Trace elements refer to elements that are extremely small in quantity but essential to life.
Trace elements usually includes zinc, selenium, iodine, copper, chromium, manganese, magnesium, diamond, cadmium, fluorine, molybdenum, lead, etc. Trace elements have important effects on many biological processes by activating or inhibiting the activity of biological enzymes. At present, there are four kinds of trace elements that have been widely studied and believed to be possibly related to blood lipid metabolism.
Firstly, the impact of zinc on blood lipids.
Zinc contains 2-3 grams in the human body and exists in the form of coenzymes, playing a wide range of regulatory roles in the body’s metabolism. Zinc is involved in metabolic pathways including serving as a major component of various enzymes (such as alkaline phosphatase, lactate dehydrogenase, etc.); and binding with some non-enzymatic organic molecules to form complexes, which affect their structural configurations.
International nutrition societies recommend a daily zinc intake of 15-20 mg for adults. Numerous epidemiological studies have shown that people who drink hard water have lower serum zinc levels, which may be related to the high calcium (Ca) and magnesium (Mg) content in hard water, forming complexes with zinc. In addition, excessive dietary calcium intake can increase zinc deposition in bones (zinc transfer from liver to bones), resulting in decreased serum zinc levels. Dietary factors such as excessive consumption of refined foods, gastrointestinal absorption problems, alcoholism, liver cirrhosis, and gastrointestinal diseases can also affect zinc metabolism and absorption, leading to zinc deficiency.
Zinc deficiency can cause abnormal lipid metabolism, which has been confirmed by numerous experimental studies. Research has shown that dietary zinc intake has a significant impact on lipid metabolism, but the intake should be appropriate.
Secondly, the impact of copper (Cu) on blood lipids.
Copper plays a catalytic role in some enzymes involved in biological metabolism. Copper-dependent enzymes are mainly metal proteins (such as cytochrome C oxidase, peroxidase, and dopamine β-hydroxylase), and they participate in the oxidation reaction of transferring ferrous iron (Fe2+) to ferric iron (Fe3+) in the body. The normal plasma copper concentration in humans is about 15.7 micromoles/litre (100 micrograms/ml), and the daily intake for adults should be 2-3 mg.
Animal experimental research has found that animals with copper deficiency have increased serum total cholesterol (TC) levels. In patients with hereditary copper transport disorder (Menkes syndrome), severe copper deficiency leads to abnormally high serum LDL-C levels, indicating that copper has a certain impact on lipid metabolism. Due to the regulatory role of the liver in copper metabolism, copper deficiency is usually not seen, but it can occur in cases of diarrhea, malabsorption accompanied by hypoproteinemia, or in patients receiving parenteral nutrition. Amino acids and fresh plant components in the diet help with copper absorption, and excessive copper intake can be excreted through bile.
High dietary copper concentrations can reduce intestinal absorption of zinc, and copper absorption is also affected by the high or low molybdenum content in the diet.
Thirdly, the impact of zinc/copper ratio on blood lipids.
Zinc and copper compete and inhibit each other during their absorption and transport in the body. Zinc can induce the liver to synthesize proteins that have a greater affinity for copper than for zinc (such as proteins rich in cysteine and sulfhydryl groups). As a result, copper binds to these proteins in large quantities, reducing the amount of free copper in the body and decreasing the activity of enzymes bound to copper, leading to abnormal lipid metabolism. Animal experiments have found that an increased zinc/copper ratio may affect lipid metabolism, but this has not yet been widely recognized.
Fourthly, the impact of chromium (Cr) on blood lipids.
Chromium usually exists in the form of organic complexes, known as glucose tolerance factor (GTF), which is an essential trace element for glucose and lipid metabolism. It is easily absorbed and required in adults in an amount of 0.05~0.2 milligrams per day. Chromium can be found in wheat germ, wheat bran, unrefined polysaccharides, and yeast. The reasons for relative chromium deficiency in the body usually include poor absorption of chromium salts or their complexes in the alkaline matrix of the intestine (only 0.5% absorbed); and the refined rice, flour, sugar, and fat can lose most of their chromium.
Eating refined carbohydrates (such as sucrose and glucose) can only supplement small amounts of chromium, which inevitably mobilize the body’s stored chromium into the plasma, resulting in a net loss of chromium content. Clinical trials have reported that healthy individuals who took chromium chloride 200 mg/day for 12 weeks had higher serum high-density lipoprotein-cholesterol (HDL-C) compared to the control group, and lower serum total cholesterol (TC) and triglycerides (TG).
Fifth, the impact of manganese (Mn) on blood lipids.
Manganese is an activator of various enzymes involved in the metabolism of glucose and fat (such as pyruvate carboxylase, superoxide dismutase, glucosyltransferase, etc.), and manganese-iron is also a cofactor for the mevalonate kinase involved in the synthesis of squalene and cholesterol. The concentration of manganese in animal tissues is relatively constant with age.
The constant level of manganese in tissues mainly depends on excretion pathways for regulation and maintenance. The content of manganese in adults is 10-20 mg, and the recommended daily essential intake is 2.5-5 mg. Research has found that manganese can inhibit the formation of atherosclerotic lesions in experimental rabbits. Manganese deficiency is similar to chromium deficiency and can cause decreased glucose tolerance and lipid metabolism abnormalities. In European countries, deficiency of manganese and chromium is related to long-term consumption of refined carbohydrates (such as wheat flour processing may lose 86%, refined rice can lose 75%, and refined sugar can lose 89% of manganese). However, the independent role and mechanism of manganese deficiency on lipid metabolism have not been elucidated.
