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ASPs and Weight Loss Stalls?

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  • ASPs and Weight Loss Stalls?

    This is an interesting concept and I wonder if any of you can interpret it? He seems to be saying that low carb/high fat works to a certain point, but that ASPs from high fat intake will eventually stall weight loss. Found the link in Gary Taubes's comments:

    A Swift Kick in the ASP


    ASP is another hormone secreted by fat cells, with several effects. First, ASP can increase LPL activity, making fatty acids available for transport into the fat cells. Second, ASP increases the expression of glucose transporters in fat cells, allowing them to bring in the glucose required to store fat. So ASP plays roughly the same role as insulin in fat storage, but rather than being generated by the pancreas in response to carbohydrates, is generated by the fat cells themselves. Better yet, ASP stimulates the production of triglycerides inside the fat cells. But what causes ASP to be secreted?

    The answer, at least in test-tubes, is chylomicrons. When fat cells are exposed to chylomicrons they generate lots of ASP. By contrast, exposing the same cells to glucose, fatty acids, VLDL, HDL, or LDL elicits little ASP response. Further, the ASP response exhibits both a time and concentration dependence on chylomicron concentration.

    This is an important clue. As discussed above, chylomicrons are the first step in transporting dietary fats into the body. When you eat a lot of fat, you make more chylomicrons, which causes the fat cells to make more ASP, which stimulates greater fat storage. But the chylomicrons only hang around for a relatively short time, being converted in the liver to VLDL. The receptor for VLDL (VLDL-R), when activated, does increase LPL activity, but to my knowledge does not stimulate glucose transport into fat cells. Thus the fat in VLDL is available to be used for energy, because the LPL frees the fatty acids for transport across cell membranes; but without some other hormonal signal (e.g. insulin), rather little of this fat can be stored in adipose tissue.

    Two questions then arise in the context of a low-carbohydrate/high-fat diet. The most obvious one is "can I get fat by eating too much fat?" Taubes lays out the case that overconsumption of carbohydrates drives fat storage through the action of insulin, but can overconsumption of fat do the same via the action of ASP? When viewed with the most narrow lens, the answer is clearly "yes". While insulin's effects on LPL and glucose transport are considerably stronger than ASP, ASP does ultimately trigger the same conditions leading to fat storage. So if you eat enough fat for a long enough time, in principle you will become obese.


    While it may be hard to gain fat through a high-fat diet, it is likely possible to keep on a certain level of body-fat. Low-carbohydrate diets are known to "stall", where the last 20 or so pounds just won't come off, regardless of carbohydrate restriction. I suspect our friend ASP plays a crucial role here. The low insulin levels on a low-carb diet will allow the fat cells to free fatty acids, but if you are consuming enough fat, at some point this effect will be balanced by that of ASP, and voila, no more fat loss.

  • #2
    In my experience, many low carb/high fat eaters 'stall' because after losing significant weight, calories begin to count. A person may simply no longer be eating at a caloric deficit, and many low carbers insist that calories don't matter so they refuse to consider the quantity of food as problematic. Most low carb/high fat menus are very calorie intensive, so it is easy to operate without a deficit, especially as the person gets smaller and caloric requirements decrease.


    • #3
      That was a bit complicated, and I can't claim to understand it all, but the one thing that I keep in mind about high fat diets is that it is extremely difficult to maintain a very high calorific intake on them due to high satiety, and lack of hunger. So I'm not sure just how much fat one would have to be eating to create the above scenario.
      My primal journal
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      • #4
        Wow. I had read that article aver a year ago but could never find it again. It makes even more sense now after having gained a bit more knowledge on how metabolism works.
        Don't be a paleotard...


        • #5
          This needs way more than 104 views.
          Don't be a paleotard...


          • #6
            The author is simplyifying the role of ASP just as many people simplify insulin.

            Just because one role of ASP is to mobilize fat for storage, a resonable response, does not mean that it is going to happen. If your body is also looking for energy and needing to burn ketones in the presence of low glucose, is your body not going to work to mobilize that fat for catabolism? Perhaps the pathways that regulate fat catabolism also downregulate ASP or some sort of precursor. This is all me just using basic biochemical knowledge to speculate on potential regulatory mechanisms.

            It is absolutely normal that the body's response to fat would include activation of storage pathways. It also makes sense that these storage pathways would be downregulated by metabolic pathways for fatty acid metabolism etc.

            This ASP molecule seems like it would be a problem if:
            1) Energy input was significantly higher than energy needs (a bit of a calories-in-calories-out idea)
            2) Excess glucose or other easily digested energy macromolecules were also being ingested (High/moderate fat + high/moderate carb)

            Disclaimer: This is all speculation, just thinking about logical ways in which the body would regulate storage and catabolism signals