From my reading I don’t think it is possible, but I’m open to learning how one can achieve a zero carbohydrate diet using only plant foods. @Resonosity@lemmy.dbzer0.com has graciously offered to look into the matter.

Motivation - Why zero carb matters:

  • Carbohydrates end up in the blood stream as glucose
  • blood glucose is a direct driver of insulin
  • persistently elevated insulin is a serious health concern
  • cancers can only metabolize glucose, and cannot perform oxidative phosphorylation - i.e. they only run on glucose, so carbohydrates feed cancers.

why chronic hyperinsulinemia is bad:

  • type 2 diabetes
  • high blood pressure
  • atherosclerosis
  • pcos
  • visceral fat
  • ectopic fat (i.e. snoring)

Functional differences between pbf and abf:

  • plant sterols interfere with human cholesterol signaling, we are made of cholesterol, this leads to higher inflammation and lower ldl (that is actually a bad thing)
  • lectins and inflammation - most pbf have lectins inside of them, these lectins bind to cells throughout the body which leads to autoimmune responses (from mild inflammation, to full anaphylactic shock)

nice to have’s on a zero carb diet:

  • local food that doesn’t have to be shipped around the world
  • regenerative agriculture, there is no top soil without ruminants
  • farming without external inputs like industrial fertilizer
  • food without pesticide residue
  • jet@hackertalks.comOPM
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    2 months ago

    Glucose Tolerance - We see human’s exhibit similar glucose tolerance issues on a keto diet. Just as with the mice in this study, reintroducing glucose resolve the glucose tolerance sensitivity. In humans, at least, the pancreas keeps a reserve of insulin ready when in demand, and in a persistent ketogenic state this reserve isn’t required - so when exogenous glucose is reintroduced it takes a day or two to refill the reserve and get “normal” glucose response. The authors of this study even demonstrated reversal of glucose tolerance in mice when keto was discontinued (consistent with the behavior in humans) https://www.eurekalert.org/news-releases/1102798 BUT they didn’t document this in the paper… calling this glucose dysregulation is disingenuous - The fact they don’t mention the human equivalent studies on this topic is telling.


    Adam Wolfberg, MD, MPH, Chief Medical Officer at Virta, who was not involved in this study, emphasized that “mice are not small humans.“

    Mice have very different metabolism then humans, they produce ketones using different pathways with different feedback loops.


    Who thought it was a good idea to give mice a 90% fat diet? This isn’t the practice in human ketogenic diets. And the fat source is industrial seed oils, thats a huge confounder as previous studies have demonstrated seed oils by themselves can impact fat metabolism.

    Regardless the hyperlipidemia and liver dysfunction are mechanisms we don’t see in humans on keto - in fact human studies show the opposite - total resolution of NAFLD, and the researches replicated the same issue on a non-keto 90% fat diet in mice… that suggests keto is not the key mechanism of action in this mouse study… so the mice are behaving totally different then the humans.


    MD Schur also covered this paper - https://youtu.be/-eA42CbEB8k


    TLDR - This study is interesting in mice, but the applicability to humans is minimal, especially as it contradicts already established human studies using a well formulated ketogenic diet (i.e. not 90% fat). I imagine if we put humans on a 90% fat diet this study could be more relevant, but no one is suggesting that.

    @forbidden_lands@quokk.au

    Thank you for the paper, I think its a good exercise to see how the literature can be weaponized to say things like :

    I wouldn’t recommend low carb diets for the long term. If you don’t use the insulin secretion mechanism for a long time, it stops working.

    • xep@discuss.onlineM
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      2 months ago

      https://pmc.ncbi.nlm.nih.gov/articles/PMC3488544/

      As a model of human obesity and insulin resistance, however, it suffers from the severe, if under-emphasized, limitation that high-fat diets do not generally cause these conditions in humans unless the diets are also high in carbohydrate.

      Mice physiology differs considerably from humans, especially C57Bl/6.

      Here is a narrative review of the KD in human beings with Type 2 Diabetes. The effects seen in mice are not typically observed: https://pmc.ncbi.nlm.nih.gov/articles/PMC12899706/

      The primary concern is muscle loss.

      • jet@hackertalks.comOPM
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        2 months ago

        I never claimed the glucose intolerance was permanent. I even gave my reason why it’s not ideal (though temporary)

        If you don’t use the insulin secretion mechanism for a long time, it stops working. - https://quokk.au/comment/4376475

        I may not be the best at English, but yes, you did.

        I said if you are not metabolically flexible even mundane things like tasting a donut on a long term keto diet can be dangerous.

