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Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.Presumably the diet he urged was low carb. But just going LC and trying to cut wheat lasted only three days. So the good Dr. Davis told Jack to get a BG meter and strive for 1 hour postprandial glucose levels to be no higher than before eating. So:
If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 mg/dl, reduce or eliminate the mashed potatoes. If slow-cooked, stone ground oatmeal causes blood glucose to increase from 115 mg/dl to 185 mg/dl (a typical response to oatmeal), then eliminate it.
Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.... Six months later, Jack came back 37 lbs lighter.
...What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise. ... And he got there without calorie-counting, without regulating portion sizes, without hunger.
No doubt, however, that alcohol can be fattening, not only because of the calories it contains, but because it slows metabolism - to quote a medical journal article I read, "Alcohol profoundly inhibits lipolysis." In English this means that alcohol slows fat-burning to a crawl. Like carbs, your body burns alcohol preferentially. Don't expect to burn any fat until you've burned through all your alcohol calories.
.....A few things to understand at the outset: First, despite the happy fact that unlike many in this field, Mr. Taubes is not out to sell you anything (other than his book), it is still a manifesto. Thus, though it is bursting with data, a reader has no way of knowing whether other data has been overlooked or minimized to support the author’s points.
Second, the new book is not really a new book at all; it is a sort of CliffsNotes version of “Good Calories, Bad Calories,” a long, dense tome Mr. Taubes published in 2007. With the new, smaller and more focused version, Mr. Taubes openly admits he is aiming for a broader audience and bigger impact. Fair enough, although one does begin to wonder if a line of protein bars is not far behind.....The highlighted statement kinda caught my eye ;-)
Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet.Firstly, we have correlation here, not causation.
Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'.
Bariatric surgery is the most effective available treatment for obesity. The most frequently performed operation, Roux-en-Y gastric bypass (RYGB), causes profound weight loss and ameliorates obesity-related comorbid conditions, especially type 2 diabetes mellitus (T2DM). Approximately 84% of diabetic patients experience complete remission of T2DM after undergoing RYGB, often before significantweight reduction. The rapid time course and disproportional degree of T2DM improvement after RYGB compared with equivalent weight loss from other interventions suggest surgery-specific, weight-independent effects on glucose homeostasis. Potential mechanisms underlying the direct antidiabetic impact of RYGB include enhanced nutrient stimulation of lower intestinal hormones (e.g. glucagon-like peptide-1), altered physiology from excluding ingested nutrients from the upper intestine, compromised ghrelin secretion, modulations of intestinal nutrient sensing and regulation of insulin sensitivity, and other changes yet to be fully characterized. Research aimed at determining the relative importance of these effects and identifying additional mechanisms promises not only to improve surgical design but also to identify novel targets for diabetes medications.
The focus cannot be only on insulin. Glucose itself is harmful via the process of endogenous glycation, i.e., glucose-driven modification of proteins. The higher the blood glucose, the greater the glycation, with the process beginning at blood glucose levels of 100 mg/dl or more. Blood glucose after a 3-egg omelet is typically 95 mg/dl. Blood glucose after a bowl of slow-cooked, stone-ground oatmeal is typically 150-200 mg/dl in non-diabetics.
It’s true that the body can store fat even when it has low insulin levels when excess calories from a high carbohydrate low fat diet are stored as fat even if insulin levels are not high. Upwards of 85% of excess carbs turns to triglycerides or fat. The body is less likely to store fat if it is primarily burning fat for fuel.
A recent undercurrent in the blogosphere is discounting the importance of insulin, instead pointing toward leptin, among other hormones, as the “master hormone.” I disagree with this slightly, not because I discount the importance of leptin, or grehlin, or any of the nearly innumerable myriad hormonal players in this crazy, complex amalgamation of meat and bones we call the human body, but because it misses the point of what I’m trying to do: maximize buy-in and discuss what works for the largest amount of people that come looking for the type of help I provide. .....
..... Even if “eat less, move more” is ineffective advice that rarely works over the long-term, it makes intuitive sense to someone who isn’t steeped in this stuff every day. We need simplicity.
That’s why I like focusing on insulin – because it simply works, and it’s easy to understand.
While carbohydrates do take precedence in the heirarchy of fuel partitioning, they never STOP fat burning. If that is ever the case, you're probably dead. There are also millions of obese folks with normal pancreatic function.Myth 1 – who’s talking about healthy individuals? We’re trying to do something about the 1.1 billion overweight and obese people in the world and the fact that we have 171 million diabetics already confirms that there is nothing healthy about the workings of the pancreas of these people. Why would you want to elevate blood glucose levels if you do admit that they stop fat burning? ...
"One of my goals here is to get the research community to understand that there is an alternative hypothesis that should actually be the null hypothesis — the hypothesis that requires remarkable evidence to reject. "
~ Gary Taubes
"Many scientists consider Popper’s idea of falsification to be the only major improvement to the scientific method since Francis Bacon came up with the idea.
Although more complex mathematically than it appears on the surface what Popper’s falsification theory does is describes a way in which hypotheses can be stated with accuracy. Remember, an hypothesis is merely a guess or an assertion that requires testing before it can be said to be viable. Hypotheses can be stated in ways that, although they seem reasonable, can never really be tested. Popper wrote that the only way an hypothesis can be considered a valid hypothesis is if it can be falsified.
What does this mean exactly?
Where to now?
