1. ANTI-RESORPTIVE DRUGS
Antiresorptive therapies are used to increase bone strength by slowing or stopping osteoclast in individuals with osteoporosis and include five principal classes of agents: bisphosphonates, estrogens, selective estrogen receptor modulators (SERMs), calcitonin and monoclonal antibodies such as denosumab.
Bisphosphonates are the most commonly prescribed antiresorptive medications and remain first-line treatment for osteoporosis. Bisphosphonates are adsorbed into the mineralized surface of bone and are internalized by osteoclasts, interfering with biochemical processes involved in bone resorption; they also induce apoptosis of osteoclasts.
Denosumab, the first biologic introduced for osteoporosis treatment, is a fully human monoclonal RANKL antibody, and by binding to RANKL, it prevents the binding of RANKL to RANK; this leads to inhibition of osteoclast activation and function.
Artificially stopping osteoclast which is a natural process our body uses to provide needed calcium for our body’s essential functions, becomes a precursor to manifold health problems. Inhibiting osteoclast to maintain the bone density may cause bigger problems than preventing fractures. SAC utilizes both osteoblast and osteoclast to build healthy bones and naturally prevents fractures.
2. ANABOLIC DRUGS
Trailing the development of antiresorptives for osteoporosis is the development of anabolic agents designed to increase bone mineral density (BMD) by stimulating bone formation, osteoblast. Sodium fluoride was a promising anabolic agent for the treatment of postmenopausal osteoporosis, but it was found to increase the risk of nonvertebral fractures despite dramatic increases in BMD and is not approved by FDA in the USA. GH (growth hormone) has also been the object of interest as an anabolic agent for the skeleton. PTH (parathyroid hormone), long known to have anabolic potential was “rediscovered” about 15 yr ago, but the bone building effect was not very impressive (only 6% increase) and also came with many side effects. The statins, cornerstones of lipid-lowering therapy, have also recently been revisited as potentially important skeletal anabolic agents, but we are too familiar with the side effects of statins.
Parathyroid hormone (PTH) and its analogue, teriparatide (Forteo) may cause unwanted side effects that require medical attention. Also, because of the way these medicines act on the body, there is a chance that they might cause other unwanted effects that may not occur until months or years after the medicine is used. These delayed effects may include certain types of cancer, such as bone cancer. More common effects include abdominal pain, confusion, constipation, depression, headache, incoherent speech, vomiting, etc.
Calcilytics increases the secretion of parathyroid hormone (PTH), which has a temporary anabolic effect on bone tissue, producing an increase in both bone volume and bone density due to increased bone deposition and resorption. However, long-term use of these causes resorption, degrading the bone to raise blood calcium. Consequently, these drugs have been researched for the treatment of osteoporosis, though with only limited success.
SAC therapy triggers TH (Thyroid Hormone), not PTH (Parathyroid Hormone), in building bones, the way our body does it naturally! Nothing works more naturally without side effects than SAC therapy.
Above indicates real bone mineral density (BMD) increase of 49 year-old male since taking SAC calcium. Measurement shows a significant increase of BMD (T-score of 1.5) over a period of 6 months. BMD is measured by FDA approved ultrasound bone densitometer by BeamMed.
Effects of SAC Calcium on bone turnover and calcium balance in ovariectomized rats.
Results reveal that the BMD of rats with induced osteoporosis has returned to normal with SAC intake. Please click the link below for the full research paper.