This will be the last of the post with this title, until perhaps sometime in September when Sam Feltham plans to do another publicity stunt the oh so insightful will fawn over and promote as science and whatnot. However, the post title is a play on "Feast or Famine" and intended to highlight the great disparity between the claims about calories in the "alternate" community and the actual practices engaged in by long time converts to the "opposite of everything we've ever been taught about nutrition" folks. See: Fast or Feltham and Fast or Feltham II.
Showing posts with label Very Low Calorie Diet. Show all posts
Showing posts with label Very Low Calorie Diet. Show all posts
Saturday, June 22, 2013
Thursday, June 13, 2013
Fast or Feltham ...
The title of this post is a play on "feast or famine". One of the things about blogging, for me anyway, is that over time you accumulate a draft bin full of posts that never get published. Some of these are on studies I never got the chance to fully flesh out, others are on the "goings on" during a particular time that never seemed appropriate to hit Publish on by the time they were ready. They are the closest thing I have to a diary and it can often be interesting to read back through the draft bin.
It is hard to believe that I've been blogging over three years now, and involved in this community for more than another year longer than that. Barely a blink of an eye compared to some but my how times have changed. This time four years ago Mark Sisson published Primal Blueprint and Jimmy Moore weighed around 245 lbs after getting down to the mid 230's earlier in the year. Nobody would have known about or considered eating nothing but eggs for weeks on end ... they would have to wait almost a year and 35 more pounds for that stunt. This was the hay day of CarbSmart and other companies selling all manner of LC fair from Dreamfields to Julian Bakery to Chocoperfection and more!
Saturday, April 14, 2012
What if Kimmer was a real 100 lb weight loss success story?
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For those not familiar with "Kimmer", allow me to fill in with a little background. Kimmer was the screen name used by one Heidi Diaz who started a subscription weight loss site KimKins.com. The website -- version 3.0 -- lives on. KimKins is essentially several low carb diets that are also low fat and low calorie. I think the most severe of them is around 300 cal/day. Kimmer used pictures of others for fake "after" pictures while remaining obese herself and promoting KK as a successful weight loss plan. You see, here is the before and apparently a real intermediate pic of Kimmer, and her "after" shot. Below that we have a montage of before/afters used by Heidi. It always amazed me that folks were apparently unquestioning of these shots, but maybe it's just me that would look at any of them and at least wonder whether this was the same person or not. Below right is a split screen of Heidi's before picture and the shot taken by a private detective.
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Monday, February 13, 2012
My Sump-Pump Analogy for the ß-Cell
I'm going to try to make this as short and to the point as possible. It's just me thinking out loud a bit, drawing on the massive amount of peer review research I've read on the topic -- a mere fraction of which I've formally blogged on -- but without any references so that I can just get this out there. No ... this is not some manifesto grand theory on diabetes and all that to be analyzed and picked apart as if I'm presenting this as fact. It's just a plausible analogy for what I think happens when metabolic mahem turns to "diabetes". I'm also going to simplify things and deal with only glucose and fatty acids here.
Our ß-cells metabolize glucose and fatty acids the same way our other cells like muscle cells do for energy. Essentially this metabolism is part of the mechanism by which the ß-cell senses the circulating levels of these energy substrates. This metabolism also produces ROS -- reactive oxidative species. While ROS are often seen as detrimental, due to the fact that they are in inappropriate amounts, the ROS molecules also play key signaling roles. The metabolism of glucose and fatty acids produce a different redox state and ROS so this is roughly how the cells can tell what's being metabolized, etc.
Insulin is secreted by ß-cells in response to both glucose and fatty acids. In response to a sharp rise in glucose (e.g. eating a carby meal), an insulin "spike" is mounted -- an acute secretion of insulin -- the GSIS = glucose stimulated insulin secretion. However we always have some basal level of circulating insulin (and it isn't as simple as some constant slow secretion) that is regulated to a significant degree by the levels of circulating free fatty acids, NEFA. The production of insulin can be simplified to modification of a precursor protein (proinsulin) to form insulin granules packaged in vesicles which eventually are released into circulation by the process of exocytosis. There is some evidence that high demand for basal insulin depletes the proinsulin stores so that the cell can no longer produce the larger amounts of insulin required for an appropriate GSIS.
Sunday, February 12, 2012
More "Crashing" Diabetes
I found this study tweeted by a follower, @JuhanaHarju, and the ever helpful MM was able to provide me with the full text.
Background: Caloric restriction in obese diabetic patients quickly improves glucose control, independently from weight loss. However, the early effects of a very-low-calorie diet (VLCD) on insulin sensitivity and insulin secretion in morbidly obese patients with type 2 diabetes are still unclear.
Objective: The objective was to study the relative contributions of insulin sensitivity, insulin secretion, or both to improvement in glucose metabolism, after 1 wk of caloric restriction, in severely obese diabetic patients.
Design: Hyperglycemic clamps were performed in 14 severely obese (BMI, in kg/m2: >40) patients with type 2 diabetes in good glucose control (glycated hemoglobin < 7.5%) before and after 7 d of a VLCD (400 kcal/d).
Results: The VLCD caused a 3.22 ± 0.56% weight loss (P < 0.001), 42.0% of which was fat loss, accompanied by decreases in fasting plasma glucose (P < 0.05) and triglycerides (P < 0.01). In parallel, the Disposition Index, which measures the body's capability to dispose of glucose load, increased from 59.0 ± 6.3 to 75.5 ± 6.3 mL⋅ min−1 ⋅ m−2 body surface area (P < 0.01), because of improvements in indexes of both first- and second-phase insulin secretion (P < 0.02), but with no changes in insulin sensitivity (P = 0.33).
Read more »Conclusion: The marked improvement in metabolic profile, observed in severely obese patients with type 2 diabetes after a 7-d VLCD, was primarily due to the amelioration of β cell function, whereas no contribution of insulin sensitivity was shown
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