Yes, it is true that losing weight requires creating a calorie deficit—whether that means increasing your daily calorie burn and/or eating less. However, sometimes your ability to burn fat isn’t that simple.
Perhaps you have tried dieting, restricting your calories, manipulating your macros and giving it your all in the gym, but you still haven’t had any luck. Burning fat off your body can actually be a little more complicated, as it isn’t simply about flipping on the single fat burning switch in your body to see a result. Multiple hormones and enzymes in the body control fat burning, and each can have a cascading effect that can impact your ability to burn fat or store it. In this post, I uncover 3 things you might not know about your fat loss and what you can do about each.
1. Your Diet Controls Fat Burning Hormones
When it comes to burning off fat, no matter if it sits on the belly, thighs, hips or glutes, you need to control your fat burning hormones in order to do so—decreasing the hormones that cause fat storing and increasing those that cause fat burning.
There are many hormones involved in fat storage, fat burning, and appetite regulation, and each one has a direct affect on the other. When one is out of balance, it can result in a cascade effect further impeding your fat burning ability.
When insulin is high, fat burning is essentially turned off. Insulin causes an increase in the fat storing enzyme LPL, or lipoprotein lipase, resulting in further storage of glucose as fat. When LPL is high, the antagonist enzyme HSL, or hormone sensitive lipase, the fat burning enzyme is low.
Following a better diet helps to reverse this response. Your diet should be lower in carbs and higher in protein to help reduce insulin spiking. Continual insulin spiking can lead to long-term insulin resistance, which is when insulin can no longer perform its function properly.
Avoid refined, high sugar carbs. Opt for more calorie-dense, nutrient-rich, high fiber carbs like sweet potato, squash, oatmeal, cruciferous vegetables or brown rice, which have lower glycemic responses in the body.
2. Lack of Sleep Disrupts Weight Loss
Whether it’s because you are just too busy or just having trouble sleeping, lack of sleep results in a negative effect on your fat loss. Missing out on sleep causes an increase in cortisol hormones and a reduction in melatonin – the sleep hormone.
When cortisol rises, insulin sensitivity and glucose intolerance also drop, along with the level of serotonin, which can cause cravings for sugar. Furthermore, lack of sleep can also disrupt the release of growth hormone, which is critical to metabolism, muscle recovery and growth. Growth hormone helps to stimulate amino acid uptake by the muscles needed for protein synthesis, while also enhancing the release and breakdown of fat!
Research has shown that those that do get enough sleep decrease their ability to lose weight. In a recent study, it was shown that those who got only 5.5 hours of sleep lost less fat and more muscle than the group that got 8.5 hours of sleep. All study participants received the same amount of calories and daily activity.
Chronic sleep loss can upset the regulation of important hormones involved in appetite, including ghrelin and leptin, and can reduce the body’s ability to process and store carbohydrates for use in the muscle…ultimately impacting metabolism!
Get into the habit of getting at least 8 hours of sleep every night. Avoid using caffeinated products within 5 hours of sleep, go to bed earlier and reap the fat burning benefits of a good nights sleep!
3. Estrogen Balance Improves Ability to Burn Fat
Estrogen can have a positive and negative effect on your body’s ability to burn off fat. When estrogen levels are regulated, so is your metabolism. But if your estrogen levels are in excess, your fat burning could be at a standstill. Excess estrogen can cause a disruption in the anti-lipolytic alpha adrenergic receptors in subcutaneous fat. Increasing the activity of these receptors causes less break down of fat to occur.
These receptors are more active in fat within the hips, thighs and glutes. Higher estrogen levels result in further receptor activation—not to mention fat cells can also produce more estrogen. Decreasing excess estrogen in the body can help restore a proper balance of estrogen to progesterone, which can help to increase beta-adrenergic receptor activity or fat burning pathways and can lead to stimulation of important fat burning hormones like norephinephrine.
Excess estrogen can cause not only a decreased metabolism, but also fatigue, bad skin, loss of libido and risk of on-set of estrogen-related diseases. Reducing excess estrogen starts with reducing your exposure. Eat organic food, and reduce chemical estrogen exposure by using sulfate free soaps and BPA-free plastics. Also, increase the fiber in your diet. Fiber binds to excess estrogen metabolites forming a complex that can be excreted out of the body. Eat a diet rich in fiber and high in anti-estrogenic compounds such as berries, which are high in flavonoids, and dark leafy cruciferous vegetables, which are high in DIM and Indole-3-Carbinol. Both of which are effective for reducing highly estrogenic compounds and reducing excess estrogen production in the body.
References
Arlet V, et al. Insufficient Sleep Undermines Dietary Efforts to Reduce Adiposity. Ann Intern Med. 2010; 153(7): 435-441.
Bradlow HL, et al. Long-term responses of women to indole-3-carbinol or a high fiber diet. Cancer Epidemiol Biomarkers Prev. 1994. 3(7): 591-5.
Cortright RN, Koves TR. Sex differences in substrate metabolism and energy homeostasis. Can J App Physiol. 2000. 25(4): 288-311.
Gann PH, et al. The effects of a low-fat/high-fiber diet on sex hormone levels of menstrual cycling in premenopausal women. Cancer. 2003. 98(9): 1870-1879.
Price T, et al. Estrogen regulation of adipose tissue lipoprotein lipase – possible mechanism of body fat distribution. Am J Obs Gynec. 1998. 178(1): 101-7.
Reding KW, et al. Fruit intake associated with urinary estrogen metabolites in healthy premenopausal women. Open J Prev Med. 2012. 2(1): 10
