The human tendency is to think in black-white/mutually exclusive terms. We love to dichotomize concepts in attempt to better organize & grasp them mentally. It’s common for people in the health & fitness space to put hormones and calories in an either-or battle, but that’s just not the reality of physiology.
FALSE: Weight loss is all about hormones, not calories.
FALSE: Weight loss is all about calories, not hormones.
TRUE: Calories and Hormones are inseparable.
Hormones regulate appetite, which influences caloric intake. This affects energy balance which ultimately dictates bodyweight. So, how we can tackle that evergreen fat loss issue?
Being overweight and obese can be understood as "energy balance disorder, which results from consuming excess calories in relation to the energy expended to sustain life and perform physical work." Paradoxically, the growing prevalence of obesity in the world’s population coincides with an increase in "dieting" as weight loss attempts, apparently unsuccessful on global range.
“People say” that approximately 7,700 calorie deficits are needed to lose one pound of body weight/body fat. Hence, every day we can come across a number of statements that "losing weight is pure mathematics".
Generally, weight loss indeed is induced by a negative energy balance; however, we typically view weight change as a static function, thinking that energy intake and energy consumption are independent variables, resulting in a fixed rate of weight loss assuming a constant energy deficit. This is, of course, wrong on multiple levels - calorie intake and calorie expenditure are NOT independent variables.
Four initial and most common misconceptions are:
1. There will be no organism-level resistance to energy restriction/increase in physical activity!?
It has been scientifically proven that energy compensation also occurs with reduced caloric intake and/or increased activity levels.
When we are on a “diet”, the presence of adaptive thermogenesis is mostly overlooked - a reduction in resting energy expenditure caused by a lack of food intake. This phenomenon is above the reduction in calorie expenditure caused by weight loss. As a result of this metabolic adaptation, the observed weight loss is disproportionately smaller, and is accompanied by an earlier plateau in weight loss, despite strict adherence to dietary intervention.
There is a wealth of scientific evidence showing mandatory and adaptive changes in TDEE (energy consumption) that occur in response to energy deficits (e.g., during weight loss process). It is clear that static modeling significantly overestimates weight loss by ignoring changes in EE observed when the body is in negative energy balance.
Understanding the impact of daily activities on energy balance is crucial. Increasing the level of activity can lead to a decrease in energy consumption feedback due to compensatory responses in inactivity part of energy consumption. This cause-and-effect relationship has profound implications for both the evolution of metabolism and human health.
The degree of energy compensation varies considerably among people of different body composition. This association between energy compensation and obesity could be due to individual differences in compensation: people who compensate more strongly may be more likely to accumulate body fat. Alternatively, the process could happen within individuals: as we get fatter, our body can more powerfully compensate for calories expended during activity, making it harder to lose fat. Establishing a causal link between energy compensation and obesity is key to improving public health strategies regarding obesity.
2. Focusing only on the number on the scale and striving for the fastest possible weight reduction?!
The simultaneous increase in the number of weight loss attempts and the global prevalence of obesity is indicative of the observation that “dieting mentality” does not necessarily lead to long-term sustainable weight loss. With great inter-individual variability in the observed weight loss outcomes, an individual’s physiological response to energy restriction must be considered to determine the success of a weight loss intervention.
Higher energy deficits caused by very low-energy “diets” on paper result in significantly greater weight loss than low-energy diets, with additional benefits in the treatment of diabetes.
Another popular way to restrict energy is the so-called 'fad diet'. Dietitians define a “fad diet” as a very restrictive diet that includes several foods or an unusual combination of foods in a short period of time, with often resulting in very rapid weight loss. Such "diets" often limit energy consumption by excluding whole food groups, macronutrients, or feeding times, with claims of drastic weight loss and health benefits. A recent review of popular fashion diets suggested that juice cleanse “diet”, paleo diet and intermittent fasting (occasional fasting) are among the most popular “diets”.
In these circumstances, excessive loss of metabolically active muscle tissue almost always occurs. This will inevitably affect the total calorie expenditure of an individual over time, there will be a decline in calorie expenditure at rest and, consequently, easier accumulation of new fat/weight in the future.
