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Thread: Help Shut my CICO Friend Up - THE GHEE CHALLENGE page 11

  1. #101
    magicmerl's Avatar
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    Quote Originally Posted by randomcow View Post
    btw I am fat-adapted.
    Keep a photolog.

    Also, ask him to predict in advance exactly how much weight you will gain by ingesting an *EXTRA* 1000 calories a day. You can make your prediction.
    Disclaimer: I eat 'meat and vegetables' ala Primal, although I don't agree with the carb curve. I like Perfect Health Diet and WAPF Lactofermentation a lot.

    Griff's cholesterol primer
    5,000 Cal Fat <> 5,000 Cal Carbs
    Winterbike: What I eat every day is what other people eat to treat themselves.
    TQP: I find for me that nutrition is much more important than what I do in the gym.
    bloodorchid is always right

  2. #102
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    Quote Originally Posted by Alan Aragon View Post
    LOL, are you serious? I have no interest in, plus I have better bedside manners than dragging folks I don't personally know into this discussion out of the blue. I'm merely suggesting that you balance out your perspective by reading White's paper. This is for your learning benefit; Mark has nothing to do with this. If you choose not to read it, then oh well, that's on you. The world will continue to turn, it's really no skin off anyone's back.
    I'm reading right now
    Would I be putting a grain-feed cow on a fad diet if I took it out of the feedlot and put it on pasture eating the grass nature intended?

  3. #103
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    I feel like pointing out that most if not all studies that implicate one particular health risk tend to do so by taking consumption levels far higher than normal consumption. This includes the other boogieman PUFA. Oh yes I went there. For me quality matters.

    Really what needs further study is the synergistic implications of various factors that are attributed to DOC in concert. As usual the whole is more than the sum of its parts, and I believe this to hold true in the human diet as well. So, its not just PUFA or just fructose overload, or just GMO, or just "insert toxic agent of neolithic origin here".... but the combination that leads to several very real and measurable adaptive changes in the human body that we call "disease".

    Alrighty then.... thats really all I got to say.... Except.... I WIN THE THREAD!
    '
    Not for this past statement but because my recommendation of a "kick to the balls then drink the ghee" is the most logical and scientific resolution to OP's issue

    Kick to the balls.... cause she don't like him... totally logical
    Drink the ghee.... prove or disprove hypothesis for your own physiology. There are those outside of the "normal" on the bell curve in each direction. Find YOUR normal. You may prove yourself wrong or right, but at least you will know a bit more about yourself in the end.

  4. #104
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    She can't drink the ghee now!
    It's not a valid experiment, she's already biased towards proving someone wrong, so it doesn't mean she'll prove anti-CICO *right*.
    And she's already fat-adapted, so clearly this isn't a reliable sample population, and it means she already has a pro-fat agenda so the conclusions will be skewed! This is just not an acceptable study.

    I know... let's make Mark analyse it and we can just make up our opinions based on his conclusions, that will be a lot easier.

  5. #105
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    Quote Originally Posted by allenete View Post
    she can't drink the ghee now!
    It's not a valid experiment, she's already biased towards proving someone wrong, so it doesn't mean she'll prove anti-cico *right*.
    And she's already fat-adapted, so clearly this isn't a reliable sample population, and it means she already has a pro-fat agenda so the conclusions will be skewed! This is just not an acceptable study.

    I know... Let's make mark analyse it and we can just make up our opinions based on his conclusions, that will be a lot easier.
    lol

  6. #106
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    Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism

    Read through it quickly but here's what I got. Most of this stuff is above my pay grade...hence I refer to experts that I trust.
    It didn't see a comparison of sugar/HFCS between babyboomers to children and young adults. It stands to reason that babyboomers would be reducing their sugar intake over the past 10 years causing the total per capita consumption to decline.

    Going back to the Lalone webinar...he said animal studies are useful but you have to allow for the differences between humans and rats. As the paper pointed out rats produce uricase and humans do not so you have to slug them with extra. And is corroborated here with this argument: Synergistic effect of uricase blo... [Am J Physiol Renal Physiol. 2013] - PubMed - NCBI
    "Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats (n = 7/group) were studied during 8 wk: water + vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose."

    I didn't google for him but one of the authors to the above quote is Dr Richard Johnson (The Fat Switch). IIRC from his book they used rats with a genetic defect (they didn't produce uricase) in an attempt to better mimic human metabolism.