        If your not consuming blood glucose spiking food, you don’t need the extra insulin. The total area under the curve of elevation is the key to glycation damage in the body - so low overall blood glucose is better then constantly spike your blood glucose (since there will be more time of elevated blood glucose). The fact people rebuild their insulin cache when eating carbs isn’t some dangerous thing in a healthy metabolic context. However, I’ll concede this is a matter of opinion.

        Why do you still keep posting it so many times?

        2 days ago, you are the one necroing a old post to continue a unproductive discussion.

        Regardless, even though I have found the last few of our interactions frustrating and unproductive - I respect you, and I want to thank you for taking the time to raise your concerns.

          • jet@hackertalks.comOPM
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            2 months ago

            I didn’t say it stops working permanently. At least that was my intention.

            That is the tricky part about communication, it’s not what is intended.

            It’s nice in theory but you have to prove that it’s significant on a wfpb diets which I am on and significant among all other factors that are working to age you and kill you. Spoilers: it’s not.

            I’m not against wfpb, I’m not saying anything about pbf. I’m talking about elevated glucose.

            Same.

            Great!

            conclusions drawn by the actual scientists writing the papers over the “analysis and rebuttals” some drunk down the street.

            The problem is your implying that the people writing papers that show benefit to keto are the “drunks down the street”, the references I gave you are the people writing papers, peer reviewed, medical doctors and everything, but this type of rebuttle is dismissive and a bit insulting.

            Which you conveniently skipped past.

            I didn’t skip past, I provided you other experts meeting your criteria, which you didn’t acknowledge. Which should at least demonstrate people involved in this publishing space are of at least two minds.

            So I assume you’re not an expert in this field. You are likely an IT with some data science or ml background if I were to guess.

            If your not willing to discuss things with me openly and honestly, why are you here? Sure you can point out the pbf group nutrition facts.org doesn’t like keto. I acknowledge they don’t like it. Fair enough, but I also have a bevy of research scientists and medical doctors who are seeing measurable benefits in human patient populations, and I’m happy to talk about that. But if we can’t talk about the papers, or data, and only pointing to third parties… why are we here in a discussion group?

              • jet@hackertalks.comOPM
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                2 months ago

                I don’t think I’ve been dishonest which you keep accusing me of. It’s only that you want to discuss the content of the papers and I am not interested.

                Fair enough. Doesn’t sound like we have anything to talk about. I acknowledge you have experts you trust who don’t like keto.

                It is a dishonest rhetorical tool, however, to drop a paper in a conversation as a “I win mechanic”, but be unwilling to read (the whole paper) or engage in a discussion of it. It would be more honest to simply link to a Dr. Gregor opinion piece, then it would be clear what is driving the opinion. It’s also vexing because I printed out the paper, read it, marked it up, and wrote up my thoughts so that we could talk about it, only to be met with “Well, I don’t actually read or talk about papers, even the one i referenced”

                I was taking the simpler and better path by pointing to the consensus of experts which wikipedia normally represents. And I’ve cited the Stanford encyclopedia of philosophy why it’s a valid path of inquiry.

                That’s fine too! I hope your pbf journey is fruitful and long term.

                Consensus beats a minority position among experts. I don’t dispute there are short term benefits to keto. That’s been proven.

                If your driven by consensus, great, I’m glad that is working for you. I only took umbrage at the demonstrably false, and inflammatory, statement at the top of this thread.


                I don’t really enjoy these non-productive non-constructive dialogs. That is why I dropped the thread 48 hours ago. I propose we just let bygones be bygones and be done with it.

                  • jet@hackertalks.comOPM
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                    2 months ago

                    Anyone well versed in the scientic method and philosophy of science knows that the consensus is statistically the least likely to be wrong.

                    I agree that is the scientic method indeed.

                    There are long term risks to a keto diet that people need to be aware of. Period.

                    Great, provide the evidence, make a post about it, and most importantly engage in the discussion.

                    I don’t care much about that one paper or Dr Greger which you have spent all the time addressing.

                    Don’t cite shit you don’t care about.

                    Dr. Greger RUNS nutritionfacts.org the source you cited and hold in high esteem- https://nutritionfacts.org/ i.e. the experts you trust, yet don’t care about…

    • jet@hackertalks.comOPM
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      2 months ago

      If we look up the mouse diet used - D16062902

      • 90% of calories from fat
      • Fat source dominated by soybean oil (very high in linoleic acid, omega-6 PUFA)
      • Extremely poor omega-6:omega-3 ratio
      • 10% protein (low for mice)
      • Virtually no carbs and no fiber

      I don’t think a high PUFA diet really is in the universe of anyone doing nutritional ketosis.

      This study is really a study of a 90% industrial seed oil on mice…