogenic diet to a diabetic, watch them lose fat, stay systemic insulin resistant (a good thing in the context of low glucose availability, because it spares glucose for the tissues that need it, and thus prevent the stress response), and then eventually become non-diabetic, and can transition to a different diet.

    Feed a moderate-SFA, very high-carb diet to that same diabetic, and watch them stay fat and diabetic.
    Feed a moderate-PUFA, very high-carb diet to that same diabetic, and maybe they have enough innate insulin sensitivity to recover (more on this in the next section).

    -----

    Next Insulin Sensitivity varies tremendously due to genetic factors. You can take the same people, at the same body composition, with the same diet, but with different ancestry, and you will find huge variations in amount of insulin secreted in response to carbohydrate loads.

    - Thieme E-Journals - Experimental and Clinical Endocrinology & Diabetes / Abstract
    - Ethnic differences in insulin sensitivity and beta-cell function among Asian men
    - International Journal of Obesity - Lean, nondiabetic Asian Indians have decreased insulin sensitivity and insulin clearance, and raised leptin compared to Caucasians and Chinese subjects

    We are literally looking at 2x or more times the amount of measured serum insulin needed in these cases. Some indices claim 10x differences in insulin sensitivity which we cannot explain by body composition, pancreatic function, or any other known metric.

    And of course, those who are more insulin resistant by nature tend to lose weight more easily on lower carb diets -- Insulin resistance is a spectrum

    And as much as I am a high-carb advocate, it is important to view other perspectives on this -- Hyperlipid: Protons (38) and ultra low fat once more

    In particular, I highlight the discussion about Walter Kempner's diet, which is extremely low fat, in sick (diabetic) patients, where they were losing fat (which would improve systemic insulin sensitivity).

    The observer will state:

    More than half of those 100 diabetic ricers—63%—actually saw their fasting blood sugar drop by at least 20 mg/dL during the diet. Only 15% had their blood sugar go up significantly. The remaining 22 saw little to no change.​

    The high-carb advocate will claim:

    Look! A 63% recovery rate.​

    The low-carb advocate will chastise them:

    Blood glucose: 15% of people were f*cked. 22% it didn’t help. 63% could maintain carbosis.​

    If we're being honest, we must admit that 2/3rds of people could adapt to an Insulin Sensitive phenotype, whereas the other 1/3rds could not, and were likely harmed by this sort of dietary protocol.

    See, this is why I keep calling for context, and self-experimentation ..... this was the whole point of the idea to experiment with either the very-low-fat or very-low-carb end of the spectrum, and then move towards a balance that is tolerable -- How The Sugar Industry Shifted Blame To Fat

    -----

    And this is all before even discussing insulin sensitivity in regards to circadian rhythms, organ level differences, etc ....

    ====

    Studying the Truth in order to Avoid it

    The goal is good health. You get there by avoiding the stuff that kills you. This is where the "eat what doesn't cause you stress" line comes from.

    "Drink coffee => feel anxious => do stupid things that cause more anxiety => not good", could easily be experienced by a person who is already having a bad day at work. The appropriate response may be "OK, I am aware to not drink coffee when I'm already high-strung. No extra stimulation required"

    The focus must be on Awareness and Experimentation. Knowledge is just knowledge :bag: ... knowledge is not power .... it is simply information. Perhaps that information could be useful in enhancing one's awareness of self, or in inspiring an experiment to be tried, but if not, file that information away in some easy-to-access location until it proves useful again.

    What cannot be brought to the surface in a practical form must be treated as nothing but entertainment :pompous:. Good entertainment perhaps, and perhaps useful in the way that you bring up a quote from a movie in order to break the ice, and start a deeper discussion about practical things ...... yet still remaining mere entertainment with no authority over oneself.

    .....
     
  10. Emstar1892

    Emstar1892 Member

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    Wow. What an incredible, well thought out, considered response from tyw. Just had to contribute to say that. Bye!
     
  11. beachbum

    beachbum Member

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    Tyw.. awesome job. Extremely helpful once again.
     
  12. Drareg

    Drareg Member

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    The true method of knowledge is experiment.

    Culture is stifling this kind of thinking,we now have cultures attached to fad diets, this is why Peat doesn't associate with forums like this as he mentioned,use this forum as a tool,
    The level of complexity in cell physiology allows anyone to take any angle of reductionism and claim this is the way back to good health,the complexity requires time investment from you which means money for their blog or books in most cases,trying to discern what is closer to the truth is difficult.

