News
Being an Evening Person Isn’t the Problem
You know the feeling. It’s 10:00 PM, and while the rest of the world is winding down, your brain is just hitting its stride. You’re sharp, creative, and finally "awake." But then 6:00 AM rolls around, and the alarm clock feels like a personal assault. For many, the struggle with obesity isn't a lack of willpower, it’s a state of internal desynchrony. If you are a "Night Owl" (Evening Chronotype) living in a "Morning Lark" world, you are likely suffering from a biological mismatch that actively sabotages your metabolism. It’s time to start understanding your Chronotype. Why do "Night Owls" even exist? Chronotype is a heritable, polygenic trait, meaning your preference for mornings or nights is partially "hardwired" into your DNA through variations in specific clock genes. In large modern population samples, most people fall in the middle, with smaller minorities at the extremes (“definitely morning” or “definitely evening”). For example, in UK Biobank (a community-based cohort with 439,933 adults aged ~40–69), chronotype assessed by a standard self-rating question showed 27.1% “definitely morning,” 63.9% intermediate (split across “more morning” and “more evening”), and 9.0% “definitely evening”. The distribution shifts with age (later during adolescence/early adulthood, earlier with aging) and differs with environment and social constraints, but the “mostly intermediate, fewer extremes” pattern remains consistent. Being a Night Owl might have saved your ancestors' lives. The Hadza are a conteporary hunter-gatherer community in northern Tanzania whose traditional lifestyle, free from the distortions of electric light and rigid industrial schedules, provides researchers with a vital "natural window" into how human sleep and circadian rhythms evolved. Researchers studying the Hadza hunter-gatherers found that in a typical camp, someone was awake nearly 99.8% of the time. While the "Larks" (morning people) slept, the "Owls" (night people) stayed awake, acting as sentinels to guard against predators. Your late-night energy isn't a "glitch"—it was once a survival gift. The problem isn't your clock; it's that we now live in a world that runs exclusively at "Lark Time." Social Jetlag Productivity culture quietly assigns moral value to waking at dawn. The early riser is praised, and the night person is treated as the one who needs “fixing.” The “problem” isn’t being a night person at all—it’s being a night person in a world that runs on morning rules. The problem isn't being an Owl; it's Social Jetlag—the discrepancy between your biological clock and your social obligations (work/school). Your Chronotype (evening person) is basically your body’s timing preference—when sleep feels easiest, when alertness rises, when your internal night begins. One-way researchers measure that internal timing is DLMO (dim-light melatonin onset), the point when your brain begins secreting melatonin under dim light. Later chronotypes tend to have later DLMO on average—meaning their biological night starts later. Your circadian rhythm is your body’s built-in 24-hour timing system. Think of it as a conductor that keeps thousands of “daily programs” coordinated: when you feel sleepy vs alert, when hormones rise and fall, when digestion is primed, when body temperature peaks, even when immune cells are more active. The master timekeeper sits in the brain, in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN gets direct input from the eyes (special light-sensitive retinal cells), so light is the strongest cue that resets the clock each day. From there, the SCN synchronizes the rest of the body through nerves, hormones, and behavior—helping keep peripheral clocks in organs like the liver, pancreas, fat, and gut aligned with the day–night cycle. Melatonin rises in the evening to signal “biological night,” while cortisol typically rises toward morning to support wakefulness and energy mobilization. Health effects When an "Owl" is forced to wake up at 6:00 AM, the Brain Clock: Says it’s midnight and time for rest. The Social Clock: Says it’s 6:00 AM and time for school or work. They will experience social jetlag. This isn't just about being tired; it’s a total internal desynchrony leading to health consequences. Research consistently shows that the evening chronotype is tied to a higher body mass index (BMI) and a more "obesogenic" lifestyle, but the reason isn't necessarily found in the "Owl" genes themselves. Instead, the risk is driven by a series of behavioral shifts that occur when your biological timing is pushed late: shorter sleep, late-night light exposure, and irregular eating. In studies of Mediterranean populations, "late eaters" lost significantly less weight than "early eaters," even when their total calorie intake and physical activity were identical. Late eaters also tended to be more evening-type and more likely to skip breakfast. This suggests that eating when your peripheral clocks (in the liver and gut) are winding down makes you metabolically inefficient. Eating a late-night "second dinner" happens when your pancreas is "asleep," leading to poor glucose control and increased fat storage. Misalignment blunts the morning cortisol surge and disrupts appetite hormones (Leptin and Ghrelin), making you crave high calorie, "ultra-processed" foods at night. When your sleep schedule swings by more than two hours between your work week and your weekend, you aren't just tired; you are statistically 1.3 to 1.7 times more likely to struggle with obesity. For the typical "Owl," this often happens. Furthermore, definite evening" types face a 15–25% higher hazard of cardiovascular events and 1.5 to 1.8 times higher odds of depression, and a BMI that is 0.3 to 0.6 kg/m² higher than their morning-oriented peers. A lot of studies link eveningness to cardiometabolic and mental-health risks. Much of the observed risk is plausibly driven by repeated exposure to sleep restriction, circadian phase misalignment, and behavior timing shifts (late eating, reduced morning light, inconsistent activity), rather than the chronotype trait itself. The takeaway is your chronotype is not a pathology. The harm stems from misalignments, which is a modifiable factor. If it’s misalignment, what helps? There is no need to change who you are. Modern life floods evenings with light and often deprives us of morning light. The goal is not to turn an owl into a lark. The goal is alignment. 