How many times have you trained a client who couldn’t lose weight no matter how hard you trained him or how “clean” he insisted his nutrition was? It’s frustrating for both fitness professional and client when the waistline doesn’t budge in spite of what seems enough effort. However, the reason belly fat can be so intractable is that it’s as much a hormonal phenomenon as it is a caloric one. In order to understand how to get rid of belly fat, it’s important to factor hormonal physiology into the overall equation.
This article looks at the many factors involved in stubborn belly fat and offers suggestions on how to help clients reach their goals.
Fat and Fat Burning
When we talk about belly fat, we’re talking not about one thing, but about three things (Ibrahim 2010). Deep fat, called visceral belly fat, lies around the organs under the abdominal muscles, and it can’t be pinched. Superficial subcutaneous belly fat hangs over the waistline and can be pinched. Deep subcutaneous belly fat is a hybrid of the two. For the purposes of this article, we will focus on visceral and superficial subcutaneous belly fat.
Visceral belly fat has greater blood supply, is richer in beta-receptors, is more responsive to cortisol and is less sensitive to insulin than subcutaneous belly fat. All of this means that visceral belly fat is harder to store and easier to burn (Ibrahim 2010). Subcutaneous belly fat has more alpha-receptors compared with visceral belly fat. This means the subcutaneous fat is less responsive to fat-burning catecholamines and has less blood supply. It is also “colder” fat, which further decreases blood flow. It is far more insulin sensitive and less cortisol reactive—meaning it is easier to store and harder to burn (Ibrahim 2010).
Three steps are required to burn fat (Ranallo & Rhodes 1998):
- Release. Fat has to be released from a fat cell. This is called lipolysis.
- Delivery. Fat then has to travel through the bloodstream and be delivered to a cell that will burn it. Therefore, blood supply to and from fat cells is important.
- Burning. Finally, fat has to enter the destination cell and be burned. This is called lipid oxidation.
It is very important to understand these three steps, which partly explain why visceral fat is usually stored last and burned first and why subcutaneous belly fat can often be so stubborn.
Introduction to Hormonal Fat Burning
Two enzymes regulate flux into and out of fat cells: lipoprotein lipase (LPL), which is responsible for fat storage, and hormone-sensitive lipase (HSL), which is involved in fat release (Langfort et al. 2003). Did you notice that the major fat-releasing enzyme is called “hormone-sensitive lipase” and not “calorie-sensitive lipase”? This gives you a hint that calories are not the only factor to consider in belly fat loss.
Several different hormones directly or indirectly impact LPL and HSL activity. A few of the most important are insulin, cortisol and the catecholamines (epinephrine and norepinephrine). Estrogen, progesterone and testosterone play an indirect role as well. Figure 1 shows how the most influential hormones impact LPL and HSL. The “+” sign means the enzyme’s activity is enhanced, while the “-” sign means its activity is repressed.
As the chart indicates, insulin enhances LPL activity while sup- pressing HSL activity. This means that as a result of insulin’s effect, fat is more likely to be stored when there is an excess of calories and less likely to be burned when there is a deficit of calories. Cortisol often gets blamed for being the “belly fat hormone,” but hormones don’t behave in isolation. Instead, they are like people and will behave differently depending on who they are “socializing” with. When cortisol is with insulin, for example, cortisol’s action on HSL is blunted, while its effect on LPL is elevated. Insulin and cortisol together are the real hormonal belly fat bullies.
Catecholamines are tricky because their impact on fat burning depends on a lesser-known nuance of fat physiology: In and around your fat cells are two types of receptors to which catechol- amines can bind: alpha-receptors, which slow fat release and constrict blood vessels; and beta-receptors, which enhance fat release and open up blood vessels. Both types work via their impact on HSL activity. To keep this straight in your head, remember “A” for alpha and antiburn and “B” for beta and burn.
As explained earlier, the location of belly fat makes a difference. Visceral fat is relatively rich in beta-receptors compared with superficial subcutaneous fat, which is richer in alpha-receptors (Ibrahim 2010). As a result, subcutaneous fat is more stubborn—harder to burn—than visceral fat.
Insulin and Belly Fat
Insulin resistance is a term thrown around a lot, but most people don’t understand what it means. Usually, insulin resistance is synonymous with fat gain; however, insulin resistance is not a global phenomenon in the body. In other words, you can remain sensitive to the action of insulin in one tissue while remaining more resistant in another “depot” (Unnikrishnan 2004). Also, insulin resistance affects different areas of the body in different ways.
