26 Jan Why Your Body Gets Fat and How Keto/Banting Works
It doesn’t take much more than an internet search or a scroll through social media to find the next diet/shake/pill/supplement or the next fitness program aimed at losing weight, usually some variation of eating less and moving more. The solution sounds so simple doesn’t it? So why then are we all still getting fatter?
You are Not a Car
Unlike a simple combustion engine the calories-in-calories-out theory would have you believe we are, our bodies are highly complex systems regulated to maintain homeostasis, the exact internal physical and chemical environment we need to keep us functioning. These body systems are regulated by hormones, chemical signals that switch bodily functions on and off, the policemen of our bodies controlling what goes where and when and what happens.
You Have Hormones
When we eat, the food is broken down into smaller molecules our bodies can absorb, carbohydrates from both simple and complex sources into glucose, proteins into amino acids and fats into triglycerides, all ready to be handled and transported to where they are needed. The most influential hormone in regulating our weight is insulin (1).
Insulin is a hormone best known for its job in moving glucose into cells to maintain steady blood glucose level as hyperglycemia (high blood glucose) has catastrophic effects on our bodies. If insulin is the policeman, glucose is the rowdy soccer crowd member, spilling into the street after a game. A couple of rowdy football fans are easily contained by a handful of police but the more there is, the more police you need to keep the peace. Over time, the body comes to expect a big crowd after a meal and the police start hanging around, taking longer and longer to disperse even with a smaller crowd. This can cause higher amounts of insulin in the blood long after a meal has been digested, hyperinsulinemia or high fasting insulin (2).
The Double Deal
This is problematic on two fronts. Firstly, high insulin creates another set of problems clinically referred to as insulin resistance, a condition which can lead to other diseases such as type 2 diabetes, non-alcoholic fatty liver disease and chronic inflammation (3) and more. Secondly, presence of insulin stops the use of fats by cells for energy, preventing the loss of body fat reserves and keeping us overweight and obese (4).
No. Don’t Take the Double Deal
By lowering dietary carbohydrates, our bodies stop needing and producing as much insulin allowing our bodies to tap into their fat reserves without the low-calorie restrictions and hunger often associated with diets or excessive workouts (5). This is the crux of Keto and Banting, and testimonials from our current members show the science isn’t wrong.
It can be overwhelming to tackle weight loss which is why we have distilled the noise to give a simple, practical, step-by-step pathway to your Awesome Weight (your medical ideal weight plus some cushion so you don’t have to be a robot) in our Online Keto Course.
(Shout out to Steph Fowler (PhD) for this piece – Steph you legend!!!)
- 1. Østergaard M, Mishra NK, Jensen KJ The abc of insulin: The organic chemistry of a small protein. Chemistry – A European Journal. 2020;26(38):8341-57.
- 2. Hamley S, Kloosterman D, Duthie T, Dalla Man C, Visentin R, Mason SA, et al. Mechanisms of hyperinsulinaemia in apparently healthy non-obese young adults: Role of insulin secretion, clearance and action and associations with plasma amino acids. 2019.
- 3. Yaribeygi H, Farrokhi F, Butler A, Sahebkar A Insulin resistance: Review of the underlying molecular mechanisms. Journal of Cellular Physiology. 2018;234(6):8152-61.
- 4. Jönsson C, Castor Batista AP, Kjølhede P, Strålfors P Insulin and β-adrenergic receptors mediate lipolytic and anti-lipolytic signalling that is not altered by type 2 diabetes in human adipocytes. The Biochemical journal. 2019;476(19):2883-908.
- 5. Dashti HM, Mathew TC, Hussein T, Asfar SK, Behbahani A, Khoursheed MA, et al. Long-term effects of a ketogenic diet in obese patients. Exp Clin Cardiol. 2004;9(3):200-5.