1- Use light strategically. Light is the main clock-reset tool. In a famous natural light experiment, adults who spent one week camping without artificial light shifted their circadian timing earlier — especially those who were later chronotypes. Light expands or shrinks the owl-lark gap. Get 15–30 minutes of outdoor sunlight as soon as you wake up which can help "pull" your rhythm earlier, making it easier to fall asleep at night. Moreover, your brain thinks the blue light from your phone is the sun. Dim your lights and use filters after 8:00 PM to allow melatonin to rise naturally. 2- Stabilize wake time. The biggest mistake is "catching up" on sleep by 4 hours on the weekend. This creates a permanent state of jetlag. Try to keep your weekend wake time within 60 minutes of your weekday alarm. 3- Watch your eating habits. If you’re an evening type, evenings are often your highest-risk window for cravings. Plan it: a structured high-protein snack before cravings hit, a “kitchen closing” routine or a default if-then plan (“If I want something at 10 pm → I have X.”) “Don’t eat late” is not about 8 p.m. or 9 p.m. It’s about your biological night. Your body shifts into night mode when melatonin — your sleep hormone — starts rising. For most people, that happens somewhere between 8:00 and 10:30 p.m., but it depends on your chronotype. When you eat close to that internal night, your body handles glucose less efficiently. Blood sugar rises higher. Insulin works less effectively. The same meal eaten earlier in your biological day produces a better metabolic response. Finish your last main meal 2–3 hours before your natural bedtime. Keep your evening timing consistent throughout the week. Conclusion Chronotypes likely exist for deep-seated biological and evolutionary reasons—ranging from your genetic "wiring" to the protective "sentinel" roles humans played in ancestral groups. However, modern life, with its early-morning schedules, artificial bright nights, and late-night eating, forces certain chronotypes to pay a much higher physiological price. The JA Method shifts the conversation away from the frustrating attempt to "fix" your nature. Instead of asking, “How do I force myself to become a morning person?” the focus becomes: “How do I reduce my internal misalignment and protect my highest-risk hours?” By identifying those windows where your biology and your environment clash, you can stop the metabolic friction. That strategic alignment is where real health wins—and sustainable weight management—actually live. References Arab, A., Karimi, E., Garaulet, M., & Scheer, F. A. J. L. (2024). Social jetlag and obesity: A systematic review and meta-analysis. Obesity Reviews, 25(3), e13664. https://doi.org/10.1111/obr.13664 Garaulet, M., Gómez-Abellán, P., Alburquerque-Béjar, J. J., Luján-Antequera, S., Ordovás, J. M., & Scheer, F. A. J. L. (2013). Timing of food intake predicts weight loss effectiveness. International Journal of Obesity, 37(4), 604–611. https://doi.org/10.1038/ijo.2012.229 Jones, S. E., Lane, J. M., Wood, A. R., van Hees, V. T., Tyrrell, J., Beaumont, R. N., Jeffries, A. R., Dashti, H. S., Hillsdon, M., Ruth, K. S., Tuke, M. A., Yaghootkar, H., Sharp, S. A., Jie, Y., Thompson, W. D., Harrison, J. W., Dawes, A. S., Budd, C. L., Lewis, D. A., . . . Weedon, M. N. (2019). Genome-wide association analyses of chronotype in 447,678 individuals identifies new loci and genetic links with self-reported diurnal preference and mental health. Nature Communications, 10(1), 481. https://doi.org/10.1038/s41467-018-08259-7 Kennaway, D. J. (2023). The dim light melatonin onset: What it is and what it is not, and its relationship with morningness/eveningness. Sleep, 46(5), zsad033. https://doi.org/10.1093/sleep/zsad033 Lotti, S., Pagliai, G., Colombini, B., Sofi, F., & Dinu, M. (2022). Chronotype differences in energy intake, dietary quality, and meal timing: A systematic review with meta-analysis of observational studies. Advances in Nutrition, 13(6), 2239–2252. https://doi.org/10.1093/advances/nmac075 Malone, S. K., Patterson, F., Lu, Y., Lozano, A., & Hanlon, A. (2016). Ethnic differences in sleep duration and morning–evening type in a population sample. Chronobiology International, 33(1), 10–21. https://doi.org/10.3109/07420528.2015.1107722 Neves, A. R., Albuquerque, T., & Quintela, T. (2022). Circadian rhythm and disease: Relationship, new insights, and future perspectives. Journal of Cellular Physiology, 237(10), 3737–3758. https://doi.org/10.1002/jcp.30815 Parsons, M. J., Moffitt, T. E., Gregory, A. M., Goldman-Mellor, S., Nolan, P. M., Poulton, R., & Caspi, A. (2015). Social jetlag, obesity and metabolic disorder: Investigation in a cohort study. International Journal of Obesity, 39(5), 842–848. https://doi.org/10.1038/ijo.2014.201 Kianersi, S., Potts, K. S., Wang, H., Sofer, T., Noordam, R., Rutter, M. K., ... & Huang, T. (2026). Chronotype, Life’s Essential 8, and risk of cardiovascular disease: a prospective cohort study in UK Biobank. Journal of the American Heart Association, 15(3), e044189. Wright, K. P., McHill, A. W., Birks, B. R., Griffin, B. R., Rusterholz, T., & Chinoy, E. D. (2013). Entrainment of the human circadian clock to the natural light-dark cycle. Current Biology, 23(16), 1554–1558. https://doi.org/10.1016/j.cub.2013.06.039
Learn more
Why Having ‘Healthy Obesity’ Is Still Dangerous for Your Health?
