Fri, Feb-13-15, 21:19
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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Quote:
Originally Posted by coachjeff
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They mention another study, with different results, here;
http://www.ncbi.nlm.nih.gov/pmc/art.../?report=reader
Quote:
In contrast, the data from previous studies found that the oral ingestion of a NNS before a glucose load augmented GLP-1 (19,20) but did not affect GIP secretion. However, in those studies total GLP-1—not the biologically active form of GLP-1—was measured (19,20). Although it is possible that the discrepancy between GLP-1 findings of those and our study is the result of this methodological difference, we think it is unlikely because active and total GLP-1 are highly correlated with each other (30). A second methodological difference is that in those studies a diet cola sweetened with both sucralose and acesulfame potassium (19,20) was used, so it is unclear whether the enhanced glucose-stimulated GLP-1 response was mediated by acesulfame potassium, a synergistic effect of both sweeteners, or other ingredients contained in the carbonated drinks (20).
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In the cola study, there isn't much difference in blood glucose or insulin when the 75 gram glucose drink was given after diet cola vs. control. They suggest that it's the type of sweetener. But I couldn't find anything in this second study suggesting that diet cola was a novel experience for the participants. Feed a rat saccharin paired with food, it gets fat. Give it a week to become used to the sweetener before giving it with the food, and the animal learns to ignore the sweetener--adding the sweetener to the chow won't make this animal fat. Carefully controlled experiments are good, they allow very specific information to be learned. Giving an artificial sweetener unpaired with a flavour, or paired with a novel flavour, and then 75 grams of glucose, gives us very specific information. It says nothing about what the diet beverages I've been drinking since I was a teenager will do to me. I really think the question shouldn't be "are artificial sweeteners harmful or safe?" but "under what conditions are artificial sweeteners harmful or safe."
Sweetness unpaired with some distinctive flavour is fairly rare in nature. And I never sweeten just water.
With the cancer thing that started this thread--feeding patterns out of phase with normal circadian rhythm can increase cancer.
Quote:
Cancer inhibition through circadian reprogramming of tumor transcriptome with meal timing.
Abstract
Circadian disruption accelerates cancer progression, whereas circadian reinforcement could halt it. Mice with P03 pancreatic adenocarcinoma (n = 77) were synchronized and fed ad libitum (AL) or with meal timing (MT) from Zeitgeber time (ZT) 2 to ZT6 with normal or fat diet. Tumor gene expression profiling was determined with DNA microarrays at endogenous circadian time (CT) 4 and CT16. Circadian mRNA expression patterns were determined for clock genes Rev-erbalpha, Per2, and Bmal1, cellular stress genes Hspa8 and Cirbp, and cyclin A2 gene Ccna2 in liver and tumor. The 24-hour patterns in telemetered rest-activity and body temperature and plasma corticosterone and insulin-like growth factor-I (IGF-I) were assessed. We showed that MT inhibited cancer growth by approximately 40% as compared with AL (P = 0.011) irrespective of calorie intake. Clock gene transcription remained arrhythmic in tumors irrespective of feeding schedule or diet. Yet, MT upregulated or downregulated the expression of 423 tumor genes, according to CT. Moreover, 36 genes involved in cellular stress, cell cycle, and metabolism were upregulated at one CT and downregulated 12 h apart. MT induced >10-fold circadian expression of Hspa8, Cirbp, and Ccna2 in tumors. Corticosterone or IGF-I patterns played no role in tumor growth inhibition. In contrast, MT consistently doubled the circadian amplitude of body temperature. Peak and trough respectively corresponded to peak expressions of Hspa8 and Cirbp in tumors. The reinforcement of the host circadian timing system with MT induced 24-hour rhythmic expression of critical genes in clock-deficient tumors, which translated into cancer growth inhibition. Targeting circadian clocks represents a novel potential challenge for cancer therapeutics.
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http://www.ncbi.nlm.nih.gov/pubmed/20395208
Palatability is often pointed at as causing overeating, and the overeating leading to various diseases. In lots of rodent models of obesity, the animals won't actually eat more than control rats on the obesity/disease-provoking diets. A very common change is in meal pattern--instead of eating mostly during their normal active period, with a smaller number of larger meals, animals will eat a large number of smaller meals, around the clock. Constant snacking. Forced to eat only when they would have if offered a more healthful chow diet, the animals are as healthy as if they had been on the more healthful chow. This is one of the things that needs to be checked for in every study in rodents showing that dietary artificial sweeteners increased cancer, at any dose, did it affect meal pattern?
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