January 28th, 2009


Positive feedback loops

...there is a difference in the bacterial taxonomic composition between obese and non-obese humans. They have shown that obese mice and people harbour in their guts a dominant population from the bacterial division Firmicutes. At the same time, lean people (or even those on a weight-loss diet) and lean mice, have less bacteria from the Firmicutes division and more from the Bacteroidetes division.

They found that in obese mice the gut bacterial population contained more enzymes that broke up complex carbohydrates, like starch. Other experiments showed that indeed, the population of bacteria in obese mice break up complex sugars more efficiently; that is, the bacterial populations of obese mice provide their hosts with smaller sugar molecules that are readily absorbed through the gut, creating a vicious feed-forward cycle: if you are a fat mouse, you will get more calories from the same piece of chow than if you are a lean mouse.

Their conclusion was that the human gut bacterial population is intimately connected with what we eat. High poly-carbohydrate foods eventually enrich their consumers’ guts with carbohydrate loving bacteria; and those, in turn, “reward” their hosts with the back-handed compliment of making more simple and easily absorbable carbohydrates available to them, making them fatter.

Consider a slice of whole wheat bread, about 100 calories.* This means that the actual caloric intake from a slice of bread will differ between individuals. Unfortunately, it is the fatter person who will, quite probably, receive more calories from eating the same slice of bread, because his gut bacteria will deliver more available calories to him.



Dhurandhar collected blood samples from 52 overweight patients. Ten of them, nearly 20 percent, showed antibody evidence of prior exposure to the SMAM-1 virus, which was a chicken virus not previously thought to have infected humans. Moreover, the once-infected patients weighed an average of 33 pounds more than those who were never infected and, most surprisingly, had lower cholesterol and triglyceride levels — the same paradoxical finding as in the chickens.

With Ad-36, Dhurandhar and Atkinson began by squirting the virus up the nostrils of a series of lab animals — chickens, rats, marmosets — and in every species the infected animals got fat.

“The marmosets were most dramatic,” Atkinson recalled. By seven months after infection, he said, 100 percent of them became obese.

Profit and risk

Last week, when RBS shares were at their lowest point (having dropped from 700p to 10p over the course of two years), I bought £100 worth.  £100 being an amount of money I could afford to have vanish into thin air if it all went horribly wrong.

The thinking being that the low price was based on people having a total loss of confidence in the bank, and didn't reflect their ability to make money in the long term.  Either they would go back up to some level of heir former value (thus massively increasing my investment) or they would be nationalised (losing me £100).  I would _never_ have put money into this that I couldn't afford to lose in its entirety.

That £100 is now worth £182.

Part of me wishes I'd put in £1000.  But I know that I don't have £1000 that I could afford to lose, and thus, although making £820 in a week would be nice, the risk level is much higher than I would be comfortable with.

I'm holding on to them for the mid-term anyway - at least a year, if not two.  I don't expect them to announce a profit this year - and possibly not next.  But there's not much point selling them on until they are back in profit, so that seems like a reasonable point to consider it.

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I didn't see the end coming

Actually, this doesn't just cover the past - it covers large chunks of the world now.  And it's the main reason why I get _so_ fed up with people who seem to think that because someone has an opinion they don't like it must mean the person is eeeevil.