News
Top blogs
Podcast
Topics
EventsInterviews with experts and kids(!) from the Low-Carb Cruise
What did the participating experts – and their kids – think about the recent Low-Carb Cruise in the Caribbean? Watch the short video above to find out!
The Full Interviews
If you want to not just watch the highlights but get to watch the full eight interviews, it’s available at the membership site (free trial one month).
Eight short interviews from the Low-Carb Cruise
In addition to these we did eleven (!) longer and higher-quality sit-down interviews at the cruise, and lots of presentations. These are coming up as soon as they are edited.
More
If you find the low-carb kids adorable and want more I recommend the “Fat Head Kids Club” videos on YouTube.
ps— mezzovoice, I don't think it's really our place to judge anyone's appearance or weight. We never know what they're going through. A lot of factors come into play when it comes to weight and overall health. :)
Meanwhile just keep those ketones up !
http://www.ncbi.nlm.nih.gov/pubmed/25863243
The role of fructose in metabolism and cancer.
Charrez B, Qiao L, Hebbard L.
Abstract
Fructose consumption has dramatically increased in the last 30 years. The principal form has been in the form of high-fructose corn syrup found in soft drinks and processed food. The effect of excessive fructose consumption on human health is only beginning to be understood. Fructose has been confirmed to induce several obesity-related complications associated with the metabolic syndrome. Here we present an overview of fructose metabolism and how it contrasts with that of glucose. In addition, we examine how excessive fructose consumption can affect de novo lipogenesis, insulin resistance, inflammation, and reactive oxygen species production. Fructose can also induce a change in the gut permeability and promote the release of inflammatory factors to the liver, which has potential implications in increasing hepatic inflammation. Moreover, fructose has been associated with colon, pancreas, and liver cancers, and we shall discuss the evidence for these observations. Taken together, data suggest that sustained fructose consumption should be curtailed as it is detrimental to long-term human health.
The Journal of Immunology May 1, 2015 vol. 194 no. 1 Supplement 48.10
Ketone body beta-hydroxy butyrate deactivates NLRP3 inflammasome in myeloid cells (CAM1P.153)
Abstract
The NLRP3 inflammasome is a major regulator of sterile inflammation. It is now known that many age-related diseases are NLRP3-dependent, including metabolic disease, cognitive decline, bone loss, and thymic demise. Therefore, decreasing inflammasome activation during aging may prevent many chronic diseases known to limit healthspan. Calorie restriction and prolonged fasting reduce inflammation. During fasting, the body uses fat for energy, leading to an increase in ketone body production as a byproduct of fatty acid oxidation. We tested the hypothesis that switching the substrates from glucose to ketones could inhibit inflammasome activation in myeloid lineage cells, macrophages and neutrophils. Here we present novel data that ketone body beta-hydroxy butyrate (BHB) inhibits NLRP3-dependent IL-1β secretion. Notably, related short chain fatty acid, butyrate does not impact the inflammasome and oxidation of ketones for energetic utilization was not required for inflammasome deactivation in myeloid cells. Instead, ketones directly inhibit inflammasome complex assembly by blocking ASC oligomerization and prionization. BHB also inhibits NLRP3 dependent inflammasome activation in vivo and in neutrophils of aged mice. Therefore, ketones may represent an anti-inflammatory intervention to prevent chronic inflammation during aging that is normally associated with functional decline and death in the elderly.
The kids were wonderful.
All the best Jan
This review (below) is iterating as well. If you dig in PubMed you'll see that ketones interact on the functional level with SIRT and mTOR.
Curr Top Med Chem. 2015 Jun 10. [Epub ahead of print]
Longevity Pathways (mTOR, SIRT, Insulin/IGF-1) as Key Modulatory Targets on Aging and Neurodegeneration.
Yokoyama Mazucanti CH1, Cabral-Costa JV, Vasconcelos AR, Andreotti DZ, Scavone C, Kawamoto EM.
Author information
Abstract
Recent data from epidemiologic studies have shown that the majority of the public health costs are related to age-related disorders, and most of these diseases can lead to neuronal death. The specific signaling mechanisms underpinning neurodegeneration and aging are incompletely understood. Much work has been directed to the search for the etiology of neurodegeneration and aging and to new therapeutic strategies, including not only drugs but also non-pharmacological approaches, such as physical exercise and low-calorie dietary intake. The most important processes in aging-associated conditions, including neurodegeneration, include the mammalian (or mechanistic) target of rapamycin (mTOR), sirtuin (SIRT) and insulin/insulin growth factor 1 signaling (IIS) pathways. These longevity pathways are involved in an array of different processes, including metabolism, cognition, stress response and brain plasticity. In this review we focus on the current advances involving the mTOR, SIRT and IIS longevity pathways during the course of healthy aging processes and neurodegenerative diseases, bringing new insights in the form of a better understanding of the signaling mechanisms underpinning neurodegeneration and how these differ from physiological normal aging processes. This also provides new targets for the therapeutic management and/or prevention of these devastating age-related disorders.