It’s time we are upfront and discuss fat loss, hunger and why you SHOULD be hungry during a diet. Yes, I have heard people say it before too.
“If you’re hungry on a diet then you’re not eating enough”
“You shouldn’t be hungry on a diet”
Or my favourite…
“My metabolism is on fire, I’m so hungry”
I hate to be the bearer of bad news, but not a single one of those statements is correct. In fact, they the complete opposite of what is going on physiologically when you place your body in a calorie deficit.
You're hungry because you are eating fewer calories than your body needs, not because your metabolism has increased, unfortunately, it is the opposite.
However, this is not necessarily a bad thing, as we can’t exactly change physiological maladaptation’s (bad) due to calorie restriction, although if we can at least understand them better than we can prepare for them and make educated decisions on how to deal with them more effectively when the time comes.
So what are some of the things that happen to our metabolism and our bodies when we diet?
And what does all that mean? Well here are some quick-fire explanations on what the relative effects of those hormones have on the body.
This is a habitual appetite regulatory hormone that tells the body to consume food and or prepare for food consumption.
During normalised dieting, Ghrelin is primarily regulated through habit (eg: if you eat every 3 hours you get hungry every 3 hours) but during times of reduced caloric intake, total circulating Ghrelin increases in an effort to induce food consumption via hunger.
Leptin is a hormone regulated by the ‘fullness’ of your fat cells, whereby during moments of lipolysis (fat breakdown) Leptin levels reduce and then signal the brain to increase appetite-enhancing hormones in an effort to refill the fat cell with the fat it has consequently lost due to being in a caloric deficit.
Decreased Leptin, which occurs during fat loss, results in increased Ghrelin.
Hedonic Brain Segment
Known as the pleasantry portion of the brain, the hedonic system is responsible for your senses such as smell and taste. During caloric restriction the body up-regulates the sensitivity of the hedonic system, causing the body to increase its sensitisation to smell and taste.
Think about it… how much better do otherwise bland foods taste during a time of caloric restriction?
The Thyroid is the gland found in your throat region that is responsible for the regulation of metabolic rate, which, among other things, helps determine how many calories you burn at rest as well as during exercise.
During times of restriction, Thyroid function down-regulates in an effort to reduce the caloric burn of the body in order to compensate for the lack of caloric intake coming from dietary sources.
To paraphrase Lyle McDonald
“Caloric restriction to your body is essentially seen as death caused by long-term starvation.”
In essence, as we restrict calories in an effort to lose aesthetically displeasing body fat stores, our system is working in the opposite direction to maintain as much fat as possible, as it provides the most amount of caloric storage the body can have and it will keep us alive longer during times of starvation.
The scary thing is just how fast this happens...
Studies suggest that even acute caloric deficits as little as 345kCal in a single day are responsible for increasing compensatory calorie intake ad libitum (without restriction) within 8 hours of eating in the days following a caloric deficit (1). What this means is that when we restrict calories and then provide people with no boundaries, they will subconsciously compensate by eating more than they normally would in order to offset the calories they missed out on, which is directly related to appetite-regulating hormone adaptations (2).
So we eat less one day, only to cancel it out the next day by eating more than we normally would.
If that’s not enough, we see that short-term hunger is increased even without Ghrelin adaptation (2) and that reported long-term hunger, alongside a reduced post feeding satiety response, is directly related to increased serum Ghrelin levels in long-term dieters (3). Similarly, long-term calorie restriction results in decreased circulating Leptin levels, with no difference in effect when comparing a low-carb versus low-fat diet (4). However, it has been postulated that this is more than likely due to the small caloric deficit used in this study (500kcal a day) and that macronutrient variability may affect hunger and hormones differently with larger caloric restrictions long term or in individuals with suboptimal body fat ranges (4) as macronutrient type becomes more important during long-term restrictive phases.
Furthermore, we also see significant reductions in Leptin, which is believed to be coordinated by Insulin, are noted in severe low-calorie dieters on less than 1000kcal per day, alongside decreased levels of the active thyroid hormone T3 as well (5). During calorie restriction, we essentially create a cocktail of sub-optimal hormones designed to make you want to EAT MORE.
