Table of Contents
If there is one disease that can be effectively prevented but is increasingly prevalent, it is obesity. We live in an era where, in developed countries, food has become so readily available that deaths from excess calories are starting to exceed deaths from a lack of them. Although this grim statistic primarily concerns the USA, obesity is a global problem. According to the WHO, one in eight people worldwide was obese in 2022. This number has doubled since 1990, and among adolescents, it has quadrupled. The number of people who are overweight, which is a precursor to obesity, exceeds 2.5 billion. If we look towards Europe, according to the OECD, in 2022, 59% of people in Slovakia and 60% in the Czech Republic were overweight or obese.[1]
Overweight and Obesity
Overweight and obesity are caused by an imbalance between calorie intake and expenditure. High-calorie and ultra-processed foods have become the most accessible form of nutrition, while the need for physical activity has practically dropped to zero, except in occupations requiring intense manual labour. This imbalance leads to excessive fat storage, which is the main cause of being overweight. When this excess fat storage exceeds a certain threshold (e.g., BMI over 30 kg/m²) and causes chronic health issues, it is termed obesity.[2]
Storing subcutaneous fat may not be a major health problem, but visceral fat, which accumulates in the abdominal cavity around internal organs, is more concerning. This type of fat is also known as toxic fat and is a source of cytokines, which mediate inflammatory responses. This chronic, long-term inflammatory process in the body leads to various chronic diseases associated with obesity.[3]
BMI Is Not Always a Reliable Parameter
The most commonly used parameter for determining obesity is the Body Mass Index (BMI). BMI simply indicates whether a person has an appropriate weight for their height. It can be easily calculated using an online BMI calculator. A person with a BMI over 25 kg/m² is considered overweight, and with a BMI over 30 kg/m², they are classified as obese.
Calculating BMI is a simple way to determine whether it is necessary to change dietary habits and increase physical activity. However, BMI’s simplicity is also its drawback. It does not account for body composition, so a person with a higher proportion of muscle mass may fall into the overweight BMI range. Elite bodybuilders can have a BMI over 30 kg/m² and only 6% body fat.[4]
A better indicator might be the waist-to-hip ratio (WHR), which directly highlights excess body fat around the abdomen.
How to Measure WHR?
- Stand straight and exhale. Use a tape measure to check the distance around the narrowest part of your waist, just above your navel. This is your waist circumference. If you cannot find the narrowest part of your waist, measure halfway between the lower edge of your ribcage and the top of your hip bone.
- Then measure the distance around the widest part of your hips – the broadest part of your buttocks. This is your hip circumference.
- Calculate your WHR by dividing your waist circumference by your hip circumference.
The table below indicates the health risks associated with WHR:
For men, a WHR between 0.95 and 1 is normal, and values above 1 indicate a high risk of obesity. For women, the critical number is 0.85. This parameter is suitable for considering fat accumulation in the abdominal area, reflecting the amount of visceral fat. However, people gain weight at different rates in different places. That means that even someone whose WHR number is within normal range can be overweight. [5]
You can complement these measurements with the waist-to-height ratio. This should range between 0.40 and 0.49. In other words, the waist circumference should not exceed half of the person’s height.[6]
All these methods together can accurately tell you about your body composition and weight. The most precise measurements are taken with devices like InBody, which can provide detailed information on body composition, body fat percentage, muscle mass, and other important parameters through bioimpedance analysis.
