Loading....
Your cart is empty
Leptin
Leptin Resistance
Leptin Resistance Causes
How To Reverse Leptin Resistance
Summary
If weight loss was only about calories in vs. calories out, then we would all be skinny. We would just not eat or eat very little until we reached our weight loss goal.
As we know, millions of people have actually tried that and many times they end up not just losing weight, but they end up gaining weight.
How can it be that we eat very few calories, but end up gaining weight?
Well, more and more scientists are discovering that it is because of a hormone called Leptin.1
When our bodies stop responding to this leptin hormone, it is called Leptin Resistance. This is now suspected to be the primary cause of people gaining fat and becoming heavier.
This article goes into detail regarding Leptin for weight loss, what you need to know, and how a person can reverse Leptin Resistance.
Leptin: What some call the “Master Fat Burning Hormone”
The Leptin hormone, believe it or not, is a hormone that is produced by the body’s fat cells.2
Leptin, when working properly, tells your brain when you have enough stored fat. Your brain then knows that you don’t have to eat more calories, and can burn calories at a normal rate without trying to store more calories as fat.
This is why Leptin sometimes gets the nickname “starvation hormone” or “hunger hormone.”
Leptin communicates with an area of the brain called the hypothalamus. Leptin’s primary role is to report to the hypothalamus how much fat is stored in the body and if the body is receiving enough calories to maintain a healthy weight.3
Essentially it keeps us from starving which it is very good at, but there is a communication error that tends to occur with the hypothalamus when it comes to overeating.
Here Is How Leptin Communicates With The Brain
Like I mentioned in the beginning, Leptin is created by the body’s fat cells and the more body fat someone carries the more Leptin that is produced.4
The Leptin hormone, once produced, is carried via the bloodstream to the brain where it targets the hypothalamus. This is the part of the brain that dictates how much you eat and when you are hungry.5
When this communication highway is working properly, the higher levels of Leptin tell the hypothalamus that we have plenty of stored fat and the brain doesn’t send out the signal to eat.
When the body has low levels of stored fat, Leptin tells the brain that we need to eat more calories.6
This form of communication is commonly known as a negative feedback loop. What I mean by this is when body fat levels increase, then Leptin levels go up since fat produces Leptin. The body then eats less calories and burns more fat to regulate the stored fat.
Now when you lose body fat or it decreases, this causes Leptin levels to drop which then signal the brain to eat more calories and to burn less calories to conserve fat stores.
Check out Christy's story and her 6 tips that she has been doing to help her finally achieve her ideal body.
"Oh and I was finally able to get into a favorite pair of jeans over the weekend"
As we know, if you are overweight or obese you have plenty of stored fat which means the level of Leptin is higher. Given how the communication pathway is supposed to work, the brain should receive the Leptin signal to start eating fewer calories.
Even though there are high levels of Leptin, the signaling and communication pathway becomes broken and the brain doesn’t get the message.
This is known as Leptin Resistance and scientists now believe this to be one of the primary contributors to so many people being overweight and obese.7
When the brain doesn’t receive the Leptin signal, it thinks that the body is starving so it sends out the signal to eat more calories.
Even though the body has plenty of stored fat, the hypothalamus’s job is to make sure the body survives so it increases appetite and hunger.
It also forces the brain to conserve energy and burn fewer calories. Now the body has created an environment to build even more fat stores even when it doesn’t need it.
For those that struggle with Leptin Resistance, thinking that you are going to overcome the brain’s hunger signal is a futile attempt. For those that believe they have Leptin Resistance, you know how strong that hunger signal is and why so many struggle with controlling their appetite.
This could also be why so many people yo-yo diet and long-term weight loss doesn’t occur. Yes, we can eat properly and restrict enough calories to lose some excess fat, but the brain still isn’t getting the signal so it increases appetite, decrease in calories burned and works to store more fat.
There are a few reasons as to what scientists believe cause Leptin Resistance.
