pixel

Leptin - the reason you're not losing weight?

For years, we considered ‘calories in vs calories out’ to be the holy grail of weight loss. If someone was overweight, they were clearly eating more calories than their body required and were therefore storing them as fat. To combat this, the same solution was always provided; eat less, move more, and the weight will drop off before you know it.

But weight loss is much more than just a numbers game. The fact is, there are numerous factors that influence whether we lose (or gain) weight – one of the most significant being a hormone called leptin.

Leptin is a hormone that many people don’t even know exists, but understanding it may help us unlock the secret to healthy, sustainable weight loss.

What is Leptin?

Leptin is a satiety hormone that regulates our appetite and our metabolism. Secreted by adipose (fat) tissue, it communicates directly with the hypothalamus in our brain and certain cells in our stomach to tell us when we are hungry and when we are satiated.

In the early years of human existence, leptin was quite literally a life-saver. When we lived through times of feast and famine, leptin would rise and fall accordingly to maintain survival:

  • When food was abundant and our body fat at a healthy level, leptin would ensure our metabolic rate increased – therefore increasing the rate at which we burn fat. After all, food is plentiful and we have enough fat cells to survive, so there is no need to store the calories we are consuming as more fat.
  • When food was scarce, our leptin levels would fall as a survival mechanism, in turn slowing our metabolism to prioritise fat storage at all costs. After all, who knows how long we need to survive before our next meal? At the same time, leptin is in constant communication with the brain telling us to search for food, resulting in an increase in appetite to encourage us to find calories – and fast.

Of course, in modern times, very rarely do we experience a true ‘feast or famine.’ Yet, our bodies still produce leptin in exactly the same way that they did when it truly assisted our survival. In healthy people, leptin is responsible for letting us know when we have eaten enough and when we have eaten too little.

Healthy leptin levels are what help the majority of people who maintain a consistent weight to do so with relative ease.

So how is leptin causing weight gain in so many people? The answer lies in what is proving to be an epidemic of modern times; leptin resistance.

What is leptin resistance?

‘Leptin resistance’ occurs when the leptin produced by our fat cells in our body cannot successfully communicate with our brain. Although leptin is still being produced by the fat cells, our bodies have become less sensitive (or resistant) to the hormone, and therefore do not adjust metabolism and appetite accordingly. The resulting physiological response is an increased appetite and a decreased metabolism; in other words, we actually become hard-wired to store fat.

But why does leptin resistance occur in the first place? As leptin is a hormone, there are many factors that could be at work:

Crash dieting:
One of the main reasons for leptin resistance is the modern ‘crash dieting’ mantra when it comes to weight loss. By embarking on a rollercoaster of excessively restrictive calorie consumption and long sessions of exercise, our leptin response becomes damaged and therefore stops working as it should do.

Ten thousand years ago, we certainly wouldn’t have gone on a ten mile run when food was scarce. Yet, in our efforts to lose weight, this is exactly what we are recommended to do. It’s all about eating less and moving more, remember?

Fructose Consumption:
Another factor that can contribute to leptin resistance is fructose consumption, especially in isolated forms like high fructose corn syrup. Excessive fructose has been shown to mute leptin responses in the hypothalamus1, whilst also elevating blood triglycerides and blocking the passage of leptin to the brain2.

Lifestyle factors:
There are also many modern lifestyle factors that could be contributing to leptin resistant. Excessive consumption of grains and soy has been strongly linked with leptin resistance, as the phytic acid they contain has been shown to bind with the leptin receptor3. A lack of sleep4 and stress5 have also been shown to interfere with leptin production.

How to fix leptin resistance

If you suspect that leptin may be the secret reason you are not losing weight, then there are steps that you can take to improve your leptin response. These are:

  • Consume high quality sources of protein and fat. to regulate your appetite and produce satiety hormones. Avoid refined sugars and simple starches. Limit your fruit consumption to 1 – 2 pieces per week in the initial period of healing.
  • Take measures to manage your stress levels; meditate, get outside in the sunshine, and do yoga.
  • Get plenty of sleep (8-9 hours each night) and try to maintain a strict circadian rhythm (I.E going to bed at 10pm and waking at 6.30am every day)
  • Avoid cardio, as this puts stress on your hormones. Limit your exercise to 2 – 3 weights or sprint sessions per week. As your system heals you can gradually start to re-introduce more exercise, if desired.
  • Avoid snacking; try to space your meals at least 4 hours apart and eat 2 / 3 larger meals each day rather than many smaller ones. This will reduce the stress on your liver, digestive system and hormones.

As you begin to heal and your leptin response improves, you should notice your appetite begin to stabilise to a more normal level. How long this will take depends on how severely leptin resistant you are, so be patient; it may take months to undo years of metabolic damage.

The key to long term weight loss

Patience and consistency; attempting to accelerate results through dramatically low calorie diets and excessive exercise is a sure fire way to damage your hormones and make maintaining your weight more of a struggle than ever before.


Sources

1) http://www.ncbi.nlm.nih.gov/pubmed/18703413
2) http://www.ncbi.nlm.nih.gov/pubmed/15111494
3) http://www.biomedcentral.com/1472-6823/5/10
4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC535701/
5) http://molpharm.aspetjournals.org/content/74/6/1610.full