Calorie restriction's effect on aging

I found this blog https://www.crvitality.com/ and it says restricting your calories slows down the biological aging process. Is there any truth to this or is this just a schizo?

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  1. 3 weeks ago
    Anonymous

    probably nonsense schizo and all the alleged "advanced aging" from consuming calories are just fatties crooking at 40 due to diabete or heart attack.

    • 3 weeks ago
      Anonymous

      so what causes diabetes and heart attacks?

      explain.

      • 3 weeks ago
        Anonymous

        You missed the point. Think harder.

  2. 3 weeks ago
    Anonymous

    we only have mouse studies, it seems to correlate with protein restriction and it's the effect can be positive or negative depending on the species of mice used.
    feast and fasting cycles to make use of autophagy intuitively make sense in humans, pure caloric restriction not really aside from mass reduction, but that would screw you over past the age of 60 because sarcopenia becomes a big issue

    • 3 weeks ago
      Anonymous

      Yes, it is true. But the effect is very limited. We can achieve similar effect by dwonregulating the insulin-IGF pathway in model organisms. It leads to a pretty significant increase in lifespan for C. elegans (9x regular lifespan), but only a mild increase in mouse model (1.2x regular lifespan) and presumably the effect is even milder in humans. And of course a dietary restriction is not the same as full pathway downregulation, and the leangth of thime and the starting age of the restriction also matter. So start now and you may get an extra 1-3 years. Unless you get acid reflux from the hunger in which case you will die earlyer of cancer (damage at areas where ectoderm and endoderm meet is a common cause of cancer).
      Ageing is a complex web of interactions, if you are genuinely interested in how it works i suggest reading the review papers López-Otín et al., 2023 and Gorbunova et al., 2021. These give you the basics and you can expand from there.

      The key mechanism behind it is reducing cell proliferation which slows down epigenetic alterations, DNA damage, (the consequent loss of proteostasis) and the telomer attrition and stem cell exhaustion that result from cell division, thereby preventing the spread os senescence.

      It only works by reducing iron intake.

      No. Not only. But i am interested to hear about the connection between iron and ageing, i have not come across this throughout my research. Please elaborate.

      >eat loads of calories
      >become fat frick moron
      >die at 40 because you're a fat frick moron
      SCIENCE!

      OP was talking about the ageing process, not premature death through disease or pathology.
      The ageing process is a distinct and recogniseable molecular mechanism (well mor like 9 to 14 mechanisms all interacting), it is by no means the same as disease related death, though ageing does contribute to various disease which we call age related diseases.

  3. 3 weeks ago
    Anonymous

    It only works by reducing iron intake.

  4. 3 weeks ago
    Anonymous

    >eat loads of calories
    >become fat frick moron
    >die at 40 because you're a fat frick moron
    SCIENCE!

  5. 3 weeks ago
    Anonymous

    There's some evidence but it seems like schizobabble and pill pushing to me tbh. Gene and stem cell therapy is the way

    • 3 weeks ago
      Anonymous

      >There's some evidence
      No, there is extenisve research. Google scholar caloric restriction ageing. Gradstudent perform this experiment for shits and giggles.
      >but it seems like schizobabble
      Well sure if anyone expects any significant results in humans from "eating healthy and maintaining a diet", they are moronic. It's far more complicated then that.
      >Gene and stem cell therapy is the way
      Nah, too complicated, error prone and dangerous and expensive.
      To effectively combat ageing, you need a combiation of senolitics, transposon silencers, targeted stem cell rejuvination through induction of telomerase family protein transcription, etc..
      It is a complex problem that will need a multi front approach.

      • 3 weeks ago
        Anonymous

        There’s no proof senolytics or anything you mention extends life.

        • 3 weeks ago
          Anonymous

          Yes there is.
          doi: 10.1038/s41591-018-0092-9
          doi: 10.1038/s41467-023-40957-9
          doi: 10.1016/j.celrep.2012.08.023
          That is why we call these (cellular senescence, genomic instability and telomer attrition) hallmarks of ageing. That is the definiton. There needs to be an experiment that shows that effecting the pathway can reduce AND increase lifespan depending on up or downregulation.
          Read López-Otín 2013 Hallmarks of ageing and Read López-Otín 2023 Hallmarks of ageing an expanding universe.
          That being said, this does not mean we have fuly uncovered the mechanisms of the ageing process, nor do the early senolitics or transposon silencing efforts cure ageing.
          My point was, that ageing has multiple overlapping mechanisms which streangthen themselves (leading to an exponent) and eachother in a multiplicative way, leading to an even steeper exponent which is our ageing rate. The point is that to combat ageing we have to adress each of these ageing hallmarks or at least many of them, and the most efficient way to do that is to find a target for small molecular (drug) intervention.
          For instance in the case of genomic stabilty, transposase is a good target, as targeting transposase reduces not only de novo transposition but also the endonuclease activity of transposase, thereby significantly reducing the rate of background mutations.
          The caloric restriction mentioned in OP is effective as it slows down stem cell exhaustion by reducing the number of divisions and through that telomer attrition.

          • 3 weeks ago
            Anonymous

            >telomer attrition
            Opninion discarded, into the trash it goes.
            Anyone who tell you telomere attrition cause aging is a pop sci tourist and shouldnt be taken seriously.

            • 3 weeks ago
              Anonymous

              offer something better then

              • 3 weeks ago
                Anonymous

                Well shit why cant you just accept that nobody know what causes aging in human and it's an extremely complex interactions that we have no clues about. It's the ISTence board, not a shilling board, admitting we dont know is part of it.

