Fri, Oct-09-15, 10:58
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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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I didn't mean to suggest that in the normal course of events, AGEs from cooked beef would be in any way dangerous. But then, in the normal course of events, peanuts wouldn't be acutely life-threatening. And as sucky as wheat may be, celiac isn't the normal course of events, either.
Part of the problem with endogenously produce AGEs isn't the presence of AGEs as such, as it is just what's getting glycated--useful proteins, with proper functions in the body that may be disrupted. Plus high endogenous AGEs pretty much pre-supposes insulin resistance.
Type II diabetics seem to be more prone to elevation of endotoxins with a fatty meal;
http://care.diabetesjournals.org/content/35/2/375.full
Quote:
High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects
Alison L. Harte, PHD1, Madhusudhan C. Varma, MRCP1, Gyanendra Tripathi, PHD1, Kirsty C. McGee, PHD1, Nasser M. Al-Daghri, PHD2, Omar S. Al-Attas, PHD2, Shaun Sabico, MD2, Joseph P. O’Hare, MD1, Antonio Ceriello, MD3, Ponnusamy Saravanan, PHD4, Sudhesh Kumar, MD1 and Philip G. McTernan, PHD1⇓
+ Author Affiliations
1Division of Metabolic and Vascular Health, University of Warwick, Coventry, U.K.
2College of Science, Biomarkers Research Programme and Center of Excellence in Biotechnology Research, King Saud University, Riyadh, Saudi Arabia
3Insititut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
4University of Warwick and George Eliot Hospital, Clinical Sciences Research Laboratories, Warwick Medical School (University Hospital Coventry and Warwickshire Campus) Coventry, U.K.
Corresponding author: Philip G. McTernan, p.g.mcternan~warwick.ac.uk.
Next Section
Abstract
OBJECTIVE To evaluate the changes in circulating endotoxin after a high–saturated fat meal to determine whether these effects depend on metabolic disease state.
RESEARCH DESIGN AND METHODS Subjects (n = 54) were given a high-fat meal (75 g fat, 5 g carbohydrate, 6 g protein) after an overnight fast (nonobese control [NOC]: age 39.9 ± 11.8 years [mean ± SD], BMI 24.9 ± 3.2 kg/m2, n = 9; obese: age 43.8 ± 9.5 years, BMI 33.3 ± 2.5 kg/m2, n = 15; impaired glucose tolerance [IGT]: age 41.7 ± 11.3 years, BMI 32.0 ± 4.5 kg/m2, n = 12; type 2 diabetic: age 45.4 ± 10.1 years, BMI 30.3 ± 4.5 kg/m2, n = 18). Blood was collected before (0 h) and after the meal (1–4 h) for analysis.
RESULTS Baseline endotoxin was significantly higher in the type 2 diabetic and IGT subjects than in NOC subjects, with baseline circulating endotoxin levels 60.6% higher in type 2 diabetic subjects than in NOC subjects (P < 0.05). Ingestion of a high-fat meal led to a significant rise in endotoxin levels in type 2 diabetic, IGT, and obese subjects over the 4-h time period (P < 0.05). These findings also showed that, at 4 h after a meal, type 2 diabetic subjects had higher circulating endotoxin levels (125.4%↑) than NOC subjects (P < 0.05).
CONCLUSIONS These studies have highlighted that exposure to a high-fat meal elevates circulating endotoxin irrespective of metabolic state, as early as 1 h after a meal. However, this increase is substantial in IGT and type 2 diabetic subjects, suggesting that metabolic endotoxinemia is exacerbated after high fat intake. In conclusion, our data suggest that, in a compromised metabolic state such as type 2 diabetes, a continual snacking routine will cumulatively promote their condition more rapidly than in other individuals because of the greater exposure to endotoxin.
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Peter at hyperlipid has pointed out that endotoxin absorption through dietary fat performs an important function in immune response. But every disease process is made up of various crucial functions, somehow gone awry.
And one more thing for now, this is all I've been able to find on endotoxins and a ketogenic diet specifically;
Quote:
Ketogenic diet exhibits anti-inflammatory properties.
Dupuis N1,2, Curatolo N1, Benoist JF1,3, Auvin S1,2,4.
Author information
Abstract
The ketogenic diet (KD) is an established treatment for refractory epilepsy, including some inflammation-induced epileptic encephalopathies. In a lipopolysaccharide (LPS)-induced fever model in rats, we found that animals given the KD for 14 days showed less fever and lower proinflammatory cytokine levels than control animals. However, KD rats exhibited a decrease in circulating levels of arachidonic acid and long-chain n-3 polyunsaturated fatty acids (PUFAs), suggesting that the anti-inflammatory effect of KD was probably not due to an increase in anti-inflammatory n-3 PUFA derivatives. These properties might be of interest in some conditions such as fever-induced refractory epileptic encephalopathy in school-aged children.
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What I was hoping for was something showing the effect of a ketogenic diet on endotoxin.
Another thing Peter has suggested, is that on a ketogenic diet, there's less for bacteria to eat-->less bacteria, less endotoxin. So even if a greater fraction of endotoxin is absorbed on a high fat diet, there might not be as much endotoxin there to absorb. Another factor might be the effect of the diet on postprandial triglycerides, take a diabetic who responds well to a ketogenic diet, and their postprandial triglycerides during a fat tolerance test are going to look more like what happens to a non-diabetic--maybe if they start handling digestion of fat more like a non-diabetic, they'll end up with a non-diabetic's exposure to endotoxin, as well.
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