Having fat floating around in the bloodstream which can happen when you are obese or significantly overweight, may be a cause. This can cause an increase in fat metabolites in the brain and possibly interfere with Leptin signaling with the brain.
The most likely cause of Leptin Resistance is inflammation. When you carry too much fat as I had mentioned earlier, the fat cells become inflamed and what some call sick. This elevated inflammation level then also occurs in the brain and hypothalamus. Scientists believe this is an important cause to Leptin Resistance.8,9
Inflammation can dull the brain’s Leptin receptor site and this causes the signaling issue which then triggers resistance.
One study reported that when someone has higher inflammation levels, they also have elevated levels of C-reactive protein (CRP) and this can inhibit Leptin’s role in controlling appetite. It also increases Cortisol levels. It can shut down the Brain-Leptin communication pathway by binding to Leptin. When this happens, it becomes nearly impossible for Leptin to cross the blood-brain barrier and reach the hypothalamus.17
Unfortunately, this can put someone into a cycle where they gain more weight and create more inflammation, which then causes more resistance with the brain and Leptin communication pathway.
How To Reverse Leptin Resistance
Science is still evolving in regards to how to reverse Leptin Resistance, but eating an inflammation-reducing diet seems to be the front runner, along with consuming nutrients that help improve the Brain-Leptin communication pathway.
Some changes you can make to adopt an inflammation-reducing diet are:
Avoid processed foods: Processed foods appear to promote inflammation.10
Eat More Soluble Fiber: This can help improve gut health which is the starting point for reducing internal inflammation in the body.11
Exercise: Burning off excess fat in the blood as energy can help with Leptin Resistance.12
Get More Sleep: It has been shown that lack of quality sleep can affect Leptin in negative ways.13
Lower Your Triglyceride Levels: Research has indicated that when you have high triglyceride levels, it can stop the movement of Leptin through the blood to your brain.14, 15
Eat More Protein: Increasing your intake of quality lean protein can help with losing weight and allow Leptin to become more sensitive.16
Take Leptin Resistance Supplements That Contain LeptiCore®: This nutrient has been shown to improve C-reactive protein levels (CRP) which can inhibit Leptin’s role in controlling appetite, and CRP may bind to the Leptin hormone which prevents it from crossing the blood-brain barrier and reaching the brain.17
If you are struggling to lose weight or seem to be dumbfounded as to why the scale won’t budge, Leptin Resistance could be the reason why.
Implement the strategies above, especially the inflammation-reducing diet and nutrients that help lower CRP levels that can cause the Leptin signal from reaching the brain.
This is the best way to regulating the Leptin hormone and reversing Leptin Resistance.
To learn more about how specific nutrients can help lower CRP levels and improve the communication between the brain and Leptin click the next page button below.
Get started and grab Your FREE 5 Blood Tests That Predict Heart Disease Better Than Cholesterol Guide!
Plus, we will send you cutting edge health news, therapies and daily strategies to maintain an optimal health status!
References:
1 https://www.ncbi.nlm.nih.gov/pubmed/25232147
2 https://www.ncbi.nlm.nih.gov/pubmed/12439643
3 https://www.ncbi.nlm.nih.gov/pubmed/9796811
4 https://www.ncbi.nlm.nih.gov/pubmed/7584987
5 https://www.ncbi.nlm.nih.gov/pubmed/10766253
6 https://www.ncbi.nlm.nih.gov/pubmed/12727933
7 https://www.ncbi.nlm.nih.gov/pubmed/23359004
8 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319208/
9 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248304/
10 https://www.ncbi.nlm.nih.gov/pubmed/19755625
11 https://www.ncbi.nlm.nih.gov/pubmed/18031592
12 https://www.ncbi.nlm.nih.gov/pubmed/11157319
13. https://www.ncbi.nlm.nih.gov/pubmed/15531540
14. https://www.ncbi.nlm.nih.gov/pubmed/15111494
15. http://www.nejm.org/doi/full/10.1056/NEJMoa022637
16. https://www.ncbi.nlm.nih.gov/pubmed/16002798
17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836327/