For example, insulin in the brain has a normal action of suppressing hunger. If you become resistant to insulin’s action in the brain, hunger will increase. Insulin’s net action in muscle cells is to aid muscle growth. It is also responsible for getting fuel into muscle cells. If muscles become resistant to insulin, it leads to muscle loss, less fuel getting into muscle and, therefore, fatigue and poor performance. In the liver, insulin decreases gluconeogenesis (sugar synthesis from glycerol and amino acids) and glycogenolysis (the breakdown of stored sugar called glycogen). Insulin resistance in the liver leads to increased sugar production and enhanced glycogen breakdown, which raises blood sugar levels (Lann & LeRoith 2007).
When it comes to the brain, muscles and liver, you want the body to be insulin sensitive. Being insulin resistant in these areas makes a person unable to burn fat and sugar or to feel satiated after eating. This is why many obese clients who are “insulin resistant” in these tissues tend to overeat (because they are hungry all the time) and, at the same time, tend to be malnourished (because fuel can’t get into muscle cells).
This discussion is critical to understanding belly fat, because insulin’s effect on fat cells can be counterintuitive if you think of insulin resistance as having the same effect on fat as it has on the brain, muscles and liver. Insulin’s normal action on fat metabolism is to increase the activity of LPL, the major fat-storing enzyme, and to suppress the action of HSL, the prime fat-releasing enzyme. This means insulin’s normal action on fat cells is to make them store and retain more fat. From that perspective, a fat cell resistant to insulin is a good thing. A fat cell that is more sensitive to the action of insulin will be a more greedy and stingy fat cell. A fat cell that is more insulin resistant will be more likely to release fat and less likely to store it.
Visceral belly fat is more resistant to insulin and therefore less likely to be stored and more likely to be burned. Subcutaneous belly fat is more sensitive to insulin and, because of this, more likely to be stored and harder to burn (Ibrahim 2010).
Cortisol and Belly Fat
Cortisol is both fat-releasing and fat-storing because it enhances the activity of both LPL and HSL. The net impact of cortisol on belly fat depends on several factors, including how much cortisol is present, for how long, and what other hormones are with it. High amounts of cortisol present for long periods of time may make people especially prone to accumulating belly fat. This is because of two interesting effects of cortisol, one in the brain and one in the body (Epel et al. 2000; Epel et al. 2001; Kuo et al. 2008).
In the brain, cortisol impacts hormones that regulate appetite. These include neuropeptide Y (NPY), corticotropin-releasing hormone (CRH) and leptin. This is why cortisol is associated with cravings for highly palatable foods (Epel et al. 2001; Appelhans et al. 2010). Too much cortisol also drives people to eat more of the wrong foods more often, making it far more likely to achieve a calorie surplus and gain fat. Additionally, excess cortisol increases NPY expression in the body, and this causes smaller, immature fat cells to become larger, mature fat cells. This is not a good thing if you are trying to lose belly fat. There are 400% more cortisol receptors in visceral fat than there are in subcutaneous fat (Epel et al. 2000; Kuo et al. 2008). This explains why cortisol may be such an issue for belly fat (Epel et al. 2001).
The final thing to know about the relationship between cortisol and belly fat involves an enzyme called 11-beta hydroxysteroid dehydrogenase (11 beta HSD). This enzyme generates its own cortisol and is present in high amounts in visceral belly fat. This has profound implications when you understand that chronic cortisol exposure causes more fat accumulation and that this chronic exposure is being generated from the area of accumulation. Visceral belly fat has a parasitic effect in this regard, perpetuating itself at the expense of its host. Another point: Insulin stimulates production of 11 beta HSD (Balachandran et al. 2008), so it is not cortisol alone that is to blame for visceral belly fat growth, but rather insulin and cortisol together.
Estrogen, Progesterone and Testosterone
No discussion of belly fat is complete without considering the impact of the sex steroids. Human fat tissue has receptors for estrogen, progesterone and testosterone, and these hormones impact fat metabolism (Mayes & Watson 2004). Receptors have varying concentrations in the different belly fat regions.
