We have the !Kung consuming anything from zero to 1000kcal/d of mongongo nuts per day, average 800kcal/d, ie about 40% of calories:
You can download the full text from Scihub. It's a nice read.
So. If this is the case you have a pair of opposing effects, from the Protons point of view the LA is insulin sensitising and will allow excess insulin signalling to distend adipocytes when they should be signalling that they are full. Under fasting it can allow relative hypoglycaemia, encouraging food intake, but that's not a feature of this study. All subjects were only fasted for four hours.
At exactly the same time the alpha eleostearic acid derived CLA will be facilitating the release of FFAs from adipocytes which means that fat cells stay approximately the correct size and those FFAs are available to be perceived by the brainstem. So, from the adipocyte point of view we have excess calories-in and excess calories-out concurrently. If the adipocytes never distend we will never have to deal with size-derived excess basal lipolysis and the associated appropriate insulin resistance.
Now we can look at how that might explain the observation in this paper
Metabolic Responses to Oral Glucose in the Kalahari Bushmen
"Since an overnight fast would probably have been broken (owing to the almost continuous eating pattern of the Bushmen when food is available), we performed tests in the afternoon, after four hours of observed rest and fasting."
The Bushmen eat very frequently when food is available but never enough in total to become obese.
What does an oral glucose tolerance test look like in a !Kung bushman?
Like this:
As the authors comment
"Mean glucose levels were higher in the Bushmen at all stages, with significant differences at 0 and 120 minutes. Indeed, by lax criteria of evaluation (Jackson et al., 1970), their mean two-hour post-glucose level of 121 mg/ 100 ml could be regarded as falling within the "diabetic" range. Conversely, the Bushmen exhibited insulinopenia throughout the test, and this was significant at 0 and 60 minutes."
"Mean glucose levels were higher in the Bushmen at all stages, with significant differences at 0 and 120 minutes. Indeed, by lax criteria of evaluation (Jackson et al., 1970), their mean two-hour post-glucose level of 121 mg/ 100 ml could be regarded as falling within the "diabetic" range. Conversely, the Bushmen exhibited insulinopenia throughout the test, and this was significant at 0 and 60 minutes."
These people are insulin sensitive, as you would expect from a high LA intake. However they don't become obese because they never secrete very much insulin, ignoring the CLA. Does anyone recall this image of an isolated, perfused rat pancreas?
The closed circles are perfusion with LA. So perhaps it's not too surprising that the !Kung are hypoinsulinaemic. And it doesn't matter because they are also very insulin sensitive. This balances out.
In some ways they remind me of Jim Johnson's reduced insulin gene dosed mice in which, during early life, some glucose intolerance was present secondary to hypoinsulinaemia but this self corrected with age. Clearly the !Kung, with normal insulin genetics, are quite capable of becoming obese on an high LA diet simply by ramping up their insulin secretion in response to a mixed diet and it is the CLA which stops this. So they never develop the problems secondary to distended adipocytes.
Other explanations welcome.
What would have been really interesting would have been an insulin tolerance test which looks at insulin sensitivity without needing any confounding contribution from (decreased) pancreatic insulin secretion. I think we can assume that there would have been a profound fall in blood glucose in response to exogenous insulin.
Peter