Introduction Obesity has long been linked to shorter lifespans, lower quality of life, and increased risk of disabilities due to cardiovascular diseases like diabetes and atherosclerosis. This raised the question: how can some individuals with obesity appear healthy over the long term, whereas others show immediate signs of health problems? The concept of metabolically healthy obesity has caused quite a stir in the medical community and beyond in recent years, as it challenges deeply held beliefs and long-standing understandings. But the recognition of this phenomenon is far from a new discovery! It dates to Jean Vague’s observations in the 1950s that certain individuals with obesity had different predispositions towards diabetes and atherosclerosis, which seemed to be related to where their fat was concentrated on their bodies. What is the definition of metabolically healthy obesity? While individuals who have metabolically healthy obesity (MHO) have been extensively researched, a consensus on a definition in adults has only recently been reached. Metabolically healthy obesity (MHO) is defined as a BMI of 30 kg/m2 or higher and no concurrent metabolic disorder or cardiovascular diseases, such as type 2 diabetes or atherosclerotic disease. A more recent definition has been proposed, requiring additional criteria such as serum triglycerides ≤150 mg/dl and HDL-cholesterol serum concentrations higher than 40 mg/dl in men or 50 mg/dl in women. Do people with “healthy obesity” exist? Recent studies show that MHO is found in 35% of the world’s population. However, there were notable differences between regions and various parts of the world. Irrespective of the definitions used and the remarkable regional and gender variation, MHO is not a rare condition. Long-term studies have suggested that MHO might be a transient state. About 30% of people with MHO develop or convert to a metabolically unhealthy obesity (MUHO) state with cardio-metabolic complications over a 5-10-year period. Aging and additional weight gain are risk factors for this conversion. Fortunately, increasing physical activity and losing weight can increase the likelihood of preserving MHO status. What are the health risks of “healthy obesity”? Metabolically healthy obesity is an interesting and complex phenomenon – on the one hand, these individuals are typically free of metabolic signs associated with “unhealthy weight”, yet they still have higher cardiovascular risks than those who maintain a normal weight. However, their cardiovascular risks are lower than those of people with metabolically unhealthy obesity (MUHO). A 2019 study, for example, found that those with metabolically unhealthy obesity (MUHO) are 5-20 times more likely to develop diabetes than those with a ‘metabolically healthy normal weight’. Even for those with metabolically healthy obesity (MHO), there is still a 4-fold increased risk of developing diabetes compared to metabolically healthy normal weight. Similarly, the risk of cardiovascular diseases is 50% greater in people with MHO at baseline than in people who are metabolically healthy at a normal weight. This means that while there are still risks involved with being classified as metabolically healthy obese, they are nowhere near as severe as those associated with those who are metabolically unhealthy. How to prevent the transition to metabolically unhealthy obesity? As MHO is not a static condition, attention has now shifted to what factors may predict metabolic deterioration from MHO to MUHO. A study in Spain identified three main factors: an increase in BMI, waist circumference, and waist-to-hip ratio. On the flip side, lifestyle choices like following a healthy diet, regular exercise, and avoiding or quitting smoking prevented the transition to MUO. It’s clear from this that good habits can help maintain our health and protect us from potentially serious conditions like MUO. Conclusion There is such a thing as metabolically healthy obesity, but it may be transient and comes with its own risks. The best way to avoid these risks is to maintain a healthy weight through diet and exercise. So, let’s take care of our health and be more mindful of what we eat and how much we exercise. References Blüher, M. (2020). Metabolically Healthy Obesity. Endocrine Reviews, 41(3), 405. Smith GI, Mittendorfer B, and Klein S. 2019. Metabolically healthy obesity: facts and fantasies. The Journal of clinical investigation 129:3978-3989. Post navigation
Learn more
Homeostatic and Hedonic Hunger
Have you ever wondered why you can’t stop eating, even when you’re full? Or why do you eat more than your body needs? Have you ever felt like starving even after eating a big meal? Or found yourself craving food, even if it wasn’t remotely close to mealtime? If so, what you experienced is called hedonic hunger. It turns out that what we think of as “hunger” is two different things. In modern times, among well-nourished populations, an increasing proportion of human food consumption appears to be driven by pleasure, not the need for calories —which isn’t necessarily bad! In this article, we’ll look at homeostatic and hedonic hunger to better understand the motivations behind food consumption. History of Human Food Consumption For most of human history and prehistory, the primary objective of seeking food was survival through maintaining energy homeostasis and avoiding starvation. Humans had to eat enough food that provided enough calories to meet their daily needs. It was essential for early humans to have enough energy to perform physical tasks such as gathering food and other resources or defending themselves from predators. In modern times, energy homeostasis is no longer an issue for most people living in developed countries who no longer need to worry about finding food for existence. The availability of an abundance of tasty foods has changed our relationship with eating from one primarily focused on survival to one also driven by pleasure. Hemeostatic vs. Hedonic Hunger Homeostatic hunger is what most people think of when they hear the word “hunger.” It refers to the body’s need for energy to maintain balance (homeostasis). When your body needs energy, it sends signals to your brain telling you to eat. Physiological needs drive this type of hunger. Hedonic hunger, however, is driven by pleasure and anticipation of reward rather than physiological needs. Hedonic hunger is an intense, psychological desire for food triggered by external cues such as the sight or smell of food, social events, time, or advertising campaigns. Unlike homeostatic hunger, which is generally limited to only what our bodies need in terms of calories, hedonic hunger is not constrained by physical limitations and can often result in over-consumption. The interplay between these two types of hunger has become increasingly complex in recent years due to the availability of calorie-dense foods with high levels of added sugar and fat. These foods are designed for maximum pleasure, making them difficult for many people to resist even if their body does not need them. How do We Know We are Hungry? Hunger is challenging to specify. We need help not only quantifying our hunger, but many need help identifying whether we are hungry at all. There may be no solid characteristic pattern of hunger symptoms when it comes to typical hunger sensations. When participants were asked about hunger sensations, there were three key identifiers. First and foremost, most people experience a growling stomach as an indicator that it’s time for food. Secondly, many people also report feeling an empty sensation in their stomach when they are hungry. Lastly, some people describe feeling mild to moderate stomach pain when hungry. In addition to these typical hunger sensations, many people experience extreme hunger sensations: headaches, lightheadedness, or dizziness, being fixated on food and feeling irritable or cranky. Understanding the distinction between homeostatic and hedonic hunger is essential for physical and mental health since it can help us make better food choices. There are distinct neural pathways associated with homeostatic and hedonic motivation for eating with animal models; however, further research should be conducted to understand how these systems interact within humans. It is sometimes hard to recognize the type of hunger in real life. However, hedonic hunger involves two constructs: liking and wanting. Liking vs. Wanting Food The primary difference between liking and wanting food lies in the motivation behind eating. Liking is a pleasure derived from oro-sensory stimulation of food – think flavors, textures, smells, etc. Conversely, wanting is defined as incentive salience or the motivation to engage in eating. When you want something, you are more likely to seek it out despite any associated costs or calories involved. By understanding these two different types of motivation when it comes to eating, we can begin to make better decisions about our diets and health goals. For example, if you “like” a specific type of food but do not necessarily need it (i.e., don’t have an urgent “want”), then it may be best to practice moderation rather than overindulge in something your body doesn’t need. On the other hand, if you want a particular type of snack despite having already eaten earlier in the day (or week!), then perhaps it’s time to take a step back and ask yourself why – are you bored? Stressed? Anxious? Identifying those underlying motivations for wanting specific foods can help us develop healthier habits and make more informed decisions about what we eat. Conclusion Enhanced hedonic response to foods can augment hunger even when satiated, meaning that even if we don’t feel hungry, we may still be tempted by tasty treats. Identifying between homeostatic and hedonic hunger can be challenging but ultimately rewarding. You will have more control over your eating habits if you understand where those cravings come from! By paying attention to cues from your body, keeping track of meals/snacks throughout the day, and taking breaks whenever necessary, you’ll be able to tell which type of hunger is driving your appetite–and make healthier choices accordingly! All this shows just how complex our relationship with food can be. References Lowe, M.R. and Butryn, M.L., 2007. Hedonic hunger: a new dimension of appetite?. Physiology & behavior, 91(4), pp.432-439. Blundell, J.E. and Finlayson, G., 2004. Is susceptibility to weight gain characterized by homeostatic or hedonic risk factors for overconsumption?. Physiology & behavior, 82(1), pp.21-25.
