I am a huge fan of Italian bitter liqueurs. I was first introduced to the idea when I was working at Memorial Sloan-Kettering in Manhattan. A co-worker brought in a six pack of bitter soda from a local pizza place. I took a sip. It was revolting. My only thought was, “this tastes like bile! …
Campari is a dual bile acid receptor agonist that activates AMPK Read More »
AMPK is a key regulator of metabolic rate and fat burning. The mainline thinking on AMPK often follows the puritanical view of classic obesity research: AMPK senses LOW cellular energy levels by monitoring the ratio of ATP to ADP and AMP.1 This suggests that the best way to stimulate AMPK is by reducing caloric intake. …
AMPK is activated by HIGH cellular energy after a starchy meal Read More »
So like I was saying, biology is weird. AMPK and SCD1 are a literal teeter totter. When SCD1 goes up, AMPK goes down. When AMPK goes up, SCD1 goes down. This matters because, as I pointed out in the last post, AMPK can help to keep us out of torpor. In hibernating animals and obese …
Summary Activating AMPK in the livers of mice prevents diet induced obesity despite higher caloric consumption Mice with activated AMPK have lower levels of cytochrome P450 enzymes that produce 12-HETE and 15-HETE – specific activators of PPAR gamma Mice with activated AMPK have higher rates of both fat and glucose metabolism AMPK blocks the pathway …
AMPK is Kryptonite to the Nuclear Receptor “Superfamily” Read More »
My last posts were viewed by some as pessimistic in a “once you’re obese, you are stuck” kind of way. I don’t believe that and very soon I will start writing about solutions. Having said that, this post will perhaps seem pessimistic if you thought the previous ones were. I’m working through the basic mechanisms …
I believe that obesity is a fuel partitioning disorder. I’ve argued that when you pack on fat, you essentially “lose” that fuel into your fat tissue. If you don’t have access to fuel, you become hungry and you eat more. In my last article, I started to delve into the mechanism of this. One thing …
In a recent post I talked about three groups of pigs with differing levels of insulin sensitivity. Group 1 was fed a low fat diet and remained insulin sensitive. Group 2 was given 40% of calories as a special soybean oil blend with the triply unsaturated alpha-linolenic acid (ALA) largely removed. These pigs became what …
PPAR gamma With Oxidized PUFA is the Gatekeeper to Metabolic Inflexibility Read More »
This is from the EPIC Potsdam study in Germany, which looked at the association between membrane phospholipid composition, diet and type 2 diabetes risk.1 Read it and weep. It looks like linoleic acid prevents diabetes after all. Time to shut down the blog, run out and buy some corn oil. KIDDING! Remember what happened to …
Hap MD asked me if I had any thoughts on Ossabaw pigs. They are interesting because they are one of the only animals other than humans who spontaneously have heart attacks (the only?). Ossabaw piings are descended from Spanish pigs that were dropped on Ossabaw island off of the coast of Georgia, United States, in …
I’ve written a lot about the strong correlation between the Desaturase Index (DI) and human obesity. DI is an indirect indicator of the activity of the SCD1 gene. I have also suggested that the consumption of linoleic acid – the primary Omega 6 polyunsaturated fat (PUFA) in the human diet found in vegetable oil, bacon …
This Is How Linoleic Acid Makes You Fat, Leptin Resistant and Torpid Read More »
I mentioned somewhere that I was leptin resistant somewhere and in the comments of the blog someone asked how I knew that I was. My immediate response was, “because I’m fat.” But also, “because I have a high desaturase index (DI), indicating high activity of the enzyme SCD1.” A high DI is an indicator that …
There are many believers in a reductionist calories in, calories out (CICO) view of the world. People in this tribe often say things like, “to lose weight, you just have to eat less and move more.” I want to be clear, I believe in calories in, calories out from a strict thermodynamic perspective. Calories you …
Introduction This is part of my Torpor, Sloth and Gluttony series where I will argue that obesity is caused not by sloth and gluttony but by specific metabolic processes. Leptin is a hormone produced by fat cells. The fatter one gets, the more circulating leptin one has. Leptin is the master hormone whose job is …
Introduction My thesis in this series is that humans get fat NOT from sloth and gluttony, human characteristics wrapped in morality and asceticism. They in fact get fat from torpor, an underlying metabolic change triggered by consuming linoleic acid. In my previous article I introduced the concepts of this series as well as the idea …
Torpor, Sloth and Gluttony: SCD1 CAUSES Humans to Store Fat Read More »
Introuction to Torpor, Sloth an Gluttony This is the first post in my new “Sloth and Gluttony” series where I will be arguing that the obesity epidemic was NOT caused by billions of people around the globe simultaneously becoming slothful and gluttonous. I will argue that in fact the reasons are biological and evolutionarily conserved. …
Torpor, Sloth and Gluttony Part 1: Americans ate a LOT in 1939 Read More »
