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Thread: Paleo Vs. Atkins page 7

  1. #61
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  2. #62
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    Quote Originally Posted by maurile View Post
    Accuracy.

    None of Banting, Atkins, or Taubes ever claimed to come at this from a paleo angle. Banting and Atkins were before paleo was a thing, and Taubes never uses evolutionary reasoning in his books.

    Banting, Atkins, and Taubes are low-carb, while paleo is not. I mean, it can be; but it can also be low-fat. Paleo isn't about macronutrient ratios. There's a huge difference in the diets of modern "primitive" people, from the high-fat diet of the traditional Eskimos to the high-carb diet of the traditional Kitavans, and the same was very likely true of ancient primitive people. If anything, the Eskimos appear to be the outliers. Most of human history occurred near the equator, where diets were likely very high in carbohydrate content in the form of tubers and fruits. Grok did not follow Atkins.
    Maybe obsessed with being too accurate and arguing over words.

    All these people were onto the same underlying principle which exists in nature. Banting didn't understand the evolutionary reason for why his diet worked, but his diet still followed it. Taubes does use evolutionary reasoning in his books, read them again. Atkins leveraged evolution same as Banting, similarly not necessarily understanding why it worked. Weston Price observed in the field the result of following evolution vs not following it.

    It's one human after another for 100s of years figuring out the same root thing, and the medical mainstream not wanting to confront it because it goes against industry. They are all part of the history of the field "paleolithic nutrition" or whatever you want to name it. If you wrote a book on the topic for a college class (which someone should do) you would include all these names.

    Hence why I say it's all basically the same shit. ^^
    Last edited by KimchiNinja; 04-06-2013 at 03:14 PM.

  3. #63
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    The Paleo diet is a low toxin diet, not a low carb diet, paleo is about eating raw and clean like our ancestors did because this is what our bodies are most adapted to, it's about getting all the processed food which are practically poison out of your diet, atkins is about achieving a state of ketosis* to force the body to burn fat. I know body builders who are on paleo, even when they are looking to gain weight they will follow paleo.

    Lo Carb diet are not sustainable or healthy in the long run, whereas paleo is more of a way of life, you're changing your lifestyle and the intention is to stick with it. Paleo makes sense, lo carb diets are about achieving results quickly.

    *Ketosis is basically when your body starts to produce a lot of ketone bodies. Your nervous system's fuel is glucose. Amino acids and triglycerides (fat) cannot be used by the brain. When there is a lack of glucose in the blood your body will use fat to produce ketone bodies which can be used by the brain. This might sound great to those wanting to lose fat, but it's not that simple, this system is designed to keep you alive during starvation (as there is a lot more fat stored in the body than glucose) your body is not designed to be in this state forever.

  4. #64
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    Quote Originally Posted by 0Angel0 View Post
    You are throwing out the Insulin Hypothesis completely and failing to grasp that just because a single hypothesis doesn't entirely explain away every single part of human metabolism, satiety, and fat storage/burning that must mean it's entirely false.
    In post #50, I described how high-carb junk foods, but not high-carb whole foods, mess with appetite regulation. In post #54, you stated that everything in my post #50 can be explained by the insulin hypothesis. In post #57, I pointed out that the insulin hypothesis does not explain how similarly glycemic and insulinogenic foods can have such different effects on appetite and weight gain. In post #59, you state that no single hypothesis must explain everything.

    That's moving the goal posts.

    I didn't give an example of something unexplained by the insulin hypothesis in order to show that the insulin hypothesis was false; I did it to rebut your claim that the insulin hypothesis explained everything I wrote about in post #50.