Learn more
Evidence on Intermittent Fasting: Reality Check
Intermittent fasting (IF) is a dietary approach involving fasting and eating periods. Unlike traditional diets that focus on what you eat, IF focuses on when you eat. The idea behind intermittent fasting is to restrict calorie intake during specific periods of the day or week while allowing for unrestricted eating during other periods. There are several types of intermittent fasting, including periodic fasting, alternate-day fasting, and time-restricted eating. Types of Intermittent Fasting Periodic fasting, also known as periodic calorie restriction, is a type of intermittent fasting that involves fasting for one or more days a week. For example, you might fast for two days a week and eat normally for the other five days. Alternate-day fasting is a type of intermittent fasting that involves fasting every other day. On fasting days, you restrict your calorie intake to 500-600 calories; on non-fasting days, you eat normally. This type of fasting is more challenging than periodic fasting because it involves fasting every other day. Time-restricted eating is intermittent fasting that restricts your eating window to a certain number of hours daily. For example, you might fast for 16 hours and eat within an eight-hour window. This approach is easier to implement than periodic fasting or alternate-day fasting because you don’t have to go without food for extended periods. Effectiveness of Intermittent Fasting Despite the increasing popularity of IF, the evidence regarding its effectiveness in promoting weight loss is conflicting. I will review the evidence from various meta-analyses. Meta-analysis is an invaluable tool to draw high-level conclusions from multiple studies centered on the same topic or research question. It is a powerful tool for providing a more accurate view of a subject or treatment. It allows researchers to combine data from multiple studies, eliminating the risk of any one study skewing the results. A review of the various meta-analyses (umbrella of meta-analyses) has found at least 28 associations between IF on BMI, body weight, fat mass, LDL-C (bad cholesterol) total cholesterol, triglycerides, fasting plasma glucose, fasting insulin, HOMA-IR (a marker of insulin resistance), and systolic and diastolic blood pressure, mostly in adults with overweight or obesity. However, most of those associations were of very low to low evidence. Only one association was supported by high-quality evidence, the effect of modified alternate-day fasting for 1-2 months on weight loss and fatty liver compared to a regular diet. IF was most successful for weight loss in the initial 1 to 6 months, followed by a plateau. A recent meta-analysis found that IF diets were not associated with a significantly different body weight at different durations ranging from 2-4 months, 6-8 months, 10-14 months, and 18-30 months compared to calorie-restricted diets. The effectiveness of IF in promoting weight loss and improving overall health is still under debate. Fasting or Calories Restriction As IF involves periods of fasting, this naturally leads to a reduction in calorie intake. Whether the effects of intermittent fasting (IF) on weight loss and health benefits are primarily due to the fasting process or the calorie restriction involved is a subject of ongoing debate and research. Although intermittent fasting may have unique metabolic and hormonal effects that go beyond simple calorie reduction based on timing (morning vs evening fasting) and pattern of fasting (alternate day vs. time restricted). However, those changes were not translated into better health outcomes or weight loss. Further research is needed to unravel the underlying mechanisms and determine the specific contributions of each factor. Some individuals may find it easier to adhere to an IF eating pattern and experience positive outcomes, while others may struggle with the restricted eating window given the social implications of eating time and symptoms of fatigue and headache during the fasting periods. Individuals should be mindful of their eating patterns during the normal eating periods. One can still consume excessive calories within the eating window, defeating IF’s purpose. Finding a balanced and sustainable approach to weight loss that aligns with one’s lifestyle and preferences is crucial for successful weight management and overall health. References Patikorn C, Roubal K, Veettil SK, et al. Intermittent Fasting and Obesity-Related Health Outcomes: An Umbrella Review of Meta-analyses of Randomized Clinical Trials. JAMA Netw Open. 2021;4(12):e2139558. doi:10.1001/jamanetworkopen.2021.39558 Harris, Leanne1; Hamilton, Sharon2,3; Azevedo, Liane B.2,3; Olajide, Joan2,3; De Brún, Caroline2,3; Waller, Gillian2,3; Whittaker, Vicki2,3; Sharp, Tracey4; Lean, Mike1; Hankey, Catherine1,∗; Ells, Louisa1,3,∗. Intermittent fasting interventions for treatment of overweight and obesity in adults: a systematic review and meta-analysis. JBI Database of Systematic Reviews and Implementation Reports 16(2):p 507-547, February 2018. | DOI: 10.11124/JBISRIR-2016-003248 Gu L, Fu R, Hong J, Ni H, Yu K, Lou H. Effects of Intermittent Fasting in Human Compared to a Non-intervention Diet and Caloric Restriction: A Meta-Analysis of Randomized Controlled Trials. Front Nutr. 2022 May 2;9:871682. doi: 10.3389/fnut.2022.871682. PMID: 35586738; PMCID: PMC9108547. Elortegui Pascual, P., Rolands, M.R., Eldridge, A.L., Kassis, A., Mainardi, F., Lê, K.A., Karagounis, L.G., Gut, P. and Varady, K.A., 2023. A meta‐analysis comparing the effectiveness of alternate day fasting, the 5: 2 diet, and time‐restricted eating for weight loss. Obesity, 31, pp.9-21. https://doi.org/10.1002/oby.23568
Learn more
Insulin Resistance: a Vicious Cycle
