The idea that there is an ideal body weight for longevity and health-related reasons has been around for quite some time. However, like most things science, weight is highly-variable, it often depends on genetics, environmental factors, and lifestyle. Therefore, speculation that there is a universally uniform ideal body weight is flat-out wrong. Very quickly, academics learned that height and muscle mass should be considered when looking at a body weight that promotes well-being. With these new considerations, a new system for measuring one's body fat in terms of mass and height was termed "body mass index". This scale uses an individual's height and weight to calculate a number. This number is directly used to categorize the individual into different categories: underweight (<18.5 kg/m^2), healthy (18.5-24.9 kg.m^2), overweight (25-29.9 kgm^2), and obese (>30 kg/m^2). The downfall of this method is that the equation totally ignores the subject's muscle mass. For example, an individual is 5 feet 6 inches, and 175 lbs, and is considerably muscular. There is no abnormal distribution of fat, this individual is just muscular. According to the BMI scale, this individual is considered overweight (28.6 kg/m^2). If this individual loses significant muscle mass to meet the BMI standards, there will be a net negative impact on this individual's health. This is because muscle promotes insulin sensitivity, higher caloric expenditure, and other important metabolic functions. With all this being said, BMI calculations must be taken with a grain of salt, however, it is a quick and easy way to determine how much body fat a patient has. Taking into account both BMI and the way the subject looks physically, a considerably accurate body fat score can be produced.
When an individual is above a BMI of 30 kg/m^2, they are considered obese. It is rarely seen that a fit/athletic person would have a BMI of above 30 kg/m^2 even considering muscle mass. Bodybuilders whose weights can hit upwards of 250-300 lbs have a lot of muscle, and while their body fat levels are not significantly high, their BMI is well above 30 kg/m^2. It should be known that these individuals typically suffer from hypertension, inflammation, and other chronic diseases. In most cases, this is due to the extremely high muscle mass and the use of anabolic-androgenic steroids, which puts strain on the cardiovascular system. Although the BMI scale is not perfect, it is a quick and easy way for someone to determine their body fat. Being significantly overweight, or obese, comes with a lot of negative health risks. There have been multiple studies to confirm that having a BMI >30 kg/m^2 is detrimental to lifespan and a variety of metabolic/health markers.
This research began quite some time ago (in academic years) and took off with a mouse model, in which mice were given food ad libitum. Over time these mice would gain excess body fat and eventually reach obesity. These obese mice outwardly expressed many physical symptoms of obesity as seen in humans. In addition to this, these obese mice were less socially inclined, and in my opinion, more susceptible to depression.
While many articles have dug deep into the physiological effects of excess fat in mice, human clinical trials are still very much at their infancy. However, in most clinical trials, researchers and physicians are looking at the benefits of weight loss and other drugs, not necessarily the negative health markers that go along with being obese. With this being said, multiple studies have concluded that weight loss led to a reduction in overall adipocyte mass, C-reactive protein, interleukin-6, and adiponectin. C-reactive protein (CRP) is a commonly used marker for inflammation thus a lower CRP value, the less systemic inflammation. Interleukin-6 (IL-6) is a member of the interleukins, a family of signaling molecules in the immune system, and is another marker for inflammation thus a reduction in IL-6 is a sign of better health. Lastly, this study found a significant reduction in adiponectin, which is a hormone released by fat cells. That is correct, fat cells (adipose) release hormones that circulate in the bloodstream and have interactions with the rest of your body.
Figure 2: Relationship between obesity (BMI >30 kg/m^2) and chronic low-grade inflammation. The obese individual (left) carries excess adipose tissue. Excess adipose tissue corresponds to overexcretion of adipocyte hormones such as IL-6, adiponectin, and leptin. Hormones travel through the blood and facilitate their effects throughout the body. An excess of these hormones can cause chronic low-grade inflammation (middle).
Specifically, it is white adipose tissue (WAT) that is responsible for releasing these potentially harmful hormones. Some of these hormones released are IL-6, adiponectin, angiotensinogen, and leptin. All of these hormones are categorized as pro-inflammatory molecules, that is, they promote inflammation, which is a naturally occurring phenomenon in the body. In general, inflammation has a bad connotation, it is used in almost every advertisement displaying a new arthritis drug, and while many conversations surrounding inflammation can be extremely negative, there are just as many ways that inflammation can protect us. It plays a vital role in the innate immune system, which is referred to as the nonspecific first line of defense. The innate immune system is quite complex. The acid in our stomach, the peptides on our skin, and digestive enzymes act as an anatomical barrier in this first line of defense. In order for a microbe to infect our inner-body cells, it must penetrate these barriers, which is much harder than you might think. After these barriers, cells can start recognizing these foreign invaders through patterns. The foreign invaders, like bacteria, are not mysterious, they require proteins, genetic material, and machinery to reproduce just like our cells. Lucky for us because if our cells can recognize "self" then they can also recognize "nonself". Briefly, our cells can recognize proteins on the invaders' surface, which are detected as foreign thus triggering a cascade of events. This cascade of events leads to the release of cytokines and other signaling molecules. These molecules travel through the bloodstream and bind to specific cells, which triggers another cascade of events. This ultimately starts the primary immune response to a specific infection. Where does inflammation play a part in all this? The small signaling molecules can act to dilate the blood vessels thus leading to more blood flow in the area of infection. Along with this, the cytokines attract immune cells like neutrophils to the area of infection, these neutrophils can essentially engulf bacteria and kill them using enzymes. With the influx of blood, chemicals released from immune cells, and byproducts of phagocytosis there is no doubt that the skin will appear red, warm, and sore. This is commonly known as inflammation.
