We all have a “master switch” in our bodies. It regulates all kinds of systems in the body like energy usage or metabolism. This master switch is called the Adenosine Monophosphate-activated Protein Kinase or AMPK.

AMPK is an enzyme found in our cells that determine body fat composition and possibly even longevity. Activated AMPK provides protection against obesity and diabetes. [1]

 

What AMPK does:

  •      Regulates energy metabolism
  •      Increases fat-burning
  •      Increases the utilization of glucose while blocking fat and cholesterol synthesis

AMPK improves glucose uptake so it lowers your blood sugar, increases the burning of stored fat, and decreases your blood triglycerides. It decreases fat-related chronic inflammation, which means that it is targeting the inflammatory fat or the abdominal fat specifically. Abdominal fat has more inflammatory potential than fats in other parts of the body.

In the Surprising Reason, You’re Gaining Weight in Your 40s, I mentioned that inflammation increases as abdominal fat accumulates. Abdominal fat is also closely linked to the liver, which controls your metabolism. The more abdominal fat you have, the more you’ll be at risk for glucose intolerance and lipid abnormalities.

When you’re able to reduce the amount of fat in the abdominal area, not only does the fat go away, but you also get rid of inflammatory chemicals that are circulating in your system. It also increases the numbers of new and healthy mitochondria, and this is partly the reason why AMPK is anti-aging.

 

2 Factors That Decrease AMPK Activation

Two factors that decrease AMPK activation:

  1. Age
  2. Chronic overeating

The activation of AMPK in the cells naturally decrease with age, increasing our risk for diseases associated with aging. Aging is something that we can’t control, but the other factor, excessive consumption of calories, is something that is completely up to us.

When you overload our bodies with calories and frequent eating, our cell’s basic or maintenance functions decrease. Cellular waste and damaged proteins accumulate and inflammatory genes start to dominate our body.

 

How to Boost AMPK Activation

There are pharmaceutical, botanical and lifestyle things that you can do to boost AMPK activation.

1. Metformin

Metformin is commonly prescribed to Type II diabetes patients. It turns out that metformin activates AMPK. A research published in the Proceedings of the National Academy of Sciences suggests that metformin may slow down aging and increase lifespan. [2]

It may be beneficial for you to stay on this medication if your doctor prescribed this to you, although like all pharmaceuticals, it has potential side effects that you should educate yourself about.

2. Fasting

Fasting can also activate AMPK. Fasting, not eating, activate longevity factors. When you fast, you’re improving the quality of the function of mitochondria. These are the powerhouses of the cell that we have discussed in the past and will do so more in future newsletters.

3. Botanicals

Gynostemma tea can help activate AMPK. Gynostemma is a distant relative of the cucumber and you can drink this tea on a regular basis. I happen to enjoy it quite a bit. There’s a brand called Dragon Herbs that I recommend.

Hesperidin (a compound found in citrus peels), green tea extract, bilberry extract, can also help activate AMPK.

4. Supplements

Life Extension Foundation has a supplement called AMPK Metabolic Activator.

For people who have very sensitive blood sugar issues, these lifestyle and botanical additions to your diet can help keep blood sugar under control while activating this enzyme.

If you have questions about AMPK, comment below or join the discussion on our Weight Loss Awakening Friendship Group on Facebook.

This post was first published on The Miracle Noodle Blog.

References:

  1. “AMPK.” LifeExtension.com, www.lifeextension.com/magazine/2014/ss/ampk/page-01.
  2. Haes, Wouter De, et al. “Metformin Promotes Lifespan through Mitohormesis via the Peroxiredoxin PRDX-2.” PNAS, National Academy of Sciences, 17 June 2014, www.pnas.org/content/111/24/E2501.