So much bullshit about insulin, so little time
Its 2016 and yet I still see people across the boards claiming that controlling insulin, not calories, is the key to fat loss.
They will go on & on about how insulin is the only fat storing hormone, timing insulin spikes are important and a bunch of other bullshit that I will conclusively shown to be false in this article.
What is Insulin?
Insulin is a hormone secreted in the pancreas by beta-cells. Its primary function is to regulate energy metabolism by controlling blood glucose levels but it also has a wide variety of other vital functions - zero insulin production would actually cause us to die.
The actions of insulin can be broken down into 3 different time frames:
- Within seconds it causes changes in the cell membranes involved in glucose transport
- Within minutes-to-hours it suppresses catabolic processes and upregulates anabolic enzymes involved in
glycogenesis, protein synthesis & lipogenesis (this is where all the bullshit comes from).
- The slowest effect is the promotion of anabolism via cell replication & mitogenesis.
Insulin is NOT the only fat storage hormone
Now given insulin's anabolic/anti-catabolic role that I highlighted earlier, it would be stupid to see it only as a "fat storage hormone".
While it can prevent fat mobilization by antagonizing things like HSL (hormone-sensitive lipase), this only translates to actual fat gain in the presence of excess calories and it is NOT the only hormone that does this.
ASP (acylation stimulating protein) is a hormone with the PRIMARY function of increasing fat storage - this is the real fat storing hormone.
It achieves this through 3 different mechanisms:
- Increasing diacyglycerol transferase activity = increased fatty acid esterification in adipocytes
- Stimulating glucose transport in preadipocytes
- Inhibiting HSL activity = limited lipolysis
- ASP does all this to increase lipogenesis INDEPENDENT of any insulin increase.
FSP2(fat-specific protein 27) is another compound that can also store fat within the body.
It does this through the promotion of triacylglycerol deposition achieved by binding to lipid droplets within adipocytes, which regulates their enlargement = inhibited lipolysis.
As with ASP earlier, FSP27 expression has been shown to occur INDEPENDENT of insulin activity.
Insulin activity is inferior to caloric balance
To illustrate how irrelevant insulin activity is when it comes to fat gain/loss, here is a brief run down of what the majority of the data, referenced at the end of this article, has shown us:
- Energy restriction improves glycaemic control & insulin metabolism regardless of carb intake.
- Plasma insulin levels decrease alongside weight regardless of dietary macros. Conversely, as weight increases insulin resistance occurs leading to higher insulin levels (so weight gain = insulin issues, NOT insulin issues = weight gain).
- Similar fat loss results among most insulin resistant & insulin sensitive individuals on the same plan.
- Glucose metabolism (impaired vs normal) & insulin response have been shown to be IRRELEVANT for fat loss.
- Despite pharmaceutical intervention, a trial using diazoxide to inhibit insulin secretion in 1 group showed no difference in fat loss, appetite or metabolism vs placebo (subjects were obese & insulin resistant).
So even pharmaceutical companies have realised that there is no money to be made from focusing on insulin for fat loss...let that sink in for a minute or two.
It's also important to consider that the lacklustre long term results of low carb diets on obese/sedentary individuals would be amplified in trained athletes (most AAS users) since they, in general, have better glucose tolerance.
Summary
The role of insulin is oversimplified and the fear of it among many is irrational.
Energy restriction ALONE is enough to improve glycaemic control & insulin metabolism regardless of carb intake.
Caloric changes influence hormonal changes - NOT the other way around.
Obesity can lead to hyperinsulinemia - NOT the other way round.
Fat loss is about calories, not carb intake, insulin levels, etc.
References
The adipocyte as an endocrine cell. - PubMed - NCBI
Adipose tissue as an endocrine organ: impact on insulin resistance. - PubMed - NCBI
Fat-specific protein 27, a novel lipid droplet protein that enhances triglyceride storage. - PubMed - NCBI
Fat-specific protein 27 regulates storage of triacylglycerol. - PubMed - NCBI
Differences in insulin resistance do not predict weight loss in response to hypocaloric diets in healthy obese women. - PubMed - NCBI
Differences in glycaemic status do not predict weight loss in response to hypocaloric diets in obese patients. - PubMed - NCBI
No effect of inhibition of insulin secretion by diazoxide on weight loss in hyperinsulinaemic obese subjects during an 8-week weight-loss diet. - PubMed - NCBI