Through many academic pieces of literature, books, and media, people are well-informed that calcium is an essential mineral to maintain our bone health. As there are many calcium supplements available in the market, calcium is aggressively advertised for its positive effects on our bodies. As many pieces of research have shown, calcium plays a critical role in treating osteoporosis, which is one of the most prevalent aging-related chronic degenerative diseases. Moreover, as the demand for calcium is increasing, many medical scientists are focusing on the effects of intracellular calcium ion on our health. While cell health translates to our overall health, calcium is closely related to the mitochondrial function, which is the key to treating aging-related chronic degenerative diseases as well as cancers. Nevertheless, even though we had already established that balancing intracellular calcium ion is crucial for cell health and offers immense potency to treat the diseases that we have not yet eradicated, there were no particular calcium treatments that could directly affect the cellular calcium homeostasis.
High-Dose Vitamin D and Calcium Attenuates Bone Loss with Antiretroviral Therapy Initiation: A Prospective, Randomized Placebo-Controlled Trial for Bone Health in HIV-Infected Individuals
Edgar Turner Overton, MD, Ellen S. Chan, MSc, Todd T. Brown, MD, PhD, Pablo Tebas, MD, Grace A. McComsey, MD, Kathleen M. Melbourne, PharmD, Andrew Napoli, PhD, William Royce Hardin, BS, Heather J. Ribaudo, PhD, and Michael T. Yin, MD MS
Antiretroviral therapy (ART) has transformed HIV infection from a terminal disease to a manageable chronic illness. While incidence of AIDS-defining conditions has declined, other comorbidities have increased (1), including osteoporosis and fragility fractures (2-7). Both viral and host factors likely contribute to bone loss and fracture risk: HIV infection mediated by certain viral proteins, HIV-associated inflammation, lifestyle and behavioral factors, underlying genetic predisposition, comorbidities, and ART (8-14).
Calcium Signalling and Calcium Transport in Bone Disease
H.C. Blair, P.H. Schlesinger, Christopher L.-H. Huang, and M. Zaidi
Calcium transport and calcium signalling mechanisms in bone cells have, in many cases, been discovered by study of diseases with disordered bone metabolism. Calcium matrix deposition is driven primarily by phosphate production, and disorders in bone deposition include abnormalities in membrane phosphate transport such as in chondrocalcinosis, and defects in phosphate-producing enzymes such as in hypophosphatasia. Matrix removal is driven by acidification, which dissolves the mineral. Disorders in calcium removal from bone matrix by osteoclasts cause osteopetrosis. On the other hand, although bone is central to management of extracellular calcium, bone is not a major calcium sensing organ, although calcium sensing proteins are expressed in both osteoblasts and osteoclasts. Intracellular calcium signals are involved in secondary control including cellular motility and survival, but the relationship of these findings to specific diseases is not clear. Intracellular calcium signals may regulate the balance of cell survival versus proliferation or anabolic functional response as part of signalling cascades that integrate the response to primary signals via cell stretch, estrogen, tyrosine kinase, and tumor necrosis factor receptors
SAC and Osteoporosis
Bone is living, growing tissue. Throughout life, our bodies are breaking down old bone cells and rebuilding new bones in a continuous cycle (bone remodeling). We gain bone by building more bone cells than we lose. After about age 40, however, this balance is typically reversed, with bone loss occurring at a much faster rate than is replaceable, leaving our bones brittle and leading to osteoporosis with increased risks of fracture, particularly of the hip, spine, wrist, and shoulder.
Osteoblasts and osteoclasts are types of cells the human body uses to repair broken bones. Osteoclasts break down old bone tissue allowing osteoblasts to replace it with new material. Together, these cells facilitate bone mending and bone growth. However, as we age osteoblast slows down and bone mineral density continues to decrease, making our bones more susceptible to fracture.
Osteoporosis weakens bones
Losing more than 25% of bone mass is considered osteoporosis. In the US, 1/3 of women and 1/4 of men have the disease, with the figure increasing each year. What may be the cause of all this?*
The 4 Functions of SAC Calcium
SAC as Hormone Regulator
Bone metabolism is controlled by the interaction of a number of hormones.
Hormonal imbalance can wreak havoc on bone metabolism. SAC assures that calcium will directly reach the bone and will not be deposited in the kidneys and blood vessels.*
SAC as Calcium Navigator
Inactive calcium molecules such as protein-bound calcium do not know where to go.
SAC navigates calcium to reach its ultimate destination – the bone. SAC calcium will not be deposited in the wrong places such as the kidneys or blood vessels.*
SAC as Calcium Activator
About 50% of the calcium in our blood is inactive.
SAC’s ionization process activates inactive calcium for use by the body.*
SAC as Bone Mineral Builder
Adequate SAC intake, as part of a healthful diet, along with physical activity, may reduce the risk of osteoporosis in life.
Serious Side Effects of Prescription Drugs
Physicians typically recommend prescription medications for the treatment of osteoporosis, but these drugs are notorious for their dangerous side effects. These drugs are designed to “increase” bone density by retaining dead bone mass through the inhibition of osteoclasts, the cells that are responsible for natural bone resorption, which provides calcium for our body’s needs. Our body takes calcium from bones – even at the risk of bone fractures, because of calcium’s urgent and crucial role in healthy cell replication, neurotransmission, heart functions, and endocrine functions.
Disrupting essential bone metabolism may lead to serious health hazards.
This is why there are so many reports that osteoporosis drugs actually make bones more brittle and that people who are treated with these drugs tend to suffer more bone fractures.*
Two Categories of Prescription Drugs
Drugs that slows bone loss
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.
Drugs that increase the rate of bone formation
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 yrs 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.
The Clinical Results of SAC
Human Trial Result
This 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.
Animal Trial Result
Lab Animal Test 2011: 27(4), 301-307
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.