You are most certainly right, and I feel I should consider myself lucky to be carrying around the healthy version of fat, as opposed to the more disease driven kind. And I do. Nevertheless I’m perceived as being unhealthy by society around me, based purely on my appearance. Every chubby person knows the stigma, which is fundamentally unfair and based upon flawed science. I think this is mostly the reason why it’s important to me to figure this out.
The article you linked to was very interesting, and thank you for explaining the content in more legman terms. I must admit I find scientific studies/articles hard to understand.
I’ve read the one I linked to as well, but this was only one study and not an analysis of many studies. It was interesting that they didn’t find statistic significant difference regarding the size of the fat cells, but I also think they used a different method of measuring.
I know it only too well… even my life insurance is tracking my BMI now and as @richard has pointed out in the past, there’s plenty of folks even if they could get to near 0% BF, their BMI would still be classed as overweight…it’s so incredibly flawed and unfair.
I’m lucky living in Norway with a public health coverage and no need for private insurance. With this in mind, the high taxes doesn’t sting so much
Edit: Bmi is hopeless as a measure for individuals! This was created for viewing large populations - I don’t see how it became acceptable to use this for any other purpose
Camomilla, thanks for posting that article link. It’s a very interesting article in that their finding is contrary to the established view which I was parroting. Sometimes I wonder how we manage to know anything at all. I got suckered into following the herd view on the healthiness of eating a very low fat, high carb diet and discounted the contrary opinions until I realized the harder I tried to follow the mainstream diet advice the fatter and sicker I got. It pays to keep an open mind and figure out how all these things actually apply to our own unique individual selves.
I’m hoping perhaps we can gather some interesting articles in this thread, it’s obviously a very complicated topic. I’m still leaning towards your initial analysis, simply because it fits so well with my own experience. In here there are mostly n=1, isn’t it? But it’s nice to have som science to back it
The thiazoladinediones drugs for type 2 diabetics improve insulin sensitivity, increase the number of adipocytes and reduce the size of adipocytes which I think lead to the idea that more smaller adipocytes = healthy fat.
Here’s a fairy recent paper showing that an increasing ratio of leptin to adiponectin is correlated to insulin resistance and more leptin is produce by big adipocytes.
Aims/hypothesis
Obesity is the dominant cause of insulin resistance. In adult humans it is characterised by a combination of adipocyte hypertrophy and, to a lesser extent, adipocyte hyperplasia. As hypertrophic adipocytes secrete more leptin and less adiponectin, the plasma leptin:adiponectin ratio (LAR) has been proposed as a potentially useful measure of insulin resistance and vascular risk. We sought to assess the usefulness of the LAR as a measure of insulin resistance in non-diabetic white adults.
Methods
Leptin and adiponectin levels were measured in 2,097 non-diabetic individuals from the Ely and European Group for the Study of Insulin Resistance (EGIR) Relationship between Insulin Sensitivity and Cardiovascular Risk (RISC) study cohorts. LAR was compared with fasting insulin and HOMA-derived insulin sensitivity (HOMA-S) in all individuals and with the insulin sensitivity index (M/I) from hyperinsulinaemic–euglycaemic clamp studies in 1,226 EGIR RISC participants.
Results
The LAR was highly correlated with HOMA-S in men (r = −0.58, p = 4.5 × 10−33 and r = −0.65, p = 1.1 × 10−66 within the Ely and EGIR RISC study cohorts, respectively) and in women (r = −0.51, p = 2.8 × 10−36 and r = −0.61, p = 2.5 × 10−73). The LAR was also strongly correlated with the clamp M/I value (r = −0.52, p = 4.5 × 10−38 and r = −0.47, p = 6.6 × 10−40 in men and women, respectively), similar to correlations between HOMA-S and the M/I value.
Conclusions/interpretation
The leptin:adiponectin ratio is a useful measure of insulin resistance in non-diabetic white adults. These data highlight the central role of adipocyte dysfunction in the pathogenesis of insulin resistance. Given that variations between fasting and postprandial leptin and adiponectin levels tend to be small, the leptin to adiponectin ratio might also have potential value in assessing insulin sensitivity in the non-fasted state.
Isn’t there such a thing as leptin resistance as well? If I remember correctly it was blown up in the media as the answer to obesity a few years back, but it’s so long ago that I might be mistaken.
I found this article on leptin resistance. I’m not familiar with the site it’s published on, but it seems to have references / sources listed, which makes it more reliable I think.
Yes, as I understand it a typical scenario is that as one gains weight the adipose tissue produces more leptin which should reduce hunger but when leptin remains chronically high it loses its impact (leptin resistance).
It seems the strength of many biological signals depends on their base levels. For example when you are long exposed to a strong scent or a loud sound the impact diminishes. Spend some time in a very clean or quiet environment and your sensitivity to odor and sound returns.
So leptin helps after a big meal to reduce hunger but it is less effective at suppressing weight gain that comes on slowly over a long period of time.
