We’ve discussed Metformin a number of times before, so the news from this latest research caught my eye:
long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice, while a higher dose (1% w/w) was toxic. Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced low-density lipoprotein and cholesterol levels without a decrease in caloric intake.
This isn’t the first time researchers have witnessed such beneficial effects, but the challenge is, of course, in understanding what significance this recent mouse study has for humans.
I know I just published my review of Cancer as a Metabolic Disease
, but I stumbled across some news that I thought was worth relating.
One of the most beautifully written and compelling parts of Seyfried’s exhaustive hypothesis is the idea that metastasis is too complex of a process to be accounted for by random genetic mutation. The idea that many different types of cancer cells would all somehow collect the right genetic mutations that would make them able to enter and exit tissues, evade detection by the immune system, and spread throughout the body seems ludicrous. From the very beginnings of Cancer as a Metabolic Disease, Seyfried begins to question this and show how the process of metastasis involves abilities already present in some macrophages and leukocytes:
A while ago Michael and I were discussing future article topics. There are truly a plethora of avenues to go down in this area of research and there is no lack of things to research and comment on. But even though I have a couple of pretty cool MCT articles sitting around on my desk, I want an interesting topic. I want something new. Something challenging. Besides, everyone is drinking the MCT koolaid these days. It’s become passe. (Also, it upsets my stomach and I have a personal vendetta against it. So there.)
I’d like to get some issues off my chest and take you along the journey I have been traveling recently.
When I first started writing for ketopia, I noticed in the journals a large amount of articles pointing to high fat diets as the end-all and be-all of obesity. There are endless articles about this:
I’m rushing out this morning so I don’t have time to share a lot of thoughts on this, but on first glance it seems like quite an inconvenient truth to the old guard: “missing” data from the Sydney Heart Study (1966-1973) has been found, and when analyzed, shows that current American Heart Association guidance on linoleic acid intake may be wrong.
If you don’t remember, the Sydney Heart Study is an intervention study in which the one group of men (30-59years) were asked to reduce animal fats to 10% of energy intake and to increase linoleic acid (“healthy” safflower oil, sunflower oil margarines). The control group
The world is becoming a sweeter place… At least in a very literal sense. In The Sweetening of the World’s Diet, Popkin and Nielsen explore the upward trend of caloric sweeteners in our lives.
The article first lays out some very basic evidence:
Ashton Kutcher has been in the news a lot recently. Normally this is something well worth ignoring, but in this instance it’s interesting: He’s been promoting the new Steve Jobs movie (in which he plays Steve Jobs) by explaining how he was hospitalized after following Steve Jobs’ diet for some time. Steve Jobs apparently ate nothing but fruit.
So what happened to poor Ashton? Well, the details are quite thin: “I was doubled over in pain [...] my pancreas levels were completely out of wack.” Media reports that he spent time in the hospital. The exact nature of his affliction and the treatment for it remain undisclosed.
Well that doesn’t sound particularly lovely, or interesting in the least bit. But to your average obesity researcher this is one of the hottest topics on the board right now. Brown is the new black, so to speak.
We’ve known for years that there are a couple different types of fat- your average lazy storage site white fat, and the active, heat-producing brown fat. Brown fat has a unique uncoupling protein (UCP1) that gets upregulated every time the sympathetic nervous system starts cranking out the catecholamines (epinephrine and norepinephrine). But there has turned out to be another player, a second hand in the brown fat pot.
It’s called TRIP-Br2, and it’s the latest-discovered protein you’ve never heard of. When it’s present, it inhibits the ability of your cells to burn fatty acids for energy. When absent, cells burn fat like it’s going out of style…
At least in mice, they do.
Ok, another article that’s behind a paywall, and it’s just a meta analysis, but still, it’s more evidence that the tide is turning in the medical, health and nutrition community. According to the abstract of a meta-analysis just published in the American Journal of Epidemiology,
persons on low-carbohydrate diets experienced a slightly but statistically significantly lower reduction in total cholesterol (2.7 mg/dL; 95% confidence interval: 0.8, 4.6), and low density lipoprotein cholesterol (3.7 mg/dL; 95% confidence interval: 1.0, 6.4), but a greater increase in high density lipoprotein cholesterol (3.3 mg/dL; 95% confidence interval: 1.9, 4.7) and a greater decrease in triglycerides (-14.0 mg/dL; 95% confidence interval: -19.4, -8.7).