Insulin resistance is a condition that can have detrimental effects on our health, including the development of diabetes, fatty liver, and obesity. Identifying the role of insulin in glucose regulation and fat metabolism is crucial to understand insulin resistance. Role of Insulin in the Body Insulin is crucial in regulating our bodies’ glucose and fat metabolism. When we consume carbohydrates, they are broken down into glucose, the primary energy source for our cells. Here’s how insulin helps in regulating glucose and fat: Glucose Regulation: When blood sugar levels rise after a meal, the pancreas releases insulin into the bloodstream. Insulin is like a key that unlocks the cells, allowing glucose to enter and be used for energy production. It also signals the liver to store excess glucose as glycogen, which can be later released when energy is needed. Insulin helps lower blood sugar levels by facilitating glucose uptake into cells, preventing them from reaching dangerous levels. Fat Regulation: Insulin also plays a role in fat metabolism. When insulin is present in the bloodstream, it inhibits the breakdown of fat stores and promotes the uptake of fatty acids into adipose (fat) tissue. It stimulates the production of lipoprotein lipase, an enzyme that helps store fat by converting it into triglycerides within fat cells. Additionally, insulin inhibits the release of stored fat from adipose tissue, preventing the breakdown of triglycerides for energy. This means that when insulin levels are high, the body favors fat storage rather than fat utilization. Insulin acts as an energy storage hormone, orchestrating the uptake and utilization of glucose by various organs and tissues in the body. It stimulates the liver and muscles to take in glucose from the blood and convert it into glycogen, a temporary storage form of energy. Additionally, insulin promotes the conversion of excess glucose into triglycerides, which are stored in fat cells (adipose tissue) as a long-term energy reserve. What is Insulin Resistance? Insulin resistance is a condition when our cells become less responsive to insulin signals. The body’s cells, particularly those in the liver, muscles, and fat tissue become less responsive to the effects of insulin. As a result, these organs cannot effectively take in glucose from the bloodstream, leading to elevated blood sugar levels (hyperglycemia). The pancreas responds by secreting more insulin to overcome this resistance and restore blood sugar levels. In other words, our bodies need to produce more insulin to get the same effect, leading to higher insulin levels in the bloodstream. Unfortunately, one of the effects of elevated insulin levels is increased fat storage. When insulin is high, our bodies prioritize storing excess energy as fat instead of using it for immediate energy needs. This can contribute to weight gain and make it harder to lose weight. In addition, insulin resistance can lead to higher blood sugar levels, which may increase the risk of developing type 2 diabetes. The persistently high insulin levels can contribute to the development of other health issues, such as fatty liver disease. Causes of Insulin Resistance Understanding the intricate mechanisms behind insulin resistance has been an ongoing challenge for researchers. While the exact cause of insulin resistance remains elusive, the most contributing factor is inflammation in adipose tissue. There exists lots of hypotheses of why inflammation occurs in the adipose tissue: quality of the diet, excessive weight gain and the role of the microbiome (the microorganisms residing in our gut). One study in mice has shown that inflammation in adipose tissue can be observed early on after the initiation of a high-fat diet and persist as long as the diet is maintained. When mice are switched back to a normal, healthier diet, the inflammation in their adipose tissue is rapidly reduced, indicating the dynamic nature of this process. This suggests a direct relationship between dietary choices and the inflammatory response within fat cells. Another intriguing hypothesis is that the rapid expansion of adipocytes, or fat cells, may be at the root of the inflammation observed. The rapid growth of the fat cells may outpace the delivery of oxygen and nutrients to the expanding fat cells, resulting in a state of inadequate oxygenation known as hypoxia. This hypoxic environment may trigger a cascade of events that ultimately lead to inflammation within the adipose tissue. Finally, the composition of the gut microbiome can be altered by a high-fat diet, which in turn may contribute to the inflammatory response within fat cells. The interplay between the gut microbiome, dietary choices, and adipose tissue inflammation is an area of active research, and scientists are working to uncover the intricate connections between these factors. Conclusion Insulin resistance is a complex condition that disrupts the normal functioning of insulin in the body. Individuals with insulin resistance may require more insulin to process the same amount of food compared to those without insulin resistance. This excessive insulin secretion can further contribute to weight gain and the accumulation of body fat, exacerbating the challenges associated with managing insulin resistance. While inflammation in adipose tissue appears to be a major culprit in the development of insulin resistance, the precise mechanisms underlying this process are still not fully understood. Researchers are actively conducting studies to unravel the intricate connections between inflammation, adipose tissue, and insulin resistance. Insulin resistance and inflammation create a vicious cycle. As fat accumulates in the body, it contributes to the development of insulin resistance. At the same time, insulin resistance promotes further weight gain, creating a self-perpetuating cycle. This cycle underscores the importance of addressing both factors in the management and prevention of obesity.
