One of the annoying tendencies of the Internet is its habit of taking preliminary findings or animal research, especially very specific findings, and spinning them out into broad statements or “the next big thing”.
This can be seen in how headlines are talking about how “copper is the key to a fast metabolism” or that “copper is key to burning fat” in response to a rather narrow mouse study. Although there is some mention of the findings being part of future obesity research, there is a large gap between the actual findings and their purported significance.
The Copper Mouse Study: Summary
- The test subjects were a group of mice that were bred to have Wilson’s disease, a genetic condition that causes accumulation of copper in the liver and other organs
- As copper built up in the mice livers, a decrease of lipid (fat) levels in the livers was also observed
- The Wilson’s mice also had higher levels of lipid deposits in the white fat (a type of body fat) compared to the control, and that the white fat also had lower levels of copper
- In other words: where there was more copper, there was less fat, and vice versa
- Cellular analysis noticed that copper can bind to the enzyme which normally attaches to and blocks something called the “cAMP signaling pathway”. The cAMP pathway is used to break down fat into fatty acids (called “lipolysis”)
What This Means
Lipolysis is the process by which fat is broken down for energy. The cAMP signaling path is how the body facilitates this process. There is an enzyme (PDE3) that can bind to the cAMP path and stops it from causing lipolysis. Copper, however, can bind to PDE3 first and prevents it from doing this. If you think of PDE3 as the stop switch for breaking down fat, then copper would be gumming up the mechanism to make that switch harder to throw.
What this all means for human obesity research is unclear. Assuming the finding is replicated, it suggests a role copper could play in human metabolism. However, whether that role is enough to have meaningful impact on obesity or weight loss in general is too speculative to say. The difference between the liver and white fat observed in the study suggests that ingesting copper is only one part of the effect—the copper must build up in the right places as well.
It is worth noting, however, that copper isn’t produced by the human body.
Dietary copper is our only source of the nutrient and it gets excreted fairly regularly. It is found in foods such as shellfish, mushrooms, greens, nuts , seeds and oysters.
Dietary copper can be found in oysters.
Although only about 25% of Americans receives the recommended 700 micrograms of copper per day, this does not necessarily mean being deficient in copper would cause a reduction in fat breakdown or if it does, if the reduction is enough to contribute to obesity or weight gain. Much more research is needed on the matter, particularly human subject research, to say anything more definitive.
The authors also caution against trying to use copper supplements since getting too much can cause drops in zinc and other toxicity effects.
Bottom Line
- Copper may have a role in blocking one of the chemical brakes for fat metabolism
- It is far too early to tell what this means for human nutrition, obesity, or weight gain/loss
Sources for Today’s Article:
“Copper is key in burning fat: Scientist says results could provide new target for obesity research,” Phys web site, June 6, 2016; http://phys.org/news/2016-06-copper-key-fat-scientist-results.html?utm_source=menu&utm_medium=link&utm_campaign=item-menu, last accessed June 7, 2016.
Krishnamoorthy, L., et. al., “Copper regulates cyclic-AMP-dependent lipolysis,” Nature Chemical Biology, 2016; 10.1038/nchembio.2098.