              • 3 weeks ago
                Anonymous

                First off, i'm not

                offer something better then

                this anon.
                Secondly, once again, you are both partially right, and completely moronic. You are right, that something can be false without you showing the correct alternative. You could show that telomer attrition is not the key cause of ageing without showing what is. So once again, you are right about something.
                But "nobody know what causes aging"? Come the frick on man, we know plenty. There is a lot of literature, and a lot of interesting experimentation. We can increase the lifespan of some organisms ten fold. The problem isn't that we don't know what causes it, we do. The problem is, we don't know how to prevent it.
                And yet there is a grain of truth to what you are saying, it is a massively complex web of interactions.
                I have to say, i prefere you brand of moronation to the schizos who think they figured out it's actually cadmium or resveratrol or metformin that is actually the cure for ageing and go buy it please...

              • 3 weeks ago
                Anonymous

                Interestingly you are both right and completely moronic at the same time.
                Telomer attrition is not the sole determinant of ageing, and indeed many popsci retrads talk about ti like it is. Congrats, you got something right.
                That being said, to think telomer attrition is completely irrelevant to ageing is moronic.
                Allow me to elaborate.
                Aging on a cellular level is the result initially of DNA damage, whioch is caused by endogenous and exogenous bacground mutations including reactive oxygen species, transposon activity, the action of topoisomearse enzyme, copying errors, etc...This results in epigenetic alterations which both result in further DNA damage, and abarrent transcription. This all results in loss of proteostasis, which will cause all the more downstream aspects of ageing.
                One of these results is an increase in senescence which will cause aseptic inflamation and loss of tissue. Another is shoreter stem cell telomers resulting in somatic cells spawned by them having a smaller Haylfick limit causing a loss of tissue.
                This increases the demand for stem cell division for replacement cells, which increases stem cell telomer attrition causing stem cell exhaustion, meaning stem cells can't replace lost cells fast enough.
                So telomer attrition plays a key role in one of the more down stream, phenotypic expressions of ageing.
                Is it a key cause of ageing? Frick no. Do popsci morons think it is? Yes. Are you moronic for dismissing the relevance of telomer attrition because you don't want to be associated with popsci gays? Yes indeed you are.

                you are just a schizo blabbling moron.
                >muh telomere attrition
                lol, lmao even. take your med, homosexual.

              • 3 weeks ago
                Anonymous

                It's iron poisoning and lack of heavy metals, telomere attrition appears to be from the lack of arsenic.

              • 3 weeks ago
                Anonymous

                You see,

                It's iron poisoning and lack of heavy metals, telomere attrition appears to be from the lack of arsenic.

                this is the kind of moron i was talking about. You are still wrong, but leaps and bounds better then him.

              • 3 weeks ago
                Anonymous

                Why is it so unbeluevable?

              • 3 weeks ago
                Anonymous

                Because we have ageing and non ageing species and cell lines, and there has been extensive analysis done on them to find the difference, and iron uptake or heavy metal uptake were not among the relevant differences.
                But if you think the researchers were not thourough enough, your model is incredibly easely testable.
                Go to the pet store, buy a box of live feeding mice (you can get like a douzen for 10$ for feeding snakes), and test various dietes with known heavy metal and iron concentrations. Also do a control group.
                Post your results here, i would be genuinely interested.
                What i don't like is the certainty in your statements of wild conjecture. But maybe i'm wrong, so show me.

              • 3 weeks ago
                Anonymous

                I wouldn't recommend to do it with white mice, or anything else albino.

            • 3 weeks ago
              Anonymous

              Interestingly you are both right and completely moronic at the same time.
              Telomer attrition is not the sole determinant of ageing, and indeed many popsci retrads talk about ti like it is. Congrats, you got something right.
              That being said, to think telomer attrition is completely irrelevant to ageing is moronic.
              Allow me to elaborate.
              Aging on a cellular level is the result initially of DNA damage, whioch is caused by endogenous and exogenous bacground mutations including reactive oxygen species, transposon activity, the action of topoisomearse enzyme, copying errors, etc...This results in epigenetic alterations which both result in further DNA damage, and abarrent transcription. This all results in loss of proteostasis, which will cause all the more downstream aspects of ageing.
              One of these results is an increase in senescence which will cause aseptic inflamation and loss of tissue. Another is shoreter stem cell telomers resulting in somatic cells spawned by them having a smaller Haylfick limit causing a loss of tissue.
              This increases the demand for stem cell division for replacement cells, which increases stem cell telomer attrition causing stem cell exhaustion, meaning stem cells can't replace lost cells fast enough.
              So telomer attrition plays a key role in one of the more down stream, phenotypic expressions of ageing.
              Is it a key cause of ageing? Frick no. Do popsci morons think it is? Yes. Are you moronic for dismissing the relevance of telomer attrition because you don't want to be associated with popsci gays? Yes indeed you are.

  6. 3 weeks ago
    Anonymous

    You’d be better to fast for 3-4 days then refeed with real high quality food. DNA repair, clean up, then regeneration.

    The path to health is going to be growth and quality control. If you restrict protein you will start to become frail or start looking like a vegan. You’ll have immune system problems.

  7. 3 weeks ago
    Anonymous

    probably schizo nonsense,
    you are better off striving to live a stress free life as that is the best thing for your health and is proven to slow down aging.

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