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Obesity as a Risk Factor for Various Diseases
The health risk associated with a high BMI and a significant proportion of adipose tissue encompasses various chronic diseases. Excess fat tissue in overweight and obese individuals produces a large number of inflammatory cytokines. These substances are normally necessary because the immune system needs to be ready with all mechanisms in case of infection or to eliminate damaged, old, and cancerous cells. However, when there are too many inflammatory cytokines, the body’s balance shifts towards continuous, chronic inflammation.[7]
Low-level chronic inflammation is closely linked to insulin resistance. Insulin resistance is a condition that once allowed our species to survive periods of food scarcity by redirecting glucose to vital organs. Nowadays, such a need is obsolete, and insulin resistance is the gateway to type 2 diabetes, where the body’s cells fail to respond adequately to insulin, leading to dangerously high blood glucose levels.[8]
Another issue with excessive fat tissue is the high concentration of free fatty acids and LDL cholesterol in the blood (dyslipidemia), which directly triggers atherosclerosis. This occurs when LDL particles begin to deposit in the walls of blood vessels, causing inflammation that results in atherosclerotic plaques that grow over time. If this condition persists, it can lead to a blocked artery and a heart attack.[9]
Overweight and obesity are also associated with metabolic syndrome, characterised by high blood pressure, high blood glucose levels, dyslipidemia, low HDL cholesterol levels, and a large waist circumference (over 102 cm in men, over 88 cm in women). If a person has at least three of these five factors, they are diagnosed with metabolic syndrome.[10]
The inflammatory process in the body and oxidative stress not only lead to cardiovascular diseases but also to certain types of cancer. An improperly regulated immune system, which is supposed to recognise and eliminate damaged and potentially cancerous cells, cannot function correctly. Oxidative stress caused by overweight and obesity can damage DNA in cells. If such mutated cells are not degraded by the immune system, the risk of cancer increases.[11]
Therefore, the motivation to lose weight, if one is overweight or obese, should not only be aesthetic but also health-related. Obesity is a disease that kills millions of people annually. While wanting a beach-ready body is a good starting point, minimising health risks should be the primary motivation for everyone.
Are Genes Responsible for a Tendency Towards Obesity?
Humans have over 19,000 genes, which allow the cells in the body to know when and what to do. Most processes are controlled by a large number of genes, whose effects are cumulative. Each person is, in their own way, a mutant with mutations in various places in different genes. Some mutations have visible effects, such as hair colour, eye colour, or skin tone. Others are less obvious and affect internal bodily processes. Sometimes, a single mutation in one gene can cause a disease.
Often, disease predispositions are only slightly influenced by one mutation, depending on lifestyle and other genes. This means that you can take a significant portion of responsibility for your health into your own hands, even though genes may complicate things. This is also true for body weight and obesity.
To the question of whether genes are responsible for overweight and obesity, we have a reasonably good answer. From a genetic perspective, we distinguish between two types of obesity, where genes have a significant or minor influence.[12]
Monogenic Obesity
The type of obesity that is 100% caused by genes is called monogenic obesity. The name indicates that it is a disease caused by a mutation in a single gene. Monogenic obesity affects only about 5% of all obese people worldwide. Because it is genetically determined, it starts in childhood and is very challenging to prevent. The impact of lifestyle on the development of monogenic obesity is minimal. At first glance, it might seem that genes causing monogenic obesity somehow lead to excessive fat storage.
The truth is that even in monogenic obesity, greatly influenced by genes, it is still about calorie balance. One of the best-studied genes causing this condition is the gene for the leptin receptor (LEPR). This receptor is crucial in regulating food intake. It is essential for leptin signalling, which gives the brain constant feedback on the state of energy (fat) reserves. Leptin is a hormone produced by fat tissue. The system is simple: the more fat a person has, the more leptin reaches the brain. Based on this, the brain knows how much fat is in the body and can regulate food intake to maintain reserves for tough times. When the amount of fat tissue decreases, leptin levels drop, signalling the brain to conserve energy or replenish it. When fat tissue increases, leptin levels rise, signalling the brain that less food is needed, and energy can be spent.