    You realized you just linked a study talking about satiety in which protein heavy meals were given to the subjects? That study was comparing the effects of protein on several different factors. Not specifically looking at how carb driven insulin spikes can casue satiety.
    If insulin itself is the problem (as is sometimes suggested), the cause of the insulin spike shouldn't matter. Nonetheless, here are some studies showing that insuiln released after carb-heavy meals does not cause increased hunger (compared to fat-heavy meals):

    The effects of high-carbohydrate vs high... [Int J Food Sci Nutr. 1999] - PubMed - NCBI

    Breakfasts high in protein, fat or carbohydr... [Eur J Clin Nutr. 1996] - PubMed - NCBI

    Meals with similar energy densities but rich ... [Am J Clin Nutr. 2003] - PubMed - NCBI

    Leptin response to carbohydrate or fat meal and... [Am J Physiol. 1999] - PubMed - NCBI

    Did you know that the insulin secreted in response to protein is accompanied by glucagon?
    Yes. I was a low-carber for a few years and an avid reader of the Eades books and blog, so I'm familiar with the standard pro-low-carb arguments. (There's a recent article on glucagon in this context here, if you're interested.)

    See this is where you need to employ some critical thinking and understand that the human body is complex and far from simple.
    That's part of my point. The insulin hypothesis treats bodyfat regulation as something that's far simpler than it really is. For example, it focuses on the hormonal effects on adipose tissue itself rather than on the brain — which is where recent research suggests the focus should be.

    Insulin and other hormones do have effects on adipose tissue directly. On a local level, insulin promotes energy storage in cells, and inhibits the burning of bodyfat. That's the grain of truth underlying the insulin hypothesis, but it seems to miss the bigger point. Local effects matter on the level of minute to minute: right after a meal, when insulin is elevated, you will not be burning bodyfat. (Indeed, why would you, when the meal itself is a source of energy?) But weight regulation on the whole is not determined minute-to-minute. It has longer cycles of feeding and fasting, and those longer cycles are regulated by the brain. It doesn't much matter that post-meal insulin spikes will keep you from burning fat for the next 60 minutes if many stretches of your life will occur in a fasted state, such as when you're sleeping. The minute-to-minute effects of post-meal insulin spikes are overwhelmed by the day-to-day (or longer) effects of appetite regulation, where insulin doesn't seem to be a major player. (And to the extent that it is a player, it seems to be an appetite suppressant.)
    Last edited by maurile; 04-08-2013 at 12:39 PM.

  5. #65
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    I've been doing Atkins for 3 days and I already lost 2 pounds so I know it works!! This has changed my life!!!

    All kidding aside, I don't see why it has to be only one or the other. I'm at a point after many years of diet tinkering where I am using some aspects of a keto diet, a paleo diet, a primal diet and intermittent fasting along with crossfit five days a week. I eat clean, keep carbs low if I need to defeat sugar cravings, eat when I am hungry, and exercise.

    Threads like these remind me that there is a ton of misinformation out there, especially when it comes to paleo and keto diets. People need to research, learn, and experiment to find what works for them. There's no one right way to do it.
    5-24-10 ................ 5-24-11
    Weight: 281.......... Weight: 203

    10-11-10
    Weight: 259
    Total Cholesterol: 243
    LDL: 188
    HDL: 40
    Trig: 96

    2-18-11
    Weight: 228
    Total Cholesterol: 239
    LDL: 183 (calc), 138 (actual)
    HDL: 46
    Trig: 49

    6-23-11
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  6. #66
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    Quote Originally Posted by Black_Diamond View Post
    The Paleo diet is a low toxin diet, not a low carb diet, paleo is about eating raw and clean like our ancestors did because this is what our bodies are most adapted to, it's about getting all the processed food which are practically poison out of your diet, atkins is about achieving a state of ketosis* to force the body to burn fat.....
    Incorrect.....

  7. #67
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    Quote Originally Posted by maurile View Post
    In post #50, I described how high-carb junk foods, but not high-carb whole foods, mess with appetite regulation. In post #54, you stated that everything in my post #50 can be explained by the insulin hypothesis. In post #57, I pointed out that the insulin hypothesis does not explain how similarly glycemic and insulinogenic foods can have such different effects on appetite and weight gain. In post #59, you state that no single hypothesis must explain everything.

    That's moving the goal posts.
    No it's not! "moving the goal posts" has become forum speak for "you said something I can't effectively counter so I'm going to say you moved a goal post". First of all the insulin hypothesis isn't one single all encompassing statement. There are several versions of it. It basically boils down to saying that elevated levels of insulin can contribute to making or keeping one fat.