    The lab studies referred to on humans were (by necessity) acute studies. Even then....
    Nutrition & Metabolism | Full text | Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein- 4, and gamma-glutamyl transferase activity in overweight/obese

    PLOS ONE: Uric Acid Stimulates Fructokinase and Accelerates Fructose Metabolism in the Development of Fatty Liver

    So you tell me...as a layman who tries to ferret out as much of this stuff as I can (which is way more than 95% of the population) and understand it as much as I can, who am I supposed to believe? You? And if so why? Guys like Dr Johnson and Lustig are doing the labs/clinicals and disseminating it (through books/videos) to people like me who want to know.

    BTW, N=1, I have a friend who was on meds for gout. He read sugar might be the cause so he gave it up. He went off med and hasn't had gout in over a year. Tell him there isn't a connection.
    Last edited by Scott F; 07-02-2013 at 04:53 PM.
    Would I be putting a grain-feed cow on a fad diet if I took it out of the feedlot and put it on pasture eating the grass nature intended?

  7. #107
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    Quote Originally Posted by Scott F View Post
    Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism

    Read through it quickly but here's what I got. Most of this stuff is above my pay grade...hence I refer to experts that I trust.
    It didn't see a comparison of sugar/HFCS between babyboomers to children and young adults. It stands to reason that babyboomers would be reducing their sugar intake over the past 10 years causing the total per capita consumption to decline.

    Going back to the Lalone webinar...he said animal studies are useful but you have to allow for the differences between humans and rats. As the paper pointed out rats produce uricase and humans do not so you have to slug them with extra. And is corroborated here with this argument: Synergistic effect of uricase blo... [Am J Physiol Renal Physiol. 2013] - PubMed - NCBI
    "Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats (n = 7/group) were studied during 8 wk: water + vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose."

    I didn't google for him but one of the authors to the above quote is Dr Richard Johnson (The Fat Switch). IIRC from his book they used rats with a genetic defect (they didn't produce uricase) in an attempt to better mimic human metabolism.
    De novo lipogenesis (DNL; the hepatic conversion of dietary carbohydrate to fat) in rats occurs at about 10-fold the rate of humans. This alone invalidates the comparison of carbohydrate feeding effects between humans & rats - and especially so, when rats are fed artificially prodigious amounts of the carbohydrate in question. This is just the tip of the iceberg in terms of physiological disparities, but it's enough. 25% of total kcals from fructose fed to a sedentary population is obviously a bad idea. But no one is arguing in favor of extremes. You linked a study examining the effects of roughly 150 g/day of isolated fructose. Achieving this dose would require 300 g sucrose (table sugar). This is obviously far-fetched, especially in populations with half a brain & a modicum of dietary consciousness.
    So you tell me...as a layman who tries to ferret out as much of this stuff as I can (which is way more than 95% of the population) and understand it as much as I can, who am I supposed to believe? You? And if so why? Guys like Dr Johnson and Lustig are doing the labs/clinicals and disseminating it (through books/videos) to people like me who want to know.
    To you as a layman, I would have you re-read White's paper, and do it with an open mind.
    BTW, N=1, I have a friend who was on meds for gout. He read sugar might be the cause so he gave it up. He went off med and hasn't had gout in over a year. Tell him there isn't a connection.
    I'm not interested in anecdotes at this point, sorry. We can share our personal anecdotes all day long, and I have 20 years of client data to bat around - ain't nobody got time fo' dat. I'd rather restrict this discussion to objective data, not subjective testimony.

  8. #108
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    More reading for you after you read White's review: Health implications of fructose consumption: A review of recent data

  9. #109
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    The whole point of eating the way we do is to nourish our bodies with high quality, whole foods. Why would you engage in such nonsense? Make a point by setting an example not by taking on such a silly challenge. I love ghee. I make my own from pastured butter. I would NEVER agree to drink it in such quantities.

    Sent from my SGH-T989 using Tapatalk 2

  10. #110
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    Quote Originally Posted by Alan Aragon View Post
    More reading for you after you read White's review: Health implications of fructose consumption: A review of recent data
    Cliffs?

    JK..haven't read this paper, thanks for sharing it. Working my way through it now.
    My nutrition/fitness/critical thinking blog:

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