    Experiment requires some level of acknowledging "I am experimenting",not day dreaming supplements and thyroid are going make you into Bradley cooper from limitless.
    You must document what you experince when experimenting as honestly as possible,this forum is good for that but sometimes your own notepad is better and easier to access.

    Majority of People on here do not need much to get back to good health imo,a paradigm shift is probably the best pill you can take.
    It's good to acknowledge if you are in a job with high stress or high stress training regimes and your choosing to stay in it even after fully comprehending Peats philosophy,this can allow you to be more realistic about your approach.
    If you are older and have fallen victim to the establishment and the culture of stress,keep in mind that Peat has acknowledged several times that some damage done is extremely difficult to reverse unfortunately,goals should be more modest at this point imo.

    The goal all round should be higher intelligence imo, adjusting expectations and meanings in life are part of this.
    If you correct or balance the biochemistry yet don't change your outlook on life and keep stepping back into the same paradigm even though the brief relief allowed you see more,you run the risk of falling back to the old way of seeing the world and your biology follows.
     
  13. Strongbad

    Strongbad Member

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    Another Hall Of Fame post by none other than the most intelligent guy in the forum :) :) Thank you for a great breakdown of real-world application in terms of how insulin works. Yes, everything is about the context and real world scenario, not just Research A says X causes Y, so Y is the answer. That's overly simplistic.
     
  14. haidut

    haidut Member

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    I think you misunderstood my context in terms chronic elevation of both cortisol and insulin. Chronic pathological (outside of normal range) elevation of cortisol due to low-grade inflammation (in the absence of stressors like exercise) has nothing to do with meeting energetic demands. Chronic elevation of insulin also has nothing to do with eating. Actually, that latter point I should re-phrase to mean chronic elevated insulin even hours post-meal is elevated because the the blood glucose levels are elevated. And those blood glucose levels are elevated not because of the meal that happened 6 hours ago but because the organism tried to compensate for the increased cortisol and keep the blood sugar from going too high. The cortisol during exercise rises as much because of increased energetic demands as it does to combat the inflammation that massively increases during and post exercise. Quite a few trials have been done where organisms have been provided with enough energetic supply to meet the demands of exercise. Cortisol still rises. Why does it stay elevated for hours or even days after a serious bout of exercise? What does that have to with energetic demands given that the person has eaten after exercise and in the days following the exercise. Cortisol stays elevated even in elite runners who are highly adapted to these energetic demands and have very efficient metabolism, adapted to fat oxidation.
    NSAID drugs lower inflammation and thus cortisol in people and that includes not just aspirin, which is direct inhibitor of 11b-HSD1. What does that have to do with eating? How come they also lower insulin given that there is no known mechanism they inhibit its release? Only one options remains - i.e insulin went down because inflammation and thus cortisol went down. Why do you think anti-serotonin drugs lower insulin and restore insulin resistance even in the presence of continued obesity? Why does aspirin do the same? Only one reason - they lower cortisol. Why do you think serotonin synthesis inhibitors are succeeding in clinical trials for obesity? Did you see this post from today?
    https://raypeatforum.com/community/threads/insulin-resistance-as-an-endocrine-disorder.15840/

    Look, I get your points. The pathway are insanely complicated and we are just beginning to understand them. But the mechanisms behind stress and disease are fairly well established at this point, at least the cause-effect part. Even mainstream medicine has moved beyond arguing whether inflammation is causative in insulin resistance/diabetes. The real question is what causes that inflammation and the cortisol that comes with it, and to me PUFA and stress are the two primary factors. To your credit, a chronic infection can also do it. You don't have to agree with this, to me the evidence is clear and my own journey so far has confirmed (to me) everything that Peat has written about PUFA and its role in disease. If you come from a different angle, the right path will probably look different to you. Again, not trying to convince you in anything, this is not a political debate. But to dismiss so much evidence just because "we don't know the exact pathway" to me is unwarranted.
     
  15. tyw

    tyw Member

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    @haidut

    As always, we separately address different topics.

    ----
    Insulin Resistance (the original topic of the thread)

    We cannot simply apply simple thinking to topics like insulin resistance. So what if it an "endocrine disorder". What is driving that disorder?

