5 Reasons Why You Need to Quit Your Diet Immediately

caveman plate it out Jan 20, 2015

The long-term success rate of dieting is 5-10% [1]. That is dismal. All the deprivation, all the stress, all the struggle, and it won’t work for most of us.

It’s not that we lack self-discipline or willpower to be successful. The problem is that dieting couldn’t be more opposite to how we’re evolutionarily designed to survive and function best. Could you ever imagine our distant ancestors going against their biological drive for survival by purposefully eating less food when it was available?

Having a crazy sweet tooth helped us survive when food was scarce, and having extra body fat was an important life insurance policy. Those who were more driven to eat and those who were better at storing fat had a better chance at survival.

Our DNA has changed very little in the past 10,000 years and we are not hardwired to eat less.

Even worse, dieting is one of the best ways to gain weight, not lose it. Continually being on and off a diet can create a cycle where the increase in stress makes us fatter over the long run. In fact, 66% of dieters don’t just gain the weight back, they gain more fat, and it’s stored preferentially as visceral fat around the midsection [2].

Dieting is one of the most physiologically and psychologically stressful things we can do. Research shows that people who diet end up gaining more weight over time than people who never do because:

1. Dieting releases cortisol. Research has shown that calorie restriction increases the production of the stress hormone cortisol [3]. Low blood glucose from not eating enough or going too long without eating signals the body that a famine is occurring. This triggers the fight-or-flight response and cortisol is released.

2. Cortisol makes us overeat. One of cortisol’s jobs is to replace the energy we theoretically spent fighting and fleeing [4]. When dieting, the only thing we’re “fighting” is the urge to eat that chocolate chip cookie, and we usually don’t win. This cortisol-induced hunger makes us seek out large amounts of food high in fat and sugar.

3. Cortisol makes us store fat. Cortisol puts the body into fat storage mode to replenish the fat stores that were released to fuel the fight-or-flight response. It takes the food we overeat and converts it into stored fat on the body, primarily around the midsection [5].

4. We lose precious muscle mass. When the body is in fat-storage mode, it breaks down stored protein from muscle mass and converts it into usable energy [6]. Less muscle mass and more fat makes us less sensitive to insulin [7, 8], an important hormone produced by the pancreas for processing blood glucose. The pancreas has to continually work harder to produce greater amounts of insulin to process glucose, which places stress on the organ. Long-term, this stress wears out cells in pancreas and can lead to diabetes.

5. Our metabolism slows. When the body goes into energy-conservation mode, it doesn’t just store fat. It also slows metabolic rate in order to conserve precious and limited energy supplies. Dieting can suppress resting metabolic rate by up to 20% [9]. Over the long run, the loss of muscle mass and decrease in metabolism can increase body fat—the exact opposite of what we’re trying to do on a diet.

Here’s how you can sustainably reduce body fat in a way that doesn’t trigger the fight-or-flight response.

1. Eat approximately every 3 hours, alternating between moderate-sized meals and small snacks. By eating small amounts all day long you keep blood glucose levels balanced and don’t trigger the fight or flight response. It prevents the release of cortisol and keeps your metabolism burning strong.

2. At meals, eat only enough to last you for about 3 hours. The goal is to eat to the point of feeling content, not full. This ensures there’s enough glucose to fuel the body, but not so much that it will be stored away in the fat cells.

3. Plate It Out at meals. Create a 50-25-25 food distribution on your plate. Your first order of business is to find a source of lean protein. It slows blood glucose levels, increases satiety, and prevents a blood glucose spike that could be stored as fat. Lean protein should comprise 25% of your plate. Next up are fruits and/or vegetables, which should take up 50% of your plate. Lastly, whole grains should make up the final 25%.

4. Make your snacks low-glycemic and in the range of 50-150 calories. Having a small snack between meals ensures blood glucose levels don’t get too low and trigger the release of cortisol. It also prevents you from getting so hungry you overeat at meals. Low-glycemic foods are broken down into glucose more slowly, make you feel fuller for longer, and are less likely to be stored as fat.

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1. Foreyt JP., Goodrick GK. (1993) “Evidence for Success of Behavior Modification in Weight Loss and Control”. Ann Intern Med. 119:698–701.

2. Benasik, J., et al. (2013) “Low-Calorie Diet Induced Weight Loss May Alter Regulatory Hormones and Contribute to Rebound Visceral Adiposity in Obese Persons with a Family History of Type-2 Diabetes.” J Am Assoc Nurse Pract. 25 (8): 440– 48.

3. Tomiyama, J., et al. (2010) “Low Calorie Dieting Increases Cortisol.” Psychosomatic Medicine. 72: 357– 64.

4. Newman, E., O'Connor, D., Conner, M. (2007) “Daily Hassles and Eating Behaviour: The Role of Cortisol Reactivity Status. Psychoneuroendocrinology. 32(2):125-132.

5. Björntorp, P. (1996) “The Regulation of Adipose Tissue Distribution in Humans. Intl J Obes Relat Metab Disord. 20(4):291-302.

6. Umpleby, A., Russell-Jones, D. (1996) “The Hormonal Control of Protein Metabolism.” Baillière’s Clin Endoc. 10(4):551– 70.

7. Srikanthan, P., Karlamangla, AS. (2012) “Relative Muscle Mass is Inversely Associated with Insulin Resistance and Prediabetes. Findings From the Third National Health and Nutrition Examination Survey.” J Clin Endocrinol Metab. 96(9):2898-903.

8. Yamashita, S., et al. (1996) “Insulin Resistance and Body Fat Distribution. Diabetes Care. 19(3):287-91.

9. Hill, A. J. (2004) “Does Dieting Make You Fat?” Br J Nutr. 92 (Suppl. 1), S15– S18.  

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