When inflammation is persistent, it can be devastating to the body. Inflammation is generally a quick reaction to a foreign invader and it is shut off very quickly after the invader is vanquished. However, if there is a problem with shutting down this inflammation, it can last years without any signs of stopping. When chronic (persistent) inflammation is present, it is often presented as a disease, such as rheumatoid arthritis and type 2 diabetes mellitus. Over the years, chronic low-grade inflammation has increased in popularity, mostly because of its association with obesity. The abundance of adipose tissue leads to excess excretion of these inflammation signals. In other words, the excess fat cells release hormones that would be released in immune cells that detected a foreign invader. This is not entirely true, as it covers part of the story. This excess fat also releases hormones that act on the hypothalamus to promote satiety, that is, the feeling of satisfaction after eating a meal. However, when excess fat accumulates, too much of this hormone is released, not only promoting low-grade inflammation but over-time results in receptor insensitivity. Receptor insensitivity has picked up steam and the term insulin resistance was coined for type 2 diabetes mellitus. Receptor insensitivity and resistance ultimately mean the same thing. Both phrases mean that a molecule that previously elicited a response upon binding no longer produces this response, or at least not to the same extent. It can be thought of as tolerance, when someone drinks a cup of coffee every day, eventually, they need another cup to feel the same wakefulness as the first cup of coffee earlier in time. This person has built a tolerance, much like when our fat cells excrete too much leptin, our leptin receptors become less likely to respond to leptin in the blood. The complications of receptor resistance (insensitivity) are far deeper than what was explained here, however, someone does not need to know molecular signaling pathways to understand that prolonged exposure to something at a supraphysiological dose is harmful.
Interestingly, weight loss is an effective anti-inflammatory signal. Losing weight by caloric restriction or surgical intervention leads to a decrease in the proinflammatory cytokine, IL-6. Increasing evidence suggests that lowering one's BMI below 30 kg/m^2 is the first step in resolving obesity-induced chronic low-grade inflammation. Once you understand the basic mechanism behind obesity and inflammation, resolving it becomes clear. Losing weight slowly at a maintainable pace is the resolution I give to everyone suffering from obesity-related symptoms. It is important to note that eating less and losing weight is extremely difficult when stuck in the vicious cycle of obesity. A later article will discuss this cycle in much more detail and offer practical tools to help break the cycle.
Now that it is well-established that being obese is detrimental to one's health, we can also establish that there is a limit to how lean someone should be. In fact, many studies have concluded that anorexia nervosa, or the lack of appetite, is a disorder that leads to extremely low body mass and body fat. This decrease in adipose tissue leads to an increase in ghrelin, the hunger hormone, which facilitates its effects mainly through the hypothalamus. Ghrelin at normal, or physiological levels, is quite beneficial., it acts as an anti-inflammatory peptide and causes a rise in growth hormone. In some cases of anorexia nervosa, ghrelin secretion (or response) is impaired thus not allowing ghrelin to facilitate its effects throughout the body. Other mechanisms explaining anorexia nervosa have pointed to impaired metabolisms, such as the inability to absorb fats thus leading to a macronutrient deficiency and putting a lot of stress on the body. While many compounding factors contribute to anorexia nervosa, one point we can take from this devastating disorder is that too little is equally as detrimental as too much.
So far, we have discussed that having too much or too little body fat is detrimental to one's health. But what is healthy? The range, in terms of BMI, is between 18.5-29 kg/m^2. Although as discussed in previous posts, health is not binary nor is it static. Someone isn't either unhealthy or healthy, in the same way, weight is not strictly healthy or unhealthy. Health itself is a range and while most people overuse the word, it shall be known that health is dynamic and only knows the boundaries within its own range. For example, one individual has a BMI of 23 kg/m^2, while another one has a BMI of 31 kg/m^2. Both of these individuals visit their physicians and receive annual blood work. Their blood work shows no deviations from the year before even though the second visitor's BMI is above 30 kg/m^2. Although the BMI indicates this individual as obese, they feel energized, happy, and sleep great. These signs should be considered in tandem with their blood work/test. Another point to be considered is longitudinal data. Longitudinal data refers to the repeating of observations/tests in a time-fixed manner. An example of this would be getting blood work done every 2 months or having your breasts examined every month for early detection of breast cancer. The point of longitudinal data is to observe patterns and make verifiable inferences. A future post regarding longitudinal data will elaborate on the importance of this method for validating health.