Scary stuff… so what do we do about it?
First of all, it is important to note that not everyone will experience the same hunger effect of dieting. Elderly individuals have been shown to have both increased leptin levels and a reduction in satiety post feeding when compared to younger participants (6). So hunger may not be as much of an issue in the elderly due to augmented feedback loops and calorie control may need to be more closely monitored.
Now while severe caloric restriction results in severe reductions in baseline Leptin, long-term reductions are more closely related to total weight loss as opposed to caloric restriction (7). Indicating that Leptin is regulated by both total weight loss, as well as actual caloric restriction.
Knowing all of the above and the fact that we know that Leptin is controlled by Insulin, weight loss, T3 and caloric restriction, it is important for us to schedule in controlled higher calorie days, or more specifically high carbohydrate days, in an attempt to override the negative adaptations of metabolic hormones as a result of re-stimulating insulin as well as attempting to momentarily repair the energy balance equation in an effort to increase Insulin and therefore Leptin and T3 hormone, which may also reduce Ghrelin momentarily as well.
Similarly, knowing that our caloric intake, our reduced fat mass and our body weight changes all cause negative hormonal responses designed to make you fail again at your weight loss efforts, the importance of long-term dietary manipulation needs to be 100% customised to suit the individuals needs.
Severe restriction, which causes severe metabolic downturn, is more likely to result in long-term dietary failure.
So when you purchase a diet from a coach or write your own diet, it MUST be physically, psychologically and socially enjoyable to minimise the likelihood of dietary binging or weight re-gain.
Remember, your body DOES NOT want you to win this fight, so you need to be armed with all the right artillery.
The reality is, that dieting is not easy.
You will and should be hungry if you are eating in a true calorie deficit, however, knowing what to expect means you can at least plan to succeed.
“Failing to prepare is preparing to fail”
It’s about as cliché as it gets, but it is 100% relevant when discussing dieting.
Hunger is, unfortunately, a necessary evil of caloric restriction and so is increased flavour and smell. However, knowing what to expect will make your journey far easier, as opposed to going in blind and hoping you will feel normal, despite asking your body to lose fat that it otherwise would rather keep.
Deighton, K., Batterham, R. and Stensel, D. (2014). Appetite and gut peptide responses to exercise and calorie restriction. The effect of modest energy deficits. Appetite, 81, pp.52-59.
OConnor, K., Scisco, J., Smith, T., Young, A., Montain, S., Price, L., Lieberman, H. and Karl, J. (2016). Altered Appetite-Mediating Hormone Concentrations Precede Compensatory Overeating After Severe, Short-Term Energy Deprivation in Healthy Adults. Journal of Nutrition, 146(2), pp.209-217.
Leidy, H., Dougherty, K., Frye, B., Duke, K. and Williams, N. (2007). Twenty-four-hour Ghrelin Is Elevated after Calorie Restriction and Exercise Training in Non-obese Women*. Obesity, 15(2), pp.446-455.
Vetter, Vetter, Alisha Wade, Leslie Womble, Cornelia Dalton-Bakes, Wadden, and Nayyar Iqbal, (2010). Effect of a low-carbohydrate diet versus a low-fat, calorie-restricted diet on adipokine levels in obese, diabetic participants. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, p.357.
Miyawaki, T., Masuzaki, H., Ogawa, Y., Hosoda, K., Nishimura, H., Azuma, N., Sugawara, A., Masuda, I., Murata, M., Matsuo, T., Hayashi, T., Inoue, G., Yoshimasa, Y. and Nakao, K. (2002). Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans. European Journal of Clinical Nutrition, 56(7), pp.593-600.
Francesco, D.V., et al. (2006). Unbalanced serum leptin and ghrelin dynamics prolong postprandial satiety and inhibit hunger in healthy elderly: another reason for the "anorexia of aging". American Journal of Clinical Nutrition. 83(5), pp 1149-52. WEB
Wadden, T. (1998). Short- and Long-Term Changes in Serum Leptin in Dieting Obese Women: Effects of Caloric Restriction and Weight Loss. Journal of Clinical Endocrinology & Metabolism, 83(1), pp.214-218.