Estrogen has anti-insulin and anticortisol effects on the belly (Yematani et al. 2013; Pallottini et al. 2008). Progesterone also has anticortisol effects. This hormone combination is very effective at controlling belly fat. This is a big part of the reason why young women tend to maintain an hourglass shape and older women tend to lose it (Björntop 1997). Testosterone is interesting because higher levels in women are associated with more belly fat, while lower levels in men are a risk factor for more belly fat. Testosterone decreases LPL activity and raises beta-receptors density, but it also opposes the action of estrogen, which explains its positive impact in male belly fat and more negative impact in women (De Pergola 2000).
Diets Don’t Work
Before we tackle the fix for belly fat, we have to talk about the elephant in the room: dieting. Diets do not work! Research has proven this over and over again. The long-term success rate of the standard dieting model is around 5% (Hafekost et al. 2013). What’s worse is that 66% of dieters don’t just gain back the weight—they gain back more fat (Mann 2007). All that regained weight or extra weight gets stored preferentially in the belly (Banasik et al. 2013). Dieting makes belly fat fatter.
If you use a standard, calorie-counting, “eat less, exercise more” approach to belly fat, you may see short-term success; however, it will almost certainly make things worse in the long run.
Why does the standard approach to dieting fail for belly fat? Burning belly fat requires a calorie deficit and balanced hormones. The problem with the “eat less, exercise more” model is that it accomplishes the calorie deficit but makes the hormone balance worse. Interestingly, if hormones are balanced it’s easier to achieve a calorie deficit. Insulin resistance makes people hungrier. Excess cortisol secretion increases hunger and cravings. Even estrogen has been shown to impact sensitivity to hunger hormones (Kok et al. 2008). This is why hormonal considerations must be addressed with calories.
The Belly Fat Fix
Since insulin and cortisol produce the greatest negative impact on belly fat, they must be controlled first. Although it is a drastic oversimplification, it is clinically useful to think of insulin as a “starch and sugar” hormone and cortisol as a “sleep and stress” hormone.
The natural inclination when dealing with belly fat is simply to focus on eating fewer carbohydrates instead of lowering calories overall. Reducing carbs is a better strategy for belly fat reduction than traditional low-fat dieting (Volek et al. 2004). However, low blood sugar stresses the body and raises cortisol levels (Ebbeling et al. 2012); therefore, you do not want to eat a diet that is too low in carbohydrates, either. The idea is to modify starch/sugar intake to provide energy and stabilize blood sugar, while at the same time lowering insulin slowly over time and keeping cortisol stable. Choosing carbohydrates that are lower in glycemic load can do this, and this approach has been shown to reduce the chance of weight regain (Gross et al. 2013).
Increasing protein intake also decreases the potential for weight regain. Higher protein, along with a lower-carbohydrate diet, has a favorable impact on belly fat as well (Volek et al. 2004; Ebbeling et al. 2012; Soenen et al. 2013).
The Belly Fat Formula
Starch and sugar combined with fat may represent the best combination if you want to gain fat. Starch and sugar raise insulin levels. Fat alone is neutral in its impact on insulin. But when fat and starch/sugar are combined, they may be especially troublesome for belly fat (La Fleur et al. 2010). A meal that combines fat and starch/sugar results in higher calories at that meal and at subsequent meals (La Fleur et al. 2010). Insulin and fat also independently raise two other fat-storing hormones: acylation-stimulating protein (ASP) and glucose-dependent insulinotrophic peptide (GIP). Add stress on top of fat and starch/ sugar and you multiply the effect (Kuo et al. 2008). The first step in beating belly fat is to avoid this fat, starch/sugar and stress combination when possible.
The Six-Pack Formula
Protein and vegetables create a high-volume, hunger-suppressing combo punch with minimal insulin production. This results in fewer calories consumed and a favorable hormone balance. Sleep and stress management aid this action by lowering cortisol. Finally, smart carbohydrate management is critical to controlling any unfavorable cortisol-elevating incident. The six-pack formula focuses on managing stress and consuming protein and fiber over starch and sugar. Both visceral fat and subcutaneous fat will respond to this approach. However, there are some differences and slight modifications.
Remember that visceral fat—compared with subcutaneous fat—is far more insulin resistant, has better blood flow, is more responsive to catecholamines (has more beta-receptors), and is helped by estrogen in women and testosterone in men. For this belly fat depot, carbohydrate reduction can be more moderate. Going too low in carbs may not help cortisol metabolism in this area. Visceral fat is also far more responsive to exercise, which is often enough to deal with it. Stress management becomes a big piece of the approach in this area, given cortisol’s central role in visceral fat metabolism.
