For nearly a century, scientists have recognized copper's importance to human health. New research from the University of California, Berkeley, sheds light on copper's crucial role in fat metabolism. This article explores the connection between copper and weight loss, drawing upon scientific studies and expert opinions.
Copper: An Essential Nutrient
Copper (Cu) is a trace element vital to human health. As early as 1928, rat studies demonstrated a link between copper deficiency and anaemia, indicating that the mineral is involved in the production of red blood cells. Scientists have long prized copper as a malleable, conductive metal used in cookware, electronics, jewelry, and plumbing. Over the past decade, it has gained increasing attention for its role in certain biological functions. Tight regulation of Cu levels in cells and tissues is necessary for normal physiologic processes. Copper is a co-factor of enzymes involved in mitochondrial function, inflammatory response, and anti-oxidative functions.
According to the Food and Nutrition Board of the Institute of Medicine, an adult's estimated average dietary requirement for copper is about 700 micrograms per day. However, various nutritional surveys suggest that as many as a quarter of Americans lack sufficient copper in their diet.
The Link Between Copper and Fat Metabolism
Researchers, led by Chris Chang at Berkeley Lab's Chemical Sciences Division, have discovered that copper is essential for breaking down fat cells so they can be used for energy. "We find that copper is essential for breaking down fat cells so that they can be used for energy," said Chang. "It acts as a regulator. The more copper there is, the more the fat is broken down." The team of researchers studied mice with a genetic mutation (called Wilson’s disease-also found in humans) that causes an accumulation of copper in the liver. Their findings: The mice with extra copper in their livers had lower than normal fat levels compared to the control group of mice.
In essence, copper keeps your body in fat-burning mode. The researchers made the copper-fat link using mice with a genetic mutation that causes the accumulation of copper in the liver. Analysis of the mice with Wilson's disease revealed that the abnormal buildup of copper was accompanied by lower than normal lipid levels in the liver compared with control groups of mice.
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How Copper Works: A Deeper Dive
To discover how copper actually works in fat metabolism, Chang chose to study mice with a genetic defect that produces symptoms similar to those of a rare human illness, Wilson’s disease. In both situations, a key enzyme that moves copper in and out of cells is mutated, causing misregulation and copper overload - often to toxic levels - in the liver. He and his team discovered that in the mice, copper is hoarded by the liver, basically starving fat cells of copper so that they cannot properly regulate fat storage and burning in organs such as the stomach and pancreas.
They succeeded in tracking down exactly how copper works: It releases a brake on fat burning. Normally, a second messenger molecule called cyclic-AMP (cAMP) activates the enzymes that break down the fat molecules. They found, however, that another enzyme (phosphodiesterase 3, or PDE3) blocks cAMP, probably to prevent fat breakdown when it is not needed. "Copper promotes fat burning by blocking a key enzyme, PDE3, that normally shuts off fat burning. When copper binds phosphodiesterase, it's like a brake on a brake," said Chang.
The mice were treated with a drug called isoproterenol, which induces lipolysis. "We studied fat cells in a culture dish, as well as fat cells in healthy and diseased mice, and discovered a new pathway showing that copper is essential for normal burning of fat in the body," explains Chang. Lipolysis is the breakdown of large pieces of fat into smaller pieces so they can circulate in the blood and be burned throughout the body.
Copper and Obesity: What the Studies Reveal
Copper misbalance has been linked to fat accumulation in animals and experimental systems; however, information about copper homeostasis in human obesity is limited. Dietary Cu deficiency combined with high fructose induces non-alcoholic fatty liver disease (NAFLD) in rats. Imbalance of Cu along with changes in the activity and abundance of Cu-dependent enzymes has been linked to diabetes and obesity. The emerging role of Cu in lipid metabolism may provide a new target for obesity research. However, information concerning Cu homeostasis in obese patients is limited. Elevation in serum Cu has been reported in obesity.
A cross-sectional study was conducted from October 2013 to March 2015 at the Johns Hopkins Medical Institutions. Obese patients (BMI > 40 kg m−2 or >35 kg m−2 with one or more obesity-associated comorbidities) undergoing bariatric surgery (Roux-en Y gastric bypass (RYGB) or vertical sleeve gastrectomy (VSG)) were recruited from the Johns Hopkins Center for Bariatric Surgery. Lean controls (BMI < 26 kg m−2) with no history of diabetes or cardiovascular disease were recruited from the Johns Hopkins Hospital. A total of 62 lean and 55 obese patients were included in this study.
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The concentrations of Cu and other trace metals (Fe, Zn, and Mn) in serum were measured for each study participant using ICP-MS. Cu levels were significantly higher in obese patients, in both males and females, relative to lean controls. Women in both the lean and the obese group had higher serum Cu compared to men. BMI positively correlated with Cu, Zn, and Fe. Following multiple regression analysis, which controlled for age, gender, ethnicity, and other metals, Cu was the only essential metal that retained its significance as a predictor of BMI. Within the obese group, only Cu levels significantly and positively correlated with BMI.
Univariate analysis of the data combined from the lean and obese groups revealed a positive association between Cu and insulin, Cu and leptin, and Cu and HbA1c. Age and ethnicity did not significantly influence serum Cu; however, gender was a predictor of serum Cu loads. Serum Cu levels were positively correlated with leptin/BMI.
In circulation, more than 95% of total Cu is bound to Cu-containing proteins. Cp is the major cuproprotein in serum, and the levels of Cp are elevated in obese patients. SSAO is another abundant Cu-dependent enzyme; the activity of SSAO in serum was shown to significantly and positively correlate with BMI.
Copper Deficiency: A Potential Factor in Obesity?
If copper is indeed key to fat metabolism, then copper deficiency could in turn play a role in obesity, causing the body to hang on to fat without breaking it down for energy. It bears mentioning that true copper deficiency is rare in the developed world. Mild deficiencies, however, may often go unrecognised.
Getting Copper Through Diet: Food Sources
"Copper is not something the body can make, so we need to get it through our diet," said Chang. "The typical American diet, however, doesn't include many green leafy vegetables. Food sources of copper include sesame seeds, cashews, soybeans, shiitake and Crimini mushrooms, leafy greens (spinach, kale, Swiss chard, mustard greens), asparagus, summer squash, and legumes.
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Caution: The Risks of Copper Supplementation
Chang cautions against ingesting copper supplements as a result of these studies. There is an additional problem too, in that too much copper can be just as dangerous as too little. It can lead to imbalances with other essential micronutrients, and can prove toxic in susceptible populations, causing oxidative damage to the body. This being the case, the research is unlikely to pave the way for a new era of copper-based obesity drugs.
The Broader Implications
"The biochemistry we have identified appears to be more widespread and can potentially occur in the pancreas, heart, and brain as well. Some of us are now thinking about obesity as a neurological disease rather than strictly a metabolic disease, because there are potentially connections between your fat tissue and the brain," he said. Chang is continuing his study of copper’s roles in the brain and in fat metabolism, looking for possible ways to target the copper pathway to treat neurodegenerative brain diseases or diseases of metabolism.