Learn more
Metformin for Weight Loss: Insights from Clinical Studies
The management of obesity and overweight revolves around lifestyle changes. However, medication can also play a role in controlling this condition. In this article, we delve into the current evidence surrounding the use of metformin for treating insulin resistance and promoting weight loss. Weight Loss The DPP, conducted from 1996 to 2001, is a landmark clinical trial that aimed to assess interventions for preventing or delaying the onset of type 2 diabetes in individuals with prediabetes. The study compared three groups: one implementing lifestyle changes, another receiving metformin treatment, and a placebo control group. The results revealed that lifestyle interventions, involving regular 150 minutes of weekly physical activity and a low-calorie, low-fat diet, were highly effective in reducing the incidence of diabetes. Specifically, the lifestyle intervention group exhibited a remarkable 58% reduction in the risk of developing diabetes compared to the placebo group. The metformin group also showed a significant reduction in diabetes incidence (31%) compared to the placebo group, albeit to a lesser extent than the lifestyle intervention group. These findings underscored the importance of lifestyle modifications as the primary approach to preventing diabetes. After one year, a significant proportion of participants in the lifestyle intervention group (62.6%) and, to a lesser extent, in the metformin group (28.5%) had lost at least 5% of their weight, compared to only 13.4% in the placebo group. In the DPP, the metformin group lost, on average, 2 kg in the first year. In a more recent study in 2013, high doses of metformin resulted in an average of 5 kg in 6 months among 154 patients with a body mass index ≥27 kg/m2 in an outpatient setting. There was a large variation in the weight outcomes from a weight loss of 335 kg in one patient and a weight gain of 13 kg in another. A meta-analysis of 21 trials (total participants is 1004) showed that metformin has a modest reduction in the BMI of almost one point. The reduction was most significant in participants with obesity and did not continue to decrease after treatment of more than 6 months. Long-term Weight Loss Maintenance The DPPOS served as an extension of the DPP study, focusing on evaluating the long-term effects of the initial interventions on diabetes development and related health outcomes. This extended study followed the participants for an additional 15 years. After an average of 10 years of follow-up, intensive lifestyle changes aimed at modest weight loss, reduced the rate of developing type 2 diabetes by 34% and delayed its onset by about 4 years. Additionally, the findings after 10 years demonstrated that metformin treatment reduced the rate of diabetes development by 18% and delayed its onset by 2 years. Approximately 6.2% of the metformin group maintained their weight loss between 6 and 15 years, as compared to 3.7% in the lifestyle group and 2.8% in the placebo group. Predictors of long-term weight loss included greater weight loss in the first year in all groups, older age and continued metformin use in the metformin group, older age, and absence of either diabetes or a family history of diabetes in the lifestyle group. Conclusion Metformin is a drug to prevent diabetes and not a weight loss drug. It is not even included in the guidelines for the treatment of obesity. Lifestyle changes remain the cornerstone for weight loss. Metformin has a very modest effect on weight loss in the first 6 months. However, it was superior to lifestyle changes in maintaining weight loss in the long term. If you decide to take metformin after a discussion with your healthcare professional, remember it must be long-term to decrease the incidence of diabetes and maintain weight loss. References Diabetes Prevention Program Research Group, 2012. Long-term safety, tolerability, and weight loss associated with metformin in the Diabetes Prevention Program Outcomes Study. Diabetes care, 35(4), pp.731-737. Seifarth, C., Schehler, B. and Schneider, H.J., 2012. Effectiveness of metformin on weight loss in non-diabetic individuals with obesity. Experimental and clinical endocrinology & diabetes, pp.27-31. Apolzan, J.W., Venditti, E.M., Edelstein, S.L., Knowler, W.C., Dabelea, D., Boyko, E.J., Pi-Sunyer, X., Kalyani, R.R., Franks, P.W., Srikanthan, P. and Gadde, K.M., 2019. Long-term weight loss with metformin or lifestyle intervention in the diabetes prevention program outcomes study. Annals of internal medicine, 170(10), pp.682-690. Pu, R., Shi, D., Gan, T., Ren, X., Ba, Y., Huo, Y., Bai, Y., Zheng, T. and Cheng, N., 2020. Effects of metformin in obesity treatment in different populations: a meta-analysis. Therapeutic advances in endocrinology and metabolism, 11, p.2042018820926000.
Learn more
The Meat Consumption Debate Unveiled
Meat consumption has long been a subject of heated debate, leaving many of us caught in the crossfire of conflicting information. With guidelines and meta-analysis findings providing diverse perspectives, it’s no wonder the topic sparks curiosity and raises questions about the impact of our food choices. Let’s dive into the meaty dilemma, exploring the controversies, health implications, and thought-provoking insights that can guide us in making informed decisions. The Clash of Guidelines The American Cancer Society (ACS) recommends limiting the consumption of red meat, including beef, pork, and lamb, and avoiding processed meats. Limit consumption to no more than about three portions per week. Three portions are equivalent to about 350–500g (about 12–18oz) cooked weight. Consume very little, if any, processed meat. The EAT-Lancet Commission suggests reducing global red meat consumption by over 50% to address environmental concerns and improve health outcomes. Aim to consume at most 98 grams of red meat (pork, beef or lamb), 203 grams of poultry, and 196 grams of fish per week. Different countries provide their own nutritional guidelines, which may have varying recommendations regarding red meat consumption. The CDC guidelines recommend 100 grams of meat per day. Advocates of Meat Consumption Let’s take a moment to explore the perspective that advocates for the consumption of red meat. As humans, we are classified as omnivores, which means our bodies are naturally adapted to consume a diverse range of foods, including plant- and animal-based sources. One look at our teeth reveals an intriguing story. We possess incisors for biting into fruits and vegetables, canines for tearing into meat, and molars for grinding both plant matter and meat. This dental composition suggests that our bodies evolved to handle a mixed diet. Proponents of red meat consumption often refer to the 4NS framework, which highlights the following aspects: Nutrients, Necessity, Nourishment, and Natural. Red meat is a rich source of essential nutrients, such as iron, vitamin B12, zinc, and selenium, vital for various bodily functions. Since plant-based sources of vitamin B12 are limited, red meat becomes an important dietary source for those following a non-vegetarian or omnivorous diet. Adequate vitamin B12 intake is crucial to prevent anemia and maintain optimal health. Therefore, it is generally recommended for vegans to obtain vitamin B12 through fortified foods or supplements to ensure they meet their dietary requirements. Furthermore, they warn about the quality of the evidence about the health effects of red meat consumption as they rely on observational studies. Advocates of Plant-Based Diets Those who argue against meat consumption claim that it is associated with an increased risk of mortality, cardiovascular diseases, and various types of cancer, especially colon rectal cancer. Additionally, they highlight the negative environmental effects of meat production. Let’s start with the environment. Agriculture, including livestock farming, watering the fields to hydrating the animals, takes many of our freshwater resources. Meat production is a significant contributor to greenhouse gas emissions. Lastly, we can’t forget about the well-being of livestock. Many organizations and initiatives promote humane and sustainable practices in livestock farming, encouraging healthier and more ethical approaches to meat production. As for health concerns, eating