The scope of health is not restricted to the amount of body fat one has accrued over a lifetime. The dynamic state of health allows individuals to be different from one another while still living in an optimal state. The weight on the scale by itself means nothing, however, in conjunction with BMI, inflammatory markers, mood, sleep quality, and other physician-recommended measurements, it becomes something meaningful. Another important aspect to consider is sustainability. Crash dieting for a short duration and then binge eating back to the starting point (or beyond) is detrimental physically and mentally. The right path is the one you can sustain over a long-time frame, which should be at minimum a decade. More than likely, the progressive gaining of body fat occurred over some years, so it should take around that time to lose that fat.
Summary
In summary, body weight, which in this case, is the number on the scale has no direct correlation with your health. Instead, when put into a simple equation (kg/m^2) weight can be used to find one's body mass index (BMI). BMI is often times used to evaluate one's physical health. The literature supports the hypothesis that there lies a healthy range, from around 19 kg/m^2 to 25 kg/m^2. Although, the aspect of health is oftentimes individual dependent. BMI should not be the only guide used when assessing health, however, obesity (>30 kg/m^2) has been correlated with many complications. Other guides one may use when assessing health are sleep quality, blood work, mood ratings, and other physician-recommended tools.
Meet The Author
Hello everyone,
My name is Joshua Giblin. I am a post-bachelor researcher/research technician at USC. My interests range from nutrition to nanomedicine and also practical science to improve everyday life. Through this blog, I aim to communicate practical scientific research and present it to curious individuals so that an educated decision can be made. Thank you for reading the blog and showing your support.
Literature cited
- Castro, A. M., Macedo-de la Concha, L. E., & Pantoja-Meléndez, C. A. (2017). Low-grade inflammation and its relation to obesity and chronic degenerative diseases. Revista Médica Del Hospital General de México, 80(2), 101–105. https://doi.org/10.1016/j.hgmx.2016.06.011
- Dalton, B., Campbell, I. C., Chung, R., Breen, G., Schmidt, U., & Himmerich, H. (2018). Inflammatory Markers in Anorexia Nervosa: An Exploratory Study. Nutrients, 10(11), 1573. https://doi.org/10.3390/nu10111573
- Guerre-Millo, M. (2002). Adipose tissue hormones. Journal of Endocrinological Investigation, 25(10), 855–861. https://doi.org/10.1007/BF03344048
- Karczewski, J., Śledzińska, E., Baturo, A., Jończyk, I., Maleszko, A., Samborski, P., Begier-Krasińska, B., & Dobrowolska, A. (2018). Obesity and inflammation. European Cytokine Network, 29(3), 83–94. https://doi.org/10.1684/ecn.2018.0415
- Liu, R., & Nikolajczyk, B. S. (2019). Tissue Immune Cells Fuel Obesity-Associated Inflammation in Adipose Tissue and Beyond. Frontiers in Immunology, 10. https://www.frontiersin.org/article/10.3389/fimmu.2019.01587
- Mathur, N., Mehdi, S. F., Anipindi, M., Aziz, M., Khan, S. A., Kondakindi, H., Lowell, B., Wang, P., & Roth, J. (2021). Ghrelin as an Anti-Sepsis Peptide: Review. Frontiers in Immunology, 11. https://www.frontiersin.org/article/10.3389/fimmu.2020.610363
- Moschen, A. R., Molnar, C., Geiger, S., Graziadei, I., Ebenbichler, C. F., Weiss, H., Kaser, S., Kaser, A., & Tilg, H. (2010). Anti-inflammatory effects of excessive weight loss: Potent suppression of adipose interleukin 6 and tumour necrosis factor α expression. Gut, 59(9), 1259–1264. https://doi.org/10.1136/gut.2010.214577
- Mraz, M., & Haluzik, M. (2014). The role of adipose tissue immune cells in obesity and low-grade inflammation. Journal of Endocrinology, 222(3), R113–R127. https://doi.org/10.1530/JOE-14-0283
- Rusu, C. C., Racasan, S., Moldovan, D., Potra, A., Tirinescu, D., Budurea, C., Orasan, R., Patiu, I. M., Bondor, C., Vladutiu, D., Delean, D., Danu, A., & Kacso, I. M. (2018). Ghrelin and acyl ghrelin levels are associated with inflammatory and nutritional markers and with cardiac and vascular dysfunction parameters in hemodialysis patients. International Urology and Nephrology, 50(10), 1897–1906. https://doi.org/10.1007/s11255-018-1933-7
- Smith Jr., D. L., Yang, Y., Nagy, T. R., Patki, A., Vasselli, J. R., Zhang, Y., Dickinson, S. L., & Allison, D. B. (2018). Weight Cycling Increases Longevity Compared with Sustained Obesity in Mice. Obesity, 26(11), 1733–1739. https://doi.org/10.1002/oby.22290
- Tanaka, T., Narazaki, M., & Kishimoto, T. (2014). IL-6 in Inflammation, Immunity, and Disease. Cold Spring Harbor Perspectives in Biology, 6(10), a016295. https://doi.org/10.1101/cshperspect.a016295
- Van Gaal, L. F., Mertens, I. L., & De Block, C. E. (2006). Mechanisms linking obesity with cardiovascular disease. Nature, 444(7121), 875–880. https://doi.org/10.1038/nature05487