    I am not dismissing any evidence whatsoever. I am taking high level mechanics (hormones), low level mechanics (mitochondria), everything in between, marrying that to circadian rhythms (which have HUGE effect on insulin activity), and then showing that one can weave an explanation that suits a particular context.

    The fact is that we have all sorts of phenotypes, and insulin resistance is just one facet of the organism as a whole, and obviously shows wildly varying levels in all sorts of different people. Or as Bill Lagakos put it:

    There are insulin sensitive obese people & IR lean people.
    Tell me again how insulin resistance causes obesity?​

    see the whole post for details -- Insulin resistance and obesity

    I am completely warranted in saying that there is no way to give generic advice regarding diet macronutrient ratios without knowing the person's context. The real world results speak for themselves, with so many different insulin sensitivity phenotypes experiencing so many different results with the same stimulus.

    ----
    Cortisol

    In clinical practice, we see all sorts of patterns that make no sense whatsoever.

    @paymanz post here is actually representative of many of the horrible cases that my doctor friends see -- Insulin Resistance As An Endocrine Disorder

    For example, one of them told me: "Super High AM, then tanked .... Most of the bad cases either have curves like this or all flat. I have never seen an upside down curve"

    Therefore, how do you know that:

    There may be a post-meal cortisol spike (which is not normal), and certainly in most cases, cortisol drops after a meal -- Cortisol responses to mental stress, exercise, and meals following caffeine intake in men and women

    See figure 1 (Cortisol responses to mental stress, exercise, and meals following caffeine intake in men and women), and note that:
    - 200mg caffeine causing increased cortisol in the face of both mental stress and exercise
    - mental stress was by far the overriding factor
    - how this sort of not-too-stressful exercise barely budges cortisol
    - how a mixed meal decreased cortisol levels

    For every study like this, I can cite another one using people in a completely different context, and show different results. (eg: chronically exercising athletes, who are consistently over-taxing their system, showing chronic cortisol dysfunction -- Increased Cortisol Production in Women Runners* | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic)

    So yes, a change in context can invalidate all mechanics. That is point that I've been trying to get across. Context-free discussions are meaningless. Context must be qualified, and then each individual can decide if the mechanics can be generalised beyond that context, and under what new conditions / constraints.

    ----

    And of course, if PUFA is such a big deal with stress, prove it ;) . Prove that there are generic mechanisms whereby PUFA is the make-it-or-break-it factor when it comes to stress, rather than just some gross trauma or energetic deficit to the tissue.

    We know the dangers of PUFA peroxidation on cell membranes, especially on high energy membranes like mitochondrial membranes. Good, scope the mechanics upon that context, and note that membrane PUFA peroxidation is bad.

    Now what? Does this randomly scale up to the inter-organ level? Of course not ...... How do we know how one person manages the PUFAs on their membranes. How do we know if they are even going to mobilise a lot of that PUFA. How do we know that they transport it into the cell. How do we differentiate between the different types of PUFA (they all have different effects). How do we know that PUFA isn't beta-oxidised instead.

    Want to talk about PUFA as hormone-like ligands? Sure, we know delve into the complicated as hell world of PPARs -- Circadian rhythms, Wnt/beta-catenin pathway and PPAR alpha/gamma profiles in diseases with primary or secondary cardiac dysfunction

    There is no answer here .... sure, we can mechanistically describe how certain PUFAs activate PPAR gamma activity (which BTW, is supposed to upregulate carbohydrate metabolism). Now what? Look at that paper, and all the life-threatening illnesses associated with PPAR gamma deficiency, and all the life-threatening illnesses associated with excess activity PPAR gamma. Screwed either way? No, this is part of a fine balancing system that is highly tuned to the context of the organism.

    The PPARs are heavily regulated by all the circadian machinery in the body -- https://www.hindawi.com/journals/ppar/2014/653017/ . RXRs, G-coupled protein receptors, etc .... They are truly "at the crossroads of circadian signalling and metabolism".

    And tying back to cortisol, look how powerful light (ie: circadian modulators) is in changing the cortisol response -- http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0155601

    Just look at Figure 3 and the huge changes in HOMA-IR just by using blue light exposure. Blue light => worst insulin sensitivity. But Blue light => less cortisol .....