Under normal conditions, this system works well. In monogenic obesity caused by a mutation in the leptin receptor gene, this system is so disrupted that the brain constantly thinks there is not enough fat and that reserves need to be replenished. This results in excessive food consumption (hyperphagia), which the person with the mutation cannot control because their brain does not respond to leptin and is in a state of “starvation”.[13]
A very rare mutation, found in fewer than 100 people worldwide, is a mutation in the leptin gene itself. This mutation often causes leptin deficiency. If leptin is not produced in the body, or a non-functional, mutated version is produced, the brain receives no signal about fat reserves, prompting continuous eating. As with leptin receptor mutations, a person with this condition cannot control their food intake.[14]
Polygenic Obesity
Obesity, where genes play a more or less significant role, is referred to as polygenic obesity. It is caused by mutations in a large number of genes, each of which has a minimal individual effect. This type of obesity affects the remaining 95% of obese individuals and is primarily influenced by lifestyle. There are numerous genes associated with polygenic obesity, and we know very little about many of them. Although the functions of many remain unknown, they can be identified in studies comparing the genes of obese and non-obese individuals. Genes that are better understood often include the same ones found in monogenic obesity but with different mutations. Different mutations can have varying effects. While one might disrupt leptin signaling so severely that food intake becomes uncontrollable, another might only slightly increase appetite. Thus, the LEPR gene is also mentioned among genes with a weaker effect.[14]
A well-known gene associated with polygenic obesity is the FTO gene (fat mass and obesity-associated). Variants of this gene have been identified in obese and overweight individuals. Its function is not completely understood, but several of its mutations are associated with increased leptin production, altered localization of leptin receptors, and increased food intake. It is hypothesized that mutations in regulatory regions affect other genes near the FTO gene.[15]
Another interesting gene is FGF21, which encodes a hormone that controls sugar cravings. People with a specific mutation in this gene produce less FGF21, which suppresses sugar cravings. Increased sugar craving and its addictive nature heighten the risk of overeating and weight gain.[16, 17]
Even though lifestyle is key in polygenic obesity and genes have a lesser effect, it is not entirely accurate to expect that lifestyle changes will be simple for an obese individual. Someone who is overweight or obese has a disrupted leptin signaling system not due to genes, but due to lifestyle. The excess body fat creates a long-term surplus of leptin to which the brain becomes accustomed. Just as insulin resistance can develop, leptin resistance can occur, where the brain no longer responds to signals from adipose tissue.
Similar to monogenic obesity, where an individual cannot control their intake due to a lack of leptin, in polygenic obesity, the brain is used to high levels of leptin. When attempting to lose weight, leptin levels decrease, and the brain receives the same signal as with a genetic disorder: “starvation, need to replenish reserves.” This occurs despite having more than enough reserves. This is one of the main reasons why losing weight is challenging for people with excess weight and obesity.
Some variants of the mentioned genes and predispositions to higher food intake and greater weight can also be detected through available genetic tests.
Conclusion
For the vast majority of obesity cases, lifestyle is the primary factor rather than genetics. Cases where it is clear that genetics are the cause of obesity are very difficult to address with lifestyle changes. The effect of mutations is so strong that making changes similar to those achievable by the remaining 95% of obese individuals is practically impossible.
While we can “point the finger” at lifestyle, it is still extremely challenging for obese individuals to abandon the lifestyle that led them to this condition. The brain, accustomed not only to chronically high levels of leptin but also to dopamine stimulation from food, is difficult to reprogram. Overweight and obesity trigger mental health disorders that make any lifestyle changes nearly impossible. Whether genes cause obesity or not, it is a condition requiring specialist intervention.