red meat has been linked to a higher risk of certain types of cancers, mostly colon cancer. For example, the risk of colorectal cancer increases by 17% (RR = 1.17; CI = 1.08-1.26) with total red and processed meat consumption. When people reduced their weekly intake of red meat by 3 servings, there were 8 fewer deaths per 1000 individuals associated with red meat consumption. For processed meat, a reduction of 3 servings per week resulted in 9 fewer deaths per 1000 individuals. Additionally, individuals who followed diets with lower consumption of red and processed meats had 15 fewer deaths per 1000 individuals. Conclusion Considering the varying perspectives, an individual’s preference and ethical stance ultimately determine whether to consume meat. To err on the side of caution, it is advisable to consume red meat in moderation, as part of a balanced diet, limiting intake to no more than 75 grams per day. Additionally, it is recommended to choose lean cuts and employ healthier cooking methods, such as baking, broiling, or stewing. Cooking methods that involve high heat and prolonged cooking times, such as grilling or frying, can generate potentially harmful compounds that contribute to the carcinogenic effect. Lastly, minimizing the consumption of processed meats is important due to the associated health risks. References Farvid, M. S., Sidahmed, E., Spence, N. D., Mante Angua, K., Rosner, B. A., & Barnett, J. B. (2021). Consumption of red meat and processed meat and cancer incidence: A systematic review and meta-analysis of prospective studies. European journal of epidemiology, 36, 937-951. Godfray, H. C. J., Aveyard, P., Garnett, T., Hall, J. W., Key, T. J., Lorimer, J., … & Jebb, S. A. (2018). Meat consumption, health, and the environment. Science, 361(6399), eaam5324. Johnston, B. C., Zeraatkar, D., Han, M. A., Vernooij, R. W., Valli, C., El Dib, R., … & Guyatt, G. H. (2019). Unprocessed red meat and processed meat consumption: dietary guideline recommendations from the Nutritional Recommendations (NutriRECS) Consortium. Annals of internal medicine, 171(10), 756-764. Leroy, F., & Cofnas, N. (2020). Should dietary guidelines recommend low red meat intake?. Critical Reviews in Food Science and Nutrition, 60(16), 2763-2772. Vernooij, R. W., Zeraatkar, D., Han, M. A., El Dib, R., Zworth, M., Milio, K., … & Johnston, B. C. (2019). Patterns of red and processed meat consumption and risk for cardiometabolic and cancer outcomes: a systematic review and meta-analysis of cohort studies. Annals of internal medicine, 171(10), 732-741. Nutrition
Learn more
Why Start Your Weight Loss Journey Today? The Science Says It All!
Have you ever wondered if consistent weight loss efforts, even small ones, can truly impact your health and lifespan? The answer is a resounding yes! Decades of research show that starting—even with modest goals—can lead to life-changing results. Whether you’ve tried and failed multiple times or are hesitant to start, the science is clear: every step you take counts toward a healthier, longer life. The Power of Cohort Studies Cohort studies are long-term research projects that follow groups of people over time, observing how their habits and health outcomes evolve. These studies are invaluable for understanding how behaviors like weight loss affect mortality. Here’s what science says: National Institutes of Health–AARP Diet and Health Study (2020):Over 160,000 participants were followed for 15 years. The study found that frequent, intentional weight loss attempts—even with small losses—significantly reduced mortality. Losing 5–23 kg (12–50 lbs) lowered the risk of death by 16% (HR = 0.84, 95% CI 0.78–0.90), and even losing as little as 2 kg (4.4 lbs) was associated with reduced mortality risk. BMC Medicine Study (2020):This study examined the relationship between weight loss frequency, magnitude, and mortality. It revealed that frequent attempts with moderate losses (e.g., 9+ attempts with 5.4 kg [12 lbs] per attempt) provided a 9% lower risk of death (HR = 0.91, 95% CI 0.84–0.98). In contrast, fewer attempts with larger losses (e.g., 30 lbs per attempt) were less beneficial and sometimes linked to a 19% increase in mortality risk (HR = 1.19, 95% CI 0.98–1.46). NHANES Study (2024):Following 48,000 adults for 15 years, this research highlighted the importance of combining multiple weight loss strategies, such as behavioral changes, physical activity, and calorie restriction. Participants using two or more strategies had significantly lower mortality rates, regardless of total weight loss. Meta-Analysis on Intentional Weight Loss (2015):Reviewing multiple trials with varied follow-up periods, this analysis showed that intentional weight loss reduced all-cause mortality by 15% (RR = 0.85, 95% CI 0.76–0.95) in people with obesity. The benefits were consistent across different weight loss methods. Consistency Beats Extremes Let’s face it: most people try to lose weight multiple times. And that’s okay! One of the most striking findings across these studies is the importance of consistent effort over perfection. For example: Frequent weight loss attempts, with smaller losses of 5.4 kg (12 lbs) per try, significantly reduced mortality by 9% (HR = 0.91). People who lost 5–23 kg (12–50 lbs) over time saw substantial health benefits, lowering their risk of death by 16% (HR = 0.84). Large, extreme weight losses (e.g., over 45 kg [100 lbs]) achieved in just a few attempts were less beneficial and sometimes linked to an increased mortality risk of 19% (HR = 1.19). The Benefits of Starting Today It’s never too late to begin, and every effort counts. Whether you’re aiming for 2 kg or 20 kg, every small effort adds up. Here’s why starting today is crucial. Here’s why starting today is critical: Small Changes Add Up: Losing even a little weight can significantly lower your risk of major health issues like heart disease and diabetes. Consistency Pays Off: Frequent, steady efforts yield more health benefits than dramatic, one-time changes. Invest in Your Future: The small steps you take today create a healthier, longer life for your future self. Practical Tips to Get Started Set Realistic Goals: Aim for 2–5 kg (4.4–11 lbs) initially and build from there. Use Multiple Strategies: Combine mindful eating, calorie tracking, and regular physical activity. Track Your Progress: Use tools or apps to monitor your habits and celebrate small wins. Be Patient: Focus on steady, sustainable changes rather than quick fixes. The Bottom Line Studies consistently show that intentional weight loss—even modest amounts—can reduce mortality risk and improve your overall quality of life. It’s not about how many times you’ve tried; it’s about consistent effort and starting today. Losing as little as 2 kg can make a measurable difference, and frequent, intentional attempts bring even greater benefits. Take that small step today. Your future self will thank you. References: Williamson DF et al. (2000). Intentional Weight Loss and Mortality Among Overweight Individuals With Diabetes. Diabetes Care. 23(12):1499-1504. BMC Medicine (2020). Frequency of Intentional Weight Loss Attempts and All-Cause Mortality in NIH-AARP Diet and Health Study. BMC Medicine. NHANES Study (2024). Effects of Weight Loss Strategies on Mortality Risk Over 15 Years. BMC Public Health. Plos One (2015). Meta-Analysis of Intentional Weight Loss and Mortality in Obesity. Plos One. Footnote: Understanding HR and RR In scientific studies, you may encounter terms like HR (Hazard Ratio) and RR (Relative Risk). Here’s a simple explanation: Hazard Ratio (HR): This compares the risk of an event (like death) happening at any point in time between two groups. For example, an HR of 0.84 means the risk is 16% lower in one group compared to another. An HR of 1.19, on the other hand, means the risk is 19% higher. Relative Risk (RR): This looks at the overall likelihood of an event occurring in one group versus another. An RR of 0.85 means the event is 15% less likely in one group compared to another. Both HR and RR are used to describe the effects of certain behaviors (like weight loss) on outcomes like mortality. A value below 1 means the behavior reduces risk, while a value above 1 means it increases risk. In short, these numbers help us understand how much a behavior like intentional weight loss can influence health risks!
