The Hypocritic Oath

Crossing The Sahara

Posted in Uncategorized by trinkwasser on September 16, 2009

There’s a theory that Type 2 is a two-strike disease, and an argument as to which comes first, the insulin resistance or the loss of pancreatic insulin output, both of which appear to be necessary. (Although breakdowns in the control circuit may have a similar effect to loss of beta cells in certain forms where the insulin could be produced but isn’t, or where insulin is produced but fails to shut down the glucagon output from the pancreatic alpha cells.) There are a whole bunch of feedback and feedforward loops involved, such that the worsening of one side of the equation worsens the other.

The classic view of Type 2 put forward by most of the meeja and all too many Medical Professionals and even some Type 1s is that it is a disease of fat lazy old people caused by the obesity.

That doesn’t even come close.

There’s a strong genetic predisposition, which has led to the theory of the Thrifty Gene: this makes evolutionary sense in that people with a predisposition to turn a temporary excess of food rapidly into fat can then live off it through the ensuing famine and outsurvive “normies”, whereas this becomes maladaptive in a world of continous feasts.

This has been parallelled with hibernatory species who feed themselves up, go torpid and live off the stored fat until food once more becomes available. Seasonal Affective Disorder, anyone?

It follows that the ability to switch insulin resistance on and then off again when required may well be what evolved originally.

Now one thing that switches insulin resistance off in humans is exercise. Growing more muscle increases glucose disposition simply because more muscle contains more GLUT-4 receptors. Actually using the muscle translocates these glucose transporters to the cell surfaces ready to grab glucose when necessary.

I have a paper by Colin Bibby on Sedge Warbler Migration but annoyingly only the first page now seems to be available FOC.

Sedge Warblers are sparrow-sized birds that breed in the UK and Northern Europe, then migrate across the Sahara to winter in subsaharan Africa.

In order to make this journey they double their body weight. They are insectivorous. Many birds which are adapted to seed eating feed their young on insects – the high protein high fat low carb diet grows the nestlings more rapidly.

Now what’s interesting about these warblers is that they stuff their faces with insects to put on all the fat they use as fuel for the migration – BUT they eat high carb insects – Plum Reed Aphids which are little bags of concentrated plant sap full of sugars. Some other insectivorous birds will eat berries prior to migration probably for the same reason – they need to put on body fat quickly and carbs are the fastest way.

Here’s my belief: they can switch on insulin resistance at will which enables them to rapidly stash carbs as body fat, driven by the ensuing high insulin levels, exactly as happens with humans. Then when they start their journey they are able to switch the IR off again and use the fat as fuel, in exactly the same way that many endurance athletes have discovered.

Next time researchers start their tinkering with genetically modified mice or rats, maybe they should consider Sedge Warblers instead?

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2 Responses

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  1. Gys de Jongh said, on March 21, 2010 at 10:40 pm

    very nice thoughts 🙂
    There is even a journal : Comparative medicine
    seen the Dolphins ?

    http://www.ncbi.nlm.nih.gov/pubmed/17803054?dopt=Citation
    Comp Med. 2007 Aug;57(4):390-5.
    Big brains and blood glucose: common ground for diabetes mellitus in humans and healthy dolphins.

    Healthy Atlantic bottlenose dolphins (Tursiops truncatus) have a sustained postprandial hyperglycemia, producing a prolonged glucose tolerance curve and a transient, diabetes mellitus-like state during 6 to 72 h of fasting. To further assess dolphins as comparative models for diabetes in humans, we hypothesized that a suite of hematological and clinical biochemistry changes during the fasting state may mimic those reported in humans with diabetes. We conducted a retrospective analysis of covariance to compare fasting and nonfasting hematologic and serum biochemical data, including 1161 routine blood samples from 52 healthy bottlenose dolphins (age, 1 to 49 y; male and female) collected during 1998 through 2005. Most changes found in dolphins during the fasting state–including significantly increased glucose, platelets, gamma-glutamyl transpeptidase, and alkaline phosphatase; significantly decreased serum uric acid; and shifts toward a metabolic acidodic state (significantly increased blood CO2)–have been previously associated with diabetes mellitus in humans. Therefore, healthy bottlenose dolphins may be the first complete and natural comparative animal model for diabetes mellitus in humans. Similarities between dolphins and humans, including metabolic changes associated with high-protein, low-carbohydrate diets; large brain-to-mass ratios; high central nervous system demands for glucose; and similarly unique blood glucose-carrying capacities should be further assessed to better understand the potential evolutionary paths of diabetes mellitus in these 2 species.

    PMID: 17803054

    http://nmmpfoundation.org/pressrelease.htm
    Big Brains and High-Protein Diets: An Evolutionary Advantage of Diabetes in Dolphins. A Fasting Switch for Diabetes in Dolphins. “Several years ago, we found an unexpected clue that healthy dolphins have a diabetes-like metabolism,” says Venn-Watson, in describing a study that compared blood values among dolphins that fasted overnight to dolphins that were recently fed. “Fasted dolphins had a series of changes in serum chemistries that matched those of people with diabetes. Interestingly, these same dolphins switched back to a non-diabetic profile after eating. There appears to be a switch that dolphins use to turn a diabetes-like state on and off.”

    • trinkwasser said, on March 21, 2010 at 11:17 pm

      Wow that’s brilliant. thanks!

      What was missing in the “thrifty gene” theory was how exercise reducing IR fitted into the plan. Migratory species make plain the way they switch from energy storage to energy usage mode in a short time period.

      Now the dolphins demonstrate this occurring over an even shorter timescale. This resembles how my own personal IR switches in after a glucose spike and remains for a few hours even after the BG has gone back down.

      I dug up some similar but different stuff here

      https://trinkwasser.wordpress.com/2009/09/01/diabetic-complications-the-motherlode/

      where again it looks like mechanisms which are of use in acute situations become hazardous when chronically engaged.

      This is the sort of pattern I’m seeing repeatedly. I’m trying to disengage the emergency genes from interfering with my everyday metabolism.

      Hmmm, now one way I do this is to eat fish. The dolphins are already doing that. I wonder if any researchers have thought to feed tham a high carb Heart Healthy diet?


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