When dealing with “love handles” (subcutaneous fat), things get trickier. This area is far more stubborn owing to its high sensitivity to insulin, its rich supply of alpha-receptors and its reduced blood flow. This fat is far less responsive to exercise and requires a stricter dietary approach. Reducing carbohydrate intake to low levels is usually the major focus when addressing this depot.
A Sample Plan
To review, there are three major considerations for a nutrition and lifestyle plan for belly fat:
- Belly fat results from a mix of calorie- and hormone-related concerns.
- Traditional “eat less, exercise more” programs have an atrocious track record and almost always cause rebound weight gain centered in the belly.
- Belly fat is dramatically impacted by stress and cortisol management.
There are two alternatives to an “eat less, exercise more” approach. Both approaches create a calorie deficit, and both seem to balance hormones. They are the “eat less, exercise less” approach and the “eat more, exercise more” approach. Both of these “plans” generate low-calorie intake and naturally pare starch intake in a way that provides enough fuel to keep hunger, energy and cravings stable, but not enough to slow fat loss.
The 3:2:1 Plan
The “eat less, exercise less” approach can be thought of as a 3:2:1 plan. The “3” stands for three meals per day. The “2” means two of those meals should be mostly protein and fiber with less starch. Healthy starch sources are higher in fiber and hypoallergenic; they include brown rice, quinoa, beans/legumes, sweet potatoes with the skin on, and oats. The “1” means one meal per day should have heavier starch. This meal is best consumed postworkout. Another way to look at the 3:2:1 designation is to visualize a plate. Three parts should be vegetables, two parts protein and one part starch. You can also think in terms of bites. For every three bites of vegetables, you have two bites of protein and one bite of starch. The 3:2:1 approach works well for people who are not heavy exercisers. Daily walking and a few weight training sessions are recommended with this plan.
The 3:2:2 Plan
The “eat more, exercise more” approach is for people who exercise regularly. It can be summed up with a 3:2:2 designation. The “3” stands for three meals per day. The first “2” means two snacks per day. The second “2” means you should double the starch intake once per day, post workout as well. You can visualize a plate and/or bites for this approach as well. The meals and snacks should be half vegetables and then equal parts protein and starch. Or, if you like, use bites. For every three bites of vegetables, take two bites of protein and two of starch.
Making It Practical
To know if you’ve been successful in helping clients reduce calories and balance hormones so that belly fat can be burned instead of stored, you need two more tools. The first tool centers on hunger, energy and cravings and is called HEC (pronounced “heck”).
Since abnormal insulin and cortisol metabolism strongly impacts all three of these sensations, HEC provides an indirect assessment of how well your clients are managing those two hormones.
Have your clients rank each parameter on a scale from 1 to 10, with 10 being high and one being low. Hunger and cravings should be less than 5. Energy should be 6 or higher. If “HEC is in check,” you have met half of the equation. Assess HEC at the end of each week, averaging the results.
The next step is to assess body shape. For women, use waist- to-hip ratio. Research shows this ratio should be 0.7 (Weeden & Sabini 2005; Platek & Singh 2010). As a client progresses and is losing weight, you want this number to approach 0.7. If it moves up toward 0.8 or does not change, this is an objective indication that you have not adequately addressed hormonal influences on belly fat. For men, the waist-to-chest ratio may be a better indicator and the optimal number is 0.77 (Price et al. 2013). Again, if this number moves past 0.8 you are going in the wrong direction.
The Fat Finale
Beating belly fat requires that a client produce calorie deficits in the context of hormone balance. Understanding how carbohydrates and stress will impact cortisol and insulin is the first critical step to understanding a more holistic approach to belly fat. From there, you can use more nuanced approaches for visceral versus subcutaneous fat and female versus male belly fat. The keys to beating belly fat include a higher-protein diet, as well as a modified carbohydrate intake, along with stress management techniques.
Appelhans, B.M., et al. 2010. HPA axis response to stress predicts short-term snack intake in obese women. Appetite, 54 (1), 217-20.
Balachandran, A., et al. 2008. Insulin and dexamethasone dynamically regulate adipo cyte 11beta-hydroxysteroid dehydrogenase type 1. Endocrinology, 149 (8), 4069-79.
