Low Fat Vs High Fat?

[Braveheart]

How can Denise Minger, "In Defense of Low Fat" and Bruce Fife, in "Ketone Therapy" sound so convincing in their opposing views of fat in the diet?.... Must everything be either, or?

 

[MrSmart]

Although the dogma of either fat or carbs in a given meal as per the natural component of food has merit behind it, even looking at a timeframe of months, I personally subscribe to the evolutionary hypothesis about ketogenic states being highly stressful as an adaptive mechanism.

 

[fradon]

How can Denise Minger, "In Defense of Low Fat" and Bruce Fife, in "Ketone Therapy" sound so convincing in their opposing views of fat in the diet?.... Must everything be either, or?

they are both right as both diets work for many people

i've read people go keto fo reverse insulin resistance and also people who go glucogenic(lowfat high carb - plant based) and also reverse insulin resitance

it works because the body has two systems in the body one to burn glucose and one to burn fat
but the successs of these diets also depends on your oxidative type

http://www.ptonthenet.com/images/articles/3284_Fig.jpg

some people do horrible on keto...no energy, high cholesterol, fatty liver and its because they have the wrong oxidation tyep for that diet as their bodies are better equipped to burn glucose and not burn fat

The Scientific Basis for Metabolic Typing, Part 2 (of a 2 part <b style="color:white;background-color:#004699">series</b>) | Article | PTontheNet

 

[Braveheart]

Thank you for your input....have read a lot of Kelley's work, found it interesting.

 

[Wagner83]

Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial
Comparison of low- and high-carbohydrate diets for type 2 diabetes management: a randomized trial. - PubMed - NCBI
Impact of High-Carbohydrate Diet on Metabolic Parameters in Patients with Type 2 Diabetes. - PubMed - NCBI

 

[ddjd]

Definitely low fat, high carb

 

[Wagner83]

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity.
Sen T1, Cawthon CR2, Ihde BT1, Hajnal A3, DiLorenzo PM4, de La Serre CB5, Czaja K6.
Author information
Abstract

Obesity is one of the major health issues in the United States. Consumption of diets rich in energy, notably from fats and sugars (high-fat/high-sugar diet: HF/HSD) is linked to the development of obesity and a popular dietary approach for weight loss is to reduce fat intake. Obesity research traditionally uses low and high fat diets and there has been limited investigation of the potential detrimental effects of a low-fat/high-sugar diet (LF/HSD) on body fat accumulation and health. Therefore, in the present study, we investigated the effects of HF/HSD and LF/HSD on microbiota composition, gut inflammation, gut-brain vagal communication and body fat accumulation. Specifically, we tested the hypothesis that LF/HSD changes the gut microbiota, induces gut inflammation and alters vagal gut-brain communication, associated with increased body fat accumulation. Sprague-Dawley rats were fed an HF/HSD, LF/HSD or control low-fat/low-sugar diet (LF/LSD) for 4weeks. Body weight, caloric intake, and body composition were monitored daily and fecal samples were collected at baseline, 1, 6 and 27days after the dietary switch. After four weeks, blood and tissues (gut, brain, liver and nodose ganglia) were sampled. Both HF/HSD and LF/HSD-fed rats displayed significant increases in body weight and body fat compared to LF/LSD-fed rats. 16S rRNA sequencing showed that both HF/HSD and LF/HSD-fed animals exhibited gut microbiota dysbiosis characterized by an overall decrease in bacterial diversity and an increase in Firmicutes/Bacteriodetes ratio. Dysbiosis was typified by a bloom in Clostridia and Bacilli and a marked decrease in Lactobacillus spp. LF/HSD-fed animals showed a specific increase in Sutterella and Bilophila, both Proteobacteria, abundances of which have been associated with liver damage. Expression of pro-inflammatory cytokines, such as IL-6, IL-1β and TNFα, was upregulated in the cecum while levels of tight junction protein occludin were downregulated in both HF/HSD and LF/HSD fed rats. HF/HSD and LF/HSD-fed rats also exhibited an increase in cecum and serum levels of lipopolysaccharide (LPS), a pro-inflammatory bacterial product. Immunofluorescence revealed the withdrawal of vagal afferents from the gut and at their site of termination the nucleus of the solitary tract (NTS) in both the HF/HSD and LF/HSD rats. Moreover, there was significant microglia activation in the nodose ganglia, which contain the vagal afferent neuron cell bodies, of HF/HSD and LF/HSD rats. Taken together, these data indicate that, similar to HF/HSD, consumption of an LF/HSD induces dysbiosis of gut microbiota, increases gut inflammation and alters vagal gut-brain communication. These changes are associated with an increase in body fat accumulation.​

We ain't rats so I don't know if this is relevant. From what I remember they don't handle sucrose/fructose as we do.