Is Leptin Resistance the Cause of Your Weight Gain?
by Amy Medling, founder of PCOS Diva
Many with Polycystic Ovary Syndrome (PCOS) struggle with weight management. There are plenty of reasons for this, the most common one being insulin resistance. However, some research suggests there might be yet another underlying factor that could be attributed to weight management problems in those with PCOS- leptin resistance.
What is Leptin?
Before we describe what leptin resistance is, it’s critical to first know what leptin is.
Leptin is a hormone produced by our body’s fat cells that is a factor when it comes to regulating our appetite and energy consumption. Because of what it does, leptin has been dubbed as a “satiety” or the “hunger” hormone.
Because it’s a hormone, it’s also a messenger and it’s supposed to send messages to the brain, letting it know when it’s time to eat and when it’s not. When it’s time to eat, the brain triggers processes that help digestion and signals hunger.
When it’s not time to eat (or when you’re full), leptin lets the brain focus on burning calories normally. Leptin is also a key hormone in immunity, brain function, and even fertility, but it’s most known as a hormone for hunger and satiety.
Naturally, when leptin balance is disturbed, it creates a chain reaction that disrupts the body’s metabolic processes which can lead to unwanted weight gain.
What is Leptin Resistance?
Leptin is produced by our fat cells, so naturally, obese people have high levels of leptin. High levels of leptin should tell our brain to stop or control food intake. However, those with leptin resistance might have malfunctioning leptin signals.
A malfunctioning leptin signaling system, specifically when the amount of leptin present is not enough to make the brain activate “stop eating” mode, is the basic definition of leptin resistance. Due to the nature of the leptin hormone and its function when it comes to hunger and satiety, experts now believe that an impairment or resistance to leptin signaling is perhaps at the root of global obesity.
Not only will the brain not tell the rest of the body to stop eating, but it will also assume that you are hungry and need to save nutrients. This sends the body into “conserve fat” mode, essentially slowing down your metabolism especially when at rest.
Leptin resistance therefore creates this environment where you always have the urge to eat even though from a nutritional viewpoint, you don’t need to.
How to tell if you have Leptin Resistance
Here are some of the things to look out for it you think you have leptin resistance
- Being overweight
- High levels of inflammation
- Difficulty controlling appetite, especially for high fat, high sugar foods
- Trouble losing weight
Being overweight is often the number one sign that you may have leptin resistance, but some also argue that even those who are underweight have the condition. At its core, leptin resistance is about a disruption in leptin signaling which results in the body’s inability to maintain a healthy balance of hunger-full.
These are also common symptoms for general obesity, insulin resistance, or metabolic syndrome, thus making it difficult to actually confirm that the issue is leptin resistance. The only surefire way to know you have leptin resistance is to have a lab test which indicates you have high leptin levels and have a professional diagnose you.
Leptin Resistance and PCOS
How does leptin resistance relate to PCOS? Is it simply a case of “If you have obesity, you have leptin resistance?”
While obesity is perhaps the number one determining factor when it comes to leptin resistance, it is more complicated to diagnose in those with PCOS due to how PCOS disrupts endocrine function. Leptin, being a hormone, is an integral part of the endocrine system and explains why PCOS complicates the idea of leptin resistance even more.
In a 2013 study, experts suggest women with PCOS have a condition known as hyperleptinemia or an abnormally high level of leptin in the bloodstream. It’s also significantly higher in obese subjects.
“…the major finding of the present investigation is that, irrespective of BMI or insulin resistance, PCOS population has higher leptin levels. This observation is quite legitimate, because leptin is predominantly synthesized by adipocytes (fat cells), and higher BMI is distributed with high frequency in the PCOS group than in control women.” [1, 2]
They also cite that insulin resistance further contributes to leptin resistance in women with PCOS because insulin stimulates leptin secretion and synthesis. They therefore speculate that high insulin levels caused leptin resistance.
Researchers also speculate that high leptin levels are associated with high testosterone levels, and quite possibly also inhibiting ovarian steroidogenesis – where ovarian cells produce hormones critical for reproductive function and ovulation – in women with PCOS.
These new findings suggest that there could be alternatives to how doctors should prescribe treatment when it comes to weight management. If more research is conducted into leptin resistance in the context of PCOS, we might soon see treatments that are meant to reduce the effects of leptin resistance or even reverse it.
Overcoming Leptin Resistance
Mentally trying to overcome leptin resistance is almost impossible because it takes more than willpower to convince your body to stop eating at a hormonal level. However, you can mitigate the “damages” done by this condition by simply upgrading your lifestyle. These include:
- Avoiding processed food: If you cannot overcome your body’s signals to eat, try to choose whole foods which are not processed. Avoid “foods” that come in boxes or packets. Stick to real fruits and veggies if you’re craving something sweet or complete meals if you’re craving something filling. Whole foods, at least, offer nutrients which your body can use and wreak less havoc on your blood sugar and hormones.
- High fiber diet: Diet plays a huge role in keeping your body healthy, and it’s the same with leptin resistance. Fibrous foods contain many vitamins and minerals, plus some antioxidants that just enable you to live a healthier lifestyle. Fiber helps you feel full and aids in digestion and much more.
- Exercising: The last thing you want to do if you suspect leptin resistance is to be sedentary. The body’s resting metabolism is at its lowest when you’re literally not moving for long periods of time. So, combat physical inactivity by moving more. It doesn’t mean you have to spend the day on a treadmill, even household chores and gardening count as exercise. The idea is to keep moving.
- Better sleep habits: Sleep is the body’s time to recover, and it can help maintain hormonal balance if you have healthy sleeping habits. Studies also indicate poor sleep is linked to leptin signaling problems.
The discovery of leptin resistance has opened new ways for experts to view obesity and how to treat it beyond the staple of diet and exercise. Moreover, the link between leptin resistance and PCOS is definitely up for consideration if not already proven. Those of us with PCOS may soon experience new insights into PCOS treatment, especially when it comes to weight management.
Amy Medling, best-selling author of Healing PCOS and certified health coach, specializes in working with women with Polycystic Ovary Syndrome (PCOS), who are frustrated and have lost all hope when the only solution their doctors offer is to lose weight, take a pill, and live with their symptoms. In response, Amy founded PCOS Diva and developed a proven protocol of supplements, diet, and lifestyle programs that offer women tools to help gain control of their PCOS and regain their fertility, femininity, health, and happiness.
References:
- Chakrabarti J. Serum leptin level in women with polycystic ovary syndrome: correlation with adiposity, insulin, and circulating testosterone. Ann Med Health Sci Res. 2013;3(2):191-196. doi:10.4103/2141-9248.113660
- Namavar Jahromi B, Dabaghmanesh MH, Parsanezhad ME, Fatehpoor F. Association of leptin and insulin resistance in PCOS: A case-controlled study. Int J Reprod Biomed. 2017;15(7):423-428.