    Foods like protein can elicit a significant insulin response yet not increase hunger because they also cause the release of other hormones that directly counteract the effects of insulin. This is why a single hypothesis cannot be used with any credibility to explain or describe every single metabolic process that occurs. Even if it's true. There are just too many confounding variables and interacting biochemical reactions that occur within the body. That's not moving a goal post that's just fact.

    I didn't give an example of something unexplained by the insulin hypothesis in order to show that the insulin hypothesis was false; I did it to rebut your claim that the insulin hypothesis explained everything I wrote about in post #50.
    I said all of those things *could* be explained by the insulin hypothesis. And they can be. That's not the same as saying the insulin hypothesis is the one and only explanation for any and all of them. Did I have to spell that out for you?

    Lets look at those studies and see if they say what you think they do, shall we?

    The effects of high-carbohydrate vs high... [Int J Food Sci Nutr. 1999] - PubMed - NCBI
    The high-fibre, carbohydrate-rich breakfast was the least palatable but most filling meal and was associated with less food intake during the morning and at lunch. Hunger returned at a slower rate after this meal than after the low-fibre, carbohydrate-rich meal.
    Both fat-rich breakfasts were more palatable but less satiating than the carbohydrate-rich meals and were followed by greater food intake during the morning, which may be a compensatory response to ingest a sufficient amount of food and/or carbohydrate to match the level of fullness produced by the subjects' habitual breakfasts. By the end of the day, the average total energy intake was significantly greater after the fat-rich EB meal than after the high-fibre, carbohydrate-rich meal (P < 0.05). Total day fat intakes were also significantly greater when the high-fat breakfasts were eaten.
    So fiber is more satiating than fat. And higher fiber more so than lower fiber. Again, no news here. Why would that be? What effect does fiber have on insulin release?

    The results confirm the relatively weak satiating power of fat-rich meals observed in controlled laboratory-based studies and indicate that a high-fibre, carbohydrate-rich breakfast may assist weight control efforts by maintaining fullness. Further research is required to determine whether satiety directly enhances alertness and whether low-GI carbohydrate-rich meals enhance alertness to a greater degree than high-GI meals.
    This study was comparing high fiber to low fiber and both to high fat. Fiber and protein are notorious for their sating effects. Protein because of the corresponding hormone releases in addition to insulin and fiber because of the dampening affect it has on blood sugar and insulin rates of release. This study boils down to fiber vs fat. You cannot claim with any certainty anything about insulin and hunger. And it certainly shows that dampening the rate of insulin release (with high fiber) is more sating than not.

    Again, doesn't specifically manipulate insulin levels so worthless in the context of this discussion. Although it does conclude again that a meal only high in fat isn't particularly satisfying. Something I agree with.

    Normal weight healthy individuals given meals at regular intervals. The take away:
    Intake of an alcohol-rich meal stimulates energy expenditure but suppresses fat oxidation and leptin more than do isoenergetically dense meals rich in protein, carbohydrate, or fat.
    Again, this study didn't specifically manipulate insulin levels and wasn't designed to support your claim that increased insulin has no effect on appetite.

    Leptin response to carbohydrate or fat meal and... [Am J Physiol. 1999] - PubMed - NCBI

    This is looking at leptin. A confounding variable with regards to appetite and insulin. Again, this study doesn't claim what you think it does.

    Internet abstract wars are silly as is evidenced above. Not a single one of those abstracts discredits the claim that unregulated and elevated insulin levels can increase the feeling of hunger. Esp long term and that chronic ever present "hunger" that occurs in response to a high carb, esp high processed (aka super fast insulin flood to the the body) food diet.

    But just for kicks lets look at a study (a whole study not just randomly picked abstracts) that actually did isolate the effects of insulin:

    JCI - Dysregulation of insulin receptor substrate 2 in &#x3B2; cells and brain causes obesity and diabetes
    a conditional knockout of insulin receptor substrate 2 (Irs2) in mouse pancreas β cells and parts of the brain including the hypothalamus increased appetite, lean and fat body mass, linear growth, and insulin resistance
    This is pretty technical and tough to wade through but shows how losing the ability to properly process and utilize insulin increases appetite and obesity....as occurs with chronically elevated insulin levels leading to insulin resistance.