Body composition is the primary determinant of REE (rest energy expenditure), explaining 60-90% of variability among individuals. Elia et al. they measured specific REEs of different body tissues, called Ki values (expressed as kcal/kg per day). Fat-free mass (FFM) has a significantly higher metabolic rate than fat mass (FM). While metabolic organs and skeletal muscle have Ki values of 200-400 and 13 respectively, adipose tissue has a Ki value of 4-5.
Therefore, an individual with a higher proportion of lean FFM mass (consisting of muscle and organs) will have a higher REE than individuals corresponding to height and weight with a higher proportion of FM. Accordingly, REE is also determined by body size, with bigger muscle related body size indicating metabolically active tissue and higher energy needs than in lower muscle mass body, despite the same proportional body composition in terms of height and weight.
3. Looking at weight loss as a linear function without influence of hormones balance?!
Such approach also ignores changes in circulating hormones (primarily ghrelin, leptin and others), and in mitochondrial efficiency itself, which will affect appetite regulation, body heat production and ultimately, you guessed it - total calorie expenditure.
Skeletal muscle is the primary site of the thermogenic effector system. This system is orchestrated by the circulation of the substrate between lipid oxidation and lipogenesis, and is regulated by hormones including insulin, leptin, and nor-epinephrine.
Leptin is secreted by adipocytes in adipose tissue in proportion to the existing adipose tissue FM. During the period of energy restriction, depleted TAG (tri-acyl-glycerols - triglycerides) stores result in decreased leptin (satiety hormone) production, which directly reduces substrate circulation in skeletal muscle. In addition, leptin indirectly reduces skeletal muscle thermogenesis through sympathetic-thyroid axis suppression, with decreased production of norepinephrine and triiodothyronine that have similar regulatory effects on substrate circulation.
Insulin is secreted by the pancreas in response to elevated blood glucose levels, so during periods of energy restriction, lower dietary carbohydrate intake results in decreased insulin production, which is said to have similar direct and indirect effects on substrate circulation and skeletal muscle thermogenesis.
However, skeletal muscle is a major consumer of glucose and a primary site for glucose metabolism, meaning that suppressed thermogenesis will result in reduced glucose utilization during the re-feeding period. The resulting hyperinsulinemia will cause redistribution of sparing glucose for lipogenesis (storage of tri-acyl-glycerides) in adipose tissue. This phenomenon, called ‘fat-compensation’, is characterized by a disproportionate FM recovery rate relative to FFM.
4. Ignoring gut health and poor microbiota diversity as obesity factor
Obesity is a disease with a complex etiology and variable prevalence across different populations, and has reached epidemic proportions in Western populations. Obesity is influenced by diet, behavior, and other environmental as well as genetic factors, and susceptibility to obesity differs by sex, age, race, ethnicity, and socio-economic status. But situation is even more complex.
Many scientific studies have reported differences in microbiota composition between obese and lean humans. One property that has been reported in multiple studies of obesity is reduced richness of microbes or their genes in obese individuals. The specific microorganism taxa reported to differ with obesity have varied across studies, so we won't go here in deep details.
But, on the other side, visible as constant through all studies, obese individuals with a low-diversity microbiota type have been characterized by more marked adiposity, greater inflammation, and poorer metabolic health compared to a high-diversity type of individuals.
So, how to improve your microbiota diversity? According to fresh scientific study published in 2021., Stanford researchers discover that a 10-week diet high in fermented foods boosts microbiome diversity and consequently improves immune responses. Regularly consuming foods such as domestic kefir, fermented cottage cheese, kimchi, kombucha fermented tea and other fermented vegetables led to an increase in overall microbial diversity.
Fermenting foods is not always practical and takes time, so you can try with ready-to-drink fermented microdrinks from Cidrani!
The more and more aggressively you lose weight below one, somewhat genetically, predetermined point, the more the body will resist - until one moment you reach the wall, when the famous yo-yo effect occur. That effect results in a rapid return of weight, probably even higher than starting point. When entering fat/weight loss process, you should take in count all four important aspects mentioned in this blog text and enter long term lifestyle change process without unreal expectations and short term goals. Ignoring even one of mentioned points could seriously undermine all efforts taken!