Learn more
Protein Bars and Weight Loss: A Guide to Smart Snacking
Losing weight is a journey, and one of the biggest challenges is maintaining lean muscle mass. So, how can you ensure you’re getting enough protein while keeping your calorie intake in check? Protein bars can be convenient, but choosing them wisely is important. Why Protein Matters When you cut calories to lose weight, your body looks for ways to save energy. Muscles burn more calories than fat, even at rest. So, if your body isn’t getting enough calories from food, it may start breaking down muscle tissue to use as fuel. This is why it’s important to eat enough protein while losing weight. Protein helps your body hold onto muscle and use fat stores for energy. Protein can help you feel fuller for longer, reducing cravings and potentially leading to lower calorie intake. Protein intake with resistance training keeps your muscles strong. The daily reference intake of protein for the healthy adult population is 0.8 g/kg body weight. However, individuals who engage in physical activity or are in a calorie deficit may require more protein. Research shows that consuming more protein, around 1.2-1.5 grams per kilogram of body weight, can help you preserve lean body mass while reducing weight. Chronic intake of greater than 2 g/kg/day in adults has been associated with negative digestive, renal, and vascular effects. Protein throughout the day: Does the Timing Matter? You might hear a lot about the perfect timing for your protein intake. The evidence is it doesn’t seem to matter much whether you have your protein before or after your workout to build muscle or strength. You should aim for 20-25 grams of protein close to your workout. As for distributing your total protein over the whole day, the research is not totally clear on that. So, focus on getting enough protein throughout the day, and don’t worry too much about the exact timing. Finding the Right Protein Bar: Needs and Ingredients Protein bars have come a long way from being just a workout snack. Today, they’re a versatile tool you can use throughout your day, depending on your needs and cravings. Here’s a breakdown of their different roles: Pre/Post-Workout Fuel: Aim for 20 grams of protein. Look for bars packed with easily digestible proteins like whey protein. Your body absorbs these proteins quickly, providing a readily available source of amino acids for muscle repair and growth. You can also check the content for additional complex carbohydrates for sustained energy. Meal Replacements on the Go: Need a quick and convenient breakfast or lunch? Look for bars packed with protein (at least 20 grams) and fiber (around 5 grams) to keep you full and satisfied until your next meal. Sweet Treats with a Protein Punch: Craving something sweet but don’t want to disrupt your goals? Protein bars can be a healthy alternative to sugary desserts. Opt for bars with a moderate protein content (around 10-15 grams) and monitor the sugar content. Look for natural sweeteners like stevia or erythritol to satisfy your sweet tooth without the sugar spike. Salty Snack Fix: Not every craving is sweet! Protein bars can also come in savory flavors to satisfy your salty snack desires. These bars might be lower in protein but contain healthy fats and fiber to keep you full. Protein Boost: If you need a protein top-up, aim for bars with 10-15 grams of protein and watch out for added sugars, saturated fats, and calories. Beyond Protein: Other Nutritional Considerations Salt: If you have high blood pressure, be mindful of sodium content. Look for bars with less than 200mg of sodium per serving. According to the American Heart Association (AHA), adults should limit their sodium intake to less than 2,300 mg daily. This is equal to about 1 teaspoon of table salt. Sugar: People with diabetes or insulin resistance should choose bars with minimal added sugars (ideally less than 5 grams per serving) and focus on sugar substitutes like stevia or erythritol. Saturated Fat: Aim for bars with less than 3 grams of saturated fat per serving. The American Heart Association recommends a dietary pattern that achieves 5-6% of calories from saturated fat. For example, if you need about 2,000 calories daily, you would need roughly 13 grams of saturated fat daily. Glucose-fructose syrup: While it may raise sweetness levels, it has been linked to increased fat storage in the liver and other health concerns, like diabetes and insulin resistance. Dietary Restrictions and Allergies The Bottom Line Protein bars can be a handy way to increase protein intake and support your weight loss goals. You can choose both nutritious and delicious bars by understanding your protein needs and considering other ingredients like salt, sugar, and saturated fat. Remember: Protein bars are not a replacement for a balanced diet. If you’re already getting enough protein from your meals, you don’t necessarily need a protein bar. References Day, L., Cakebread, J.A. and Loveday, S.M., 2022. Food proteins from animals and plants: Differences in the nutritional and functional properties. Trends in Food Science & Technology, 119, pp.428-442. Naclerio, F. and Seijo, M., 2019. Whey protein supplementation and muscle mass: current perspectives. Nutrition and Dietary Supplements, pp.37-48. Huecker, M., Sarav, M., Pearlman, M. and Laster, J., 2019. Protein supplementation in sport: source, timing, and intended benefits. Current nutrition reports, 8, pp.382-396. Wirth, J., Hillesheim, E. and Brennan, L., 2020. The role of protein intake and its timing on body composition and muscle function in healthy adults: a systematic review and meta-analysis of randomized controlled trials. The Journal of nutrition, 150(6), pp.1443-1460.
Learn more