And what about some positive conclusions? The majority of obesity cases can be easily prevented. If a person does not fall into the endless cycle of overeating and lack of physical activity, they can effectively prevent obesity and associated health problems. This holds true regardless of whether they have a predisposition to higher appetite. There is a high likelihood that 95 out of 100 people have their health in their own hands. There is no such thing as “healthy obesity.” This term arose from cases where overweight individuals did not yet show symptoms of metabolic syndrome. However, this is only a transitional state, and the risk of chronic diseases increases with a BMI over 30.[17] What is the best prevention method? Sufficient physical activity, which should include at least 150 minutes of aerobic activity and at least two strength training sessions per week.[18, 19]
Any physical activity alone is not enough if caloric intake exceeds calories burned, so a well-balanced diet with adequate protein and fibre is also crucial. Ideally, one should avoid highly processed foods that are easy to overeat. Getting enough sleep is a good way to avoid overeating sweets and other tasty but unhealthy foods. In extreme cases, weight loss medications like Ozempic might be an option. These have gained popularity in recent years but come with the drawback in the form of rapid muscle loss. While they can save lives, their misuse can cause more harm than good in the long run. Therefore, such treatment should be managed and monitored by a healthcare professional.
[1] OECD and E. Union- Health at a Glance: Europe 2022 – https://doi.org/10.1787/507433b0-en
[2] Lin, X., H. Li – Obesity: Epidemiology, Pathophysiology, and Therapeutics – https://pubmed.ncbi.nlm.nih.gov/34552557/
[3] Shuster, A., et al. – The clinical importance of visceral adiposity: a critical review of methods for visceral adipose tissue analysis – https://pubmed.ncbi.nlm.nih.gov/21937614/
[4] Khanna, D., et al. – Body Mass Index (BMI): A Screening Tool Analysis – https://pubmed.ncbi.nlm.nih.gov/35308730/
[5] Khan, I., et al. – Surrogate Adiposity Markers and Mortality – https://pubmed.ncbi.nlm.nih.gov/37728925/
[6] Bener, A., et al. – Obesity index that better predict metabolic syndrome: body mass index, waist circumference, waist hip ratio, or waist height ratio – https://pubmed.ncbi.nlm.nih.gov/24000310/
[7] Kolb, H. – Obese visceral fat tissue inflammation: from protective to detrimental? – https://pubmed.ncbi.nlm.nih.gov/36575472/
[8] Tsalamandris, S., et al. – The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives – https://pubmed.ncbi.nlm.nih.gov/31131037/
[9] Jebari-Benslaiman, S., et al. – Pathophysiology of Atherosclerosis – https://pubmed.ncbi.nlm.nih.gov/35328769/
[10] Saklayen, M.G. – The Global Epidemic of the Metabolic Syndrome – https://pubmed.ncbi.nlm.nih.gov/29480368/
[11] Pati, S., et al. – Obesity and Cancer: A Current Overview of Epidemiology, Pathogenesis, Outcomes, and Management – https://pubmed.ncbi.nlm.nih.gov/36672434/
[12] Loos, R.J.F. and G.S.H. Yeo – The genetics of obesity: from discovery to biology – https://pubmed.ncbi.nlm.nih.gov/34556834/
[13] Park, H.K., R.S. Ahima – Leptin signaling – https://pubmed.ncbi.nlm.nih.gov/25343030/
[14] Huvenne, H., et al. – Rare Genetic Forms of Obesity: Clinical Approach and Current Treatments in 2016 – https://pubmed.ncbi.nlm.nih.gov/27241181/
[15] Fawcett, K.A. and I. Barroso – The genetics of obesity: FTO leads the way – https://pubmed.ncbi.nlm.nih.gov/20381893/
[16] Tezze, C., V. Romanello, and M. Sandri – FGF21 as Modulator of Metabolism in Health and Disease – https://pubmed.ncbi.nlm.nih.gov/31057418/
[17] Avena, N.M., P. Rada, and B.G. Hoebel – Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake – https://pubmed.ncbi.nlm.nih.gov/17617461/
[18] Marcus, Y., et al. – Metabolically Healthy Obesity Is a Misnomer: Components of the Metabolic Syndrome Linearly Increase with BMI as a Function of Age and Gender – https://pubmed.ncbi.nlm.nih.gov/37237531/
[19] Bull, F.C., et al. – World Health Organization 2020 guidelines on physical activity and sedentary behaviour – https://pubmed.ncbi.nlm.nih.gov/33239350/
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