Unless a diet can tackle insulin resistance, it will fail. Here’s why.
As anyone who has ever tried to lose weight can testify, weight loss isn’t about willpower. People who chalk up phenomenal achievements in their professional lives can spend a lifetime trying and failing to lose a few extra inches from their waistlines. Likewise, you can be the kind of human powerhouse who holds a whole family together, and still struggle with high-calorie food.
What’s going on?
In two words: insulin resistance.
The weight piles on and stays on. Not because you are weak, or because you aren’t prepared to work hard, but because your body’s ability to detect when it is full is no longer doing its job.
Think of your appetite as an energy-thermostat. When it is working properly, your drive to eat should cut out as soon as you have taken in enough calories. Unlike a thermostat, though, your appetite is not a box on a wall with a dial – it is the outcome of complex cross-talk between body chemicals, which alters according to your activity levels and eating patterns.
Insulin, and insulin resistance, are key to this process. Without insulin, your body would have no means to vary the rate at which sugar passes from the bloodstream into cells. The result would be a glucose yo-yo, sending blood sugar soaring after meals, and crashing at times of hunger. This would quickly become lethal: while too little circulating glucose can kill, too much of it causes serious damage to nerves and blood vessels.
To remain alive, then, you need a chemical that can ramp up your sugar absorption when there is plenty of glucose around, but that allows just enough sugar to remain in your blood when you’re not eating.
This, in essence, is what insulin does. After a meal, insulin opens glucose receptors on muscle cells, and (in the brain) switches off your appetite. Sugar rushes into the cells for burning, and you also stop feeling hungry. When you are not producing much insulin, though – a couple of hours after your last meal, say – the energy reserves in your liver start to release exactly enough glucose to stop your blood sugar levels from falling too low.
Insulin resistance: a disease of modernity
It’s a system that works beautifully – provided you live an active lifestyle and don’t overeat, which is easier said than done.
In the food-abundant modern world, continuous eating and little activity can lead to insulin resistance.
So, insulin’s job is to regulate your blood sugar levels after you have eaten food. In a state of health, it pushes the sugar from your food into muscle cells to be burnt as fuel. But if you are “insulin resistant” then your muscles find it hard to absorb these calories. Instead, they get dumped into your fat cells.
The trouble is, your body still craves fuel, so you continue to feel hungry. So you eat, again. Because you are insulin resistant many of the calories you absorb get diverted into your fat cells. You get fatter but still stay hungry.
During this process, your fat cells will become inflamed, as your body is trying to cram more and more energy into them. At some point you exceed your “personal fat” threshold. There is no space left to store fat internally, so it starts to overflow into your internal organs, such as your pancreas and liver, forming a type of fat called “visceral fat”.
This is when the real trouble begins. As visceral fat lays itself down in your liver, it interferes with your body’s ability to regulate its blood sugar. And as fat deposits accumulate in your pancreas, they place stress on your insulin-producing cells.
Insulin resistance and bad health
Caught in a vicious spiral of insulin resistance, elevated blood sugar, raging appetite and a failing pancreas, your body is firmly on the path to obesity, type 2 diabetes, and a frightening array of diseases.
Rising levels of abdominal fat also create a state of chronic inflammation, which contributes not only to cardiovascular disease, but can also exacerbate conditions such as asthma, eczema and rheumatoid arthritis. Insulin resistance can also cause blood pressure to rise, along with triglycerides – a type of fat that circulates in the blood.
Taken together, abdominal fat, raised blood sugar, high blood pressure and triglycerides are termed the “metabolic syndrome”, which is a known risk factor for heart disease and stroke. And as if insulin resistance could not do more damage, the fat that infiltrates your liver may, in time, lead to non-alcoholic fatty liver disease (NAFLD) and – in some – cause scarring and lead to liver failure.
Very low calorie diets: a medical revolution
Type 2 diabetes, according to the textbooks, was irreversible. In fact the NHS calls it a ‘lifelong condition’. In the early 2010s, though, doctors began to observe a curious phenomenon. In many patients who had recently undergone gastric bypass surgery, insulin resistance (and diabetes) seemed to reduce, reverse, or even disappear.
When recovering from bypass surgery, patients have to eat a very low calorie diet. Further investigation showed that it was this that was the cause of their diabetes reversal. In part, this is due to the interaction between visceral fat and adrenaline. The less you eat, the more adrenaline you make. The more adrenaline you make, the faster your visceral fat burns away. And the more tummy fat you lose, the more insulin resistance you lose with it.
Taking these findings further, a team of researchers in 2017 published the results of the DiRECT weight loss trial, based in GP surgeries1. A group of 149 overweight patients with type 2 diabetes were placed on a diet of 850 calories per day for 3-5 months, followed by 2-8 weeks of stepped food reintroduction, with structured healthy eating support for the remainder of the year. Another group were given standard healthy eating advice only.
The results astonished the medical world. Of the group on the low-calorie diet, fully 24 per cent lost 15 kg or more, compared to no members of the control group. Diabetes remission was achieved in 46 per cent of the low-calorie group, compared to 4 per cent of the control group. And, perhaps the most surprising of all, those in the low-calorie group rated their quality of life at a level that was more than double that of those receiving standard healthy living advice.
Very low calorie diets: a revolution in weight loss
Insulin resistance, we now know, is reversible. Applying the principles of studies such as the DiRECT trial, The Fast 800 represents something that has never existed before: an evidence-based, fast and effective way to lose weight, and keep it off – for life.
No two lifestyles are the same, which is why The Fast 800 is not so much a diet, as a bespoke weight loss planner. Designed to fit around your own needs, The Fast 800 comprises three tracks:
- The Very Fast 800, a twelve-week very low calorie plan for rapid weight loss
- The New 5:2, which counters insulin resistance with a regular two-day fasting regime; and
- The Way of Life, which works either as a great maintenance plan for those who have achieved their goals, or as an entry-level plan for those considering their next options
Combined with advice on planning, exercise and mindfulness, The Fast 800 is a weight loss plan based on cutting-edge medical research. It works!
Life is about much, much more than calorie counting. So why condemn yourself to years of struggling with pointless weight loss regimes, when a focused and structured intervention can switch your cravings off for life? Left unchecked, insulin resistance leads to obesity, type 2 diabetes, and serious disease. With our help, you can reverse it!
The Fast 800 is an innovative approach to healthy living and weight loss based on the latest scientific research. Developed in conjunction with Dr Michael Mosley, the online programme is for those that need more support and guidance for achieving long lasting health. For more tips and tricks, subscribe to our monthly newsletter here.
- Lean, M.E.J., Leslie, W.S., Barnes, A.C. et al (2017), ‘Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial’, The Lancet vol. 391, issue 10120, p 541-551, doi https://doi.org/10.1016/S0140-6736(17)33102-1, available at https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)33102-1/fulltext?cc=y=#articleInformation