Banasik, J.L., et al. 2013. Low-calorie diet induced weight loss may alter regulatory hormones and contribute to rebound visceral adiposity in obese persons with a family history of type-2 diabetes. Journal of the American Association of Nurse Practitioners, 25 (8), 440-48.
Bj├Ârntorp, P. 1997. Hormonal control of regional fat distribution. Human Reproduction, 12 (1), S21-S25. De Pergola, G., 2000. The adipose tissue metabolism: Role of testosterone and dehydroepiandrosterone. International Journal of Obesity and Related Metabolic Disorders, 24 (2), S59-63.
Ebbeling, C.B., et al. 2012. Effects of dietary composition on energy expenditure during weight-loss maintenance. The Journal of the American Medical Association, 307 (24), 2627-34.
Epel, E., et al. 2000. Stress and body shape: Stress-induced cortisol secretion is consistently greater among women with central fat. Psychosomatic Medicine, 62 (5), 623-32.
Epel, E., et al. 2001. Stress may add bite to appetite in women: A laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology, 26 (1), 37-49.
Goss, A.M., et al. 2013. Effects of diet macronutrient composition on body composition and fat distribution during weight maintenance and weight loss. Obesity, 21 (6), 1139-42.
Hafekost, K., et al. 2013. Tackling overweight and obesity: Does the public health message match the science? BMC Medicine, 11, 41.
Ibrahim, M.M. 2010. Subcutaneous and visceral adipose tissue: Structural and functional differences. Obesity Reviews, 11 (1), 11-18.
Kok, P., Paulo, R.C., & Veldhuis, J.D. 2008. Estrogen supplementation selectively enhances hypothalamopituitiary sensitivity to ghrelin in postmenopausal women. Journal of Clinical Endocrinology, 93 (10), 4020-26.
Kuo, L.E. et al. 2008. Chronic stress, combined with a high-fat/high-sugar diet, shifts sympathetic signaling toward neuropeptide Y and leads to obesity and the metabolic syndrome. Annals of New York Academy of Science, 1148, 232-37.
La Fleur, S.E., et al. 2010. A free-choice high-fat high-sugar diet induces changes in arcuate neuropeptide expression that support hyperphagia. International Journal of Obesity, 34 (3), 537-46.
Langfort, J., et al. 2003. Hormone-sensitive lipase in skeletal muscle: Regulatory mechanisms. Acta Physiology Scandanavia, 178 (4), 397-403.
Lann, D., & LeRoith, D. 2007. Insulin resistance as the underlying cause for metabolic syndrome. Medical Clinics of North America, 91 (6), 1063-77.
Mann, T., et al. 2007. Medicare’s search for effective obesity treatments: Diets are not the answer. American Psychologist, 62 (3), 220-33.
Mayes, J.S., & Watson, G.H. 2004. Direct effects of sex steroid hormones on adipose tissue and obesity. Obesity Reviews, 5 (4), 197-216.
Pallottini, V., et al. 2008. Estrogen regulation of adipose tissue functions: Involvement of estrogen receptor isoforms. Infectious Disorders—Drug Targets, 28 (1), 52-60.
Platek, S.M., & Singh, D. 2010. Optimal waist-to-hip ratios in women activate neural reward centers in men. PLOS One, 5 (2), e9042.
Price, M.E., et al. 2013. Body shape preferences: Associations with rater body shape and sociosexuality. PLOS One, 8 (1), e52532.
Ranallo, R.F., & Rhodes, E.C. 1998. Lipid metabolism during exercise. Sports Medicine, 26 (1), 29-42.
Soenen, S., et al. 2013. Normal protein intake is required for body weight loss and weight maintenance, and elevated protein intake for additional preservation of resting energy expenditure and fat free mass. The Journal of Nutrition, 143 (5), 591-96.
Unnikrishnan, A.G. 2004. Tissue-specific insulin resistance. Postgraduate Medicine Journal, 80 (946), 435.
Volek, J.S., et al. 2004. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition and Metabolism, 1 (1), 13.
Weeden, J., & Sabini, J. 2005. Physical attractiveness and health in Western societies: A review. Psyhological Bulletin, 131 (5), 635-53.
Yematani, H., et al. 2013. Association of estrogen with glucocorticoid levels in visceral fat in postmenopausal women. Menopause, 20 (4), 437-42.