    JCI - Obesity and insulin resistance
    Insulin promotes adipocyte triglyceride stores by a number of mechanisms, including fostering the differentiation of preadipocytes to adipocytes and, in mature adipocytes, stimulating glucose transport and triglyceride synthesis (lipogenesis), as well as inhibiting lipolysis
    Isn't that what's at the base of the insulin hypothesis? Is it so unreasonable to acknowledge that chronic and persistent elevated insulin levels are fattening?

    I don't randomly post abstracts to studies I've never read and cross my fingers that the person I'm debating isn't smart enough to understand them either. So in the interest of time right now those two will have to do!

  8. #68
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    Yes. I was a low-carber for a few years and an avid reader of the Eades books and blog, so I'm familiar with the standard pro-low-carb arguments. (There's a recent article on glucagon in this context here, if you're interested.)
    I'm familiar with that blog post. I've read it and think it was well done. How exactly does it conflict with the pro-low carb arguments? Unles you think the smoking gun is here Regarding hunger, glucagon is often suggested to oppose the hunger-inducing effects of insulin. However, contrary to popular claims, insulin doesn't increase hunger or food intake in humans unless it causes frank hypoglycemia, so there is nothing to oppose (1, 2, 3, 4)*. Nevertheless, glucagon probably does play a role in satiety, independently of insulin. So that claim is partially true.

    Elevated insulin levels causing hypoglycemia is exactly why they can lead to hunger! It's not as simple as increase insulin increase hunger. I never claimed that and nobody with half a brain would. It is the metabolic disease that *too much* insulin can have under chronic conditions that is the problem. It may not be as simple as 2+2=4 but it's not rocket science!

    That's part of my point. The insulin hypothesis treats bodyfat regulation as something that's far simpler than it really is. For example, it focuses on the hormonal effects on adipose tissue itself rather than on the brain which is where recent research suggests the focus should be.
    No, it treats insulin as a primary driver of body fat storage. There is a difference!

    Insulin and other hormones do have effects on adipose tissue directly. On a local level, insulin promotes energy storage in cells, and inhibits the burning of bodyfat. That's the grain of truth underlying the insulin hypothesis, but it seems to miss the bigger point. Local effects matter on the level of minute to minute: right after a meal, when insulin is elevated, you will not be burning bodyfat. (Indeed, why would you, when the meal itself is a source of energy?) But weight regulation on the whole is not determined minute-to-minute. It has longer cycles of feeding and fasting, and those longer cycles are regulated by the brain. It doesn't much matter that post-meal insulin spikes will keep you from burning fat for the next 60 minutes if many stretches of your life will occur in a fasted state, such as when you're sleeping. The minute-to-minute effects of post-meal insulin spikes are overwhelmed by the day-to-day (or longer) effects of appetite regulation, where insulin doesn't seem to be a major player. (And to the extent that it is a player, it seems to be an appetite suppressant.)
    I agree with the bolded part! I've never argued that insulin is toxic and dangerous. It is a necessary hormone. What I've always argued is that it is a primary regulator of body fat and an unhealthy diet that chronically elevates it, without other accompanying and dampening hormones, is fattening.

    I've also always argued that chronically elevated insulin is far more dangerous than the occasional insulin spike in a healthy person. Although if one is diseased then even what would otherwise be a temporary insulin spike can be unhealthy.

    Every reason you are giving can only be assumed in a healthy individual with a fully functioning metabolism. You cannot apply that across the board to everyone. I would go further to argue that long term elevated insulin levels can eventually make a healthy person unhealthy. That was my N=1 when low fat high carb eating every 3 hours diets entered my life. I went from battling 20 pounds to 100 lbs.

  9. #69
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    Quote Originally Posted by Kaminokamen View Post
    I should stop because it is like the Atkins diet and the guy died
    What did Atkins die from?

    If a man eating a particular type of diet dies on the footpath from a piano falling out a window on to his head - Does that mean it shows his particular diet is unhealthy and you should stop this diet because he died?

    If someone dies at 110 years old (from old age ???) - do we avoid their diet too? ("the guy died, so it's not really healthy").

  10. #70
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    0Angel0,

    You go girl!
    JoreyTK
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