    I can just as easily claim that chronic unnatural light exposure in today's world, coupled with night-time eating, is responsible for systemic Insulin Resistance. There is more than enough evidence to prove this as a dominant factor in people's lives, but it is a dominant factor in "this particular person's life"? No clue, experiment and find out.

    Context mang! :woot::woot: Take someone, deprive them of sleep for a day, and all metabolic parameters change.

    The practical takeaway from that should have been, "Night time .... Go to sleep!", instead of worrying about macronutritional balances and PUFA mechanics.

    SIDENOTE: as an aside, it is usually much better for recovery of circadian cycles, to skip eating during circadian disruption, and then re-start eating during the next circadian morning.

    This generalises to everything from staying up too late (no late night snacks), to flying across multiple time zones (try to time flight arrival in morning, do not eat along the way).​

    ----

    Mechanics be come with qualified Context :blackalien:, and that includes all up- and down-stream side effects of that particular mechanic.

    I will always err on the side of uncertainty, and never claim to generalise any mechanics beyond the exact context that there were elucidated within.

    I have also provided so much counter evidence to show how all these various mechanics at the various hierarchies of the organism can interact in seemingly wildly contradicting ways.

    eg: high serum FFA can lead to insulin resistance via the Randle Cycle (serum level). high PUFA flux through mitochondria leads to insulin sensitivity (intercellular level). Which one dominates? Dunno, ask the organism .....

    The type of narrative one wants to weave can be completely biased by working only on a particular hierarchy of the system. I'd rather stay honest and say, "wow this is complex, I try my best to tell an accurate story based on existing observations, but you guys interpret this for yourself".


    "What is the context of the mechanics I am discussing?", and of course, "How can I apply this to my life? And how do I know if the intervention is working?"

    .....
     
  16. Liubo

    Liubo Member

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    Reading one of tyw's posts is like watching a nature documentary complete with a view of the earth from outer space...you just realize how small you are in the scheme of things
     
  17. Westside PUFAs

    Westside PUFAs Member

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    zrL8_f-maxage-0.gif
     
  18. Hitoshi

    Hitoshi Member

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    Agree with @tyw that many of the Peat memes/dogma are context dependent and often plain wrong at the mechanical level. I was hoping tyw would alert to the insulin-permissive role of PUFA in this thread, as it seems a commonly held misinterpretation that it is responsible for IR, and that SFA is not. At the mitochondrial reverse flow level, the opposite is true.
    This of course is not to say pufa is nit damaging, as reverse flow is the key motochondrial signal to limit caloric ingress in order to protect mitochondria.
     
  19. nikolabeacon

    nikolabeacon Member

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    food and environment ≤=≥ digestion and internal hormonal profile and state
     
  20. Drareg

    Drareg Member

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    Your taking Peat out of context here as a has tyw on multiple occasions. Why the subtle strawmans is beyond me,subtle as in they are hidden in information overload with selective/cherry picked context ironically! Stepping back and then claiming complexity and balance adds to the confusion.

    Peat speaks about context on multiple occasions, threads like these end up going down obvious paths which is here are a load of studies for my view and for yours with little understanding of the techniques used in research,I think Chris masterjohn who works in a laboratory understands the complexity and nuances and seems to be speaking more about said topics.
    Peat mentioned some interesting points recently about the studies that make it onto pubmed not being everything we have uncovered,there is also the clear issue with funding for the other view.

    The measurement and behaviour of PUFA at the cell membrane where Peat believes it is damaging the membrane hence the speeding up is what a lot of this is based on.
    He may have recently mentioned insulins level of importance to @DaveFoster I believe?

    Peats theories evolve and are not static,no doors are closed here as more research is needed.
    To add to that I have seen nothing in any of these posts or previous that can outright refute what Peat puts forward.
    We get there are other views on what's going on in the body,at some point you must experiment,the body was functioning before we knew a lot about it and most great leaps forward were through tinkering and experiment.
    Peat calls for more experiment yet it's stifled when it doesn't fit the establishments view.

    A Peat dogma doesn't really exist imo,the term dogma gets thrown around too easily,we could start an argument about the "views " you currently support being dogma by you or others with "viewpoints".
    Using the term Peat dogma is a subtle attempt to discredit and redundant when apply the same reasoning to you and others we get dogma based on your definitions.
     
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