Does CoQ10 help with osteoporosis?

Osteoporosis (OP) is a systemic disease characterized by bone metabolism disorders. The World Health Organization defines it as a bone mineral density (BMD) that is 2.5 standard deviations or more below the average BMD of young healthy patients. Epidemiological surveys show that the incidence of female OP increases with age, and the prevalence of women over 65 years old is 51.6%. The rate of bone resorption in postmenopausal women is about twice that of bone formation, which is related to decreased ovarian function, oxidative stress, increased levels of inflammatory factors, and fluctuations in estrogen and follicle-stimulating hormone (FSH).

Although exogenous estrogen therapy can reduce the incidence of postmenopausal osteoporosis (PMOP), long-term use of non-antagonistic estrogen therapy may lead to an increase in the incidence of other diseases and the clinical application of other anti-OP drugs will also be limited due to their respective side effects.

Coenzyme Q10 is often used to improve ovarian reserve function and enhance fertility in the treatment of gynecological diseases because of its antioxidant properties. In recent years, studies have found that coenzyme Q10 also has good efficacy and safety in the treatment of OP.

Structure and function of coenzyme Q10

Coenzyme Q10 is a lipophilic electron carrier that participates in the transfer of electron chains and is the core of cell metabolism. Under normal circumstances, it exists in the body in two forms: redox. Most of the coenzyme Q10 required by the human body is synthesized by its tissues. After the age of 25, the content of coenzyme Q10 in the human body will decrease with age. The continuous accumulation of reactive oxygen species (ROS) in women's bodies will gradually increase the risk of OP. In the early days, coenzyme Q10 was often widely promoted as a dietary supplement. It has been used in the treatment of many diseases, such as diabetes, Parkinson's syndrome, male asthenospermia, premature ovarian failure, cardiovascular disease, etc. As the clinical application of coenzyme Q10 becomes popular, its new functions have also begun to be explored. Coenzyme Q10 has important research value in the treatment of PMOP, but the potential mechanism of action needs further exploration.

Mechanism of Coenzyme Q10 in the Treatment of Postmenopausal Osteoporosis

1. Obesity Leads to Decreased Testosterone Levels

Estrogen deficiency in postmenopausal women can inhibit the oxidation of mitochondrial β-fatty acids in the body's cells and increase the production of oxygen free radicals. ROS-induced bone loss is mainly induced by RANKL. After menopause, the level of RANKL in the bone microenvironment will increase due to estrogen deficiency, and the increase in FSH concentration will enhance T cell activation. The activated T cells will lead to RANKL-induced osteoclast activation and bone destruction. Coenzyme Q10, also known as ubiquitin ketone, is easily soluble in lipid solvents and has good tolerance and safety. In the treatment of PMOP, Coenzyme Q10 can replace estrogen to fight oxidative stress and inhibit the formation of RANKL-induced osteoclasts. In addition, Coenzyme Q10 can also directly remove intracellular oxygen free radicals and prevent bone loss.

2. Inhibit the expression of inflammatory factors

Inflammation is a self-protective response of cells to harmful external stimuli, but long-term inflammatory reactions caused by abnormal stress can cause bone destruction. Inflammatory cytokines play an important role in the development of PMOP in both human and animal models. To effectively prevent PMOP, in addition to increasing the level of estrogen in the body, it is also crucial to inhibit the expression of inflammatory factors. Coenzyme Q10 is similar to many antioxidants and has potential anti-inflammatory ability. "Anti-inflammatory" is actually "anti-oxidation" to some extent. Coenzyme Q10 may activate the pathway where nuclear factor E2-related factor 2 (Nrf2) is located, activate the downstream antioxidant enzymes of the pathway to fight oxidative stress and inhibit the expression of inflammatory factors.

3. Regulate the apoptosis of RAW264.7 cell mitochondria

RAW264.7 cells are one of the family members of the mononuclear/macrophage lineage and can differentiate into multinuclear cells with osteoclast ability. This cell is similar to most macrophages and can phagocytose cell fragments and consume pathogens. In the normal bone metabolism process of women, RAW264.7 can acidify bone, degrade collagen, and promote bone remodeling. In the absence of external stimulation, RAW264.7 cells will only proliferate. However, the loss of estrogen in postmenopausal women increases, causing RAW264.7 to rapidly differentiate into mature osteoclasts, resulting in an abnormal increase in the number of osteoclasts and an imbalance in bone metabolism. Coenzyme Q10 can enhance the expression of mitochondrial apoptosis proteins in RAW264.7 cells to inhibit the formation of osteoclasts and is expected to become a candidate drug for the treatment of PMOP in the future.

4. Reduce serum FSH levels

After menopause, women suffer the most severe bone loss, and serum FSH levels will rise rapidly and maintain a high level for several years. The decrease in estrogen secretion weakens the inhibitory effect on the hypothalamus-pituitary axis, causing an increase in FSH concentration, resulting in weakened osteoblast activity, active osteoclast differentiation, and continued increase in bone resorption. Coenzyme Q10 can effectively reverse the serum FSH concentration in elderly women, so it is speculated that coenzyme Q10 may treat PMOP by reducing serum FSH. In the future, the detailed mechanism of action of coenzyme Q10 in reducing FSH to treat PMOP can be studied in depth from the perspective of molecular biology.

Ultimately, PMOP is related to the aging of ovarian function and the fluctuation of sex hormones in the body. Estrogen deficiency and elevated FSH are key factors that lead to the increase of inflammatory factors and ROS, which in turn indirectly induce RAW264.7 cells to differentiate into osteoclasts. Numerous animal studies have shown that coenzyme Q10 can not only improve OP through multiple pathways, but also help restore ovarian function, and its safety is higher than other anti-OP drugs in clinical practice. However, so far, most of the treatment processes of coenzyme Q10 for PMOP are mainly animal studies, and clinical studies are relatively lacking; some conclusions of animal experiments are also drawn through speculation, which need further verification and exploration.

HSF Biotech's Coenzyme Q10

To enhance the bioavailability of Coenzyme Q10, it is important to select appropriate formulations based on different application needs, enabling better release and function within the body. Relying on our separation and extraction technology platform, HSF Biotech produces Coenzyme Q10 using cold water dispersion microencapsulation technology. This ensures stable performance, strict control over trace pollutants, and good flowability. It quickly disperses in cold water, making it suitable for various applications such as solid beverages, gummies, and premixes. It can be combined with vitamin E/plant oils and is widely used in functional foods and soft capsules, among other products.

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