“The Calcium Paradox” 2017-05-24T11:03:02+00:00

“The Calcium Paradox”

Both men and women are losing calcium when they become older. From the age of 35 we are losing bone mass and height as the illustrations shows below. Especially when women enter menopause, they simultaneously lose calcium from bone and increase its deposition in arteries – a negative “double whammy” called the “calcium paradox,” which greatly increases the risk of both osteoporosis and cardiovascular disease. The drop in oestrogen causes both problems, but vitamin K can help rectify them.

The Osteoporosis process

Among postmenopausal women not using oestrogen replacement, low levels of vitamin K or high levels of undercarboxylated (vitamin K-dependent) osteocalcin are associated with low spine BMD, but a 3-year study of 325 postmenopausal women, receiving either K2 or placebo, shows that supplementation with K2 can prevent bone loss associated with oestrogen decline. In the women given K2, bone mineral content increased, and hip and bone strength remained unchanged, whereas in the placebo group, bone mineral content and bone strength decreased significantly.

Vitamin K-dependent MGP that inhibits vascular calcification also helps maintain the elasticity of postmenopausal women’s blood vessels.

Peak bone mass

The “peak bone mass” is the amount of bone tissue present at the end of skeletal maturation¹. It is a major determinant of the risk of fracture due to osteoporosis since the mass of bone tissue at any time during adult life is the difference between the amount accumulated at maturity and that lost with ageing. There is, therefore, considerable interest in exploring ways to increase peak bone mass. Epidemiological studies indicate a 10% increase in peak bone mass in the Caucasian female population would decrease the risk of hip fracture by about 30%². Such an increase would roughly correspond to the difference between male and female peak bone mass as measured at the radial or femoral diaphyseal site

Osteoporosis after Organ Transplantation

Within the past 2 decades, organ transplantation has become established as effective therapy for end-stage renal, hepatic, cardiac, and pulmonary disease. Regimens to prevent rejection after transplantation commonly include high-dose glucocorticoids and calcineurin-calmodulin phosphatase inhibitors (the cyclosporines and tacrolimus), which are detrimental to bone and mineral homeostasis, and are associated with rapid bone loss that is often superimposed upon an already compromised skeleton. The incidence of fracture ranges from 8% to 65% during the first year after transplantation. In general, fracture rates are lowest in renal transplant recipients and highest in patients who receive a liver transplant for primary biliary cirrhosis.

Rates of bone loss and fracture are greatest during the first 6 to 12 months after transplantation. Postmenopausal women and hypogonadal men appear to be at increased risk. Although no pretransplant densitometric or biochemical parameter has yet been identified that adequately predicts fracture risk in the individual patient, low pretransplant bone mineral density does tend to increase the risk of fracture, particularly in women. However, patients may sustain fractures despite normal pretransplant bone mineral density. Although the pathogenesis of the rapid bone loss is multifactorial, prospective biochemical data suggest that uncoupling of bone formation from resorption may be in part responsible, at least during the first 3 to 6 months.

We believe that prevention of transplantation osteoporosis should begin well before transplantation. Patients awaiting transplantation should be evaluated with among other, Menacin™. (Rodino & Shane 2008, sugest that the platients also should be evaluated with spine radiographs, bone densitometry, thyroid function tests, serum calcium, vitamin D, parathyroid hormone, testosterone (in men))³. Therapy for osteoporosis, low bone mass, and potentially reversible biochemical causes of bone loss should be instituted during the waiting period before transplantation. In patients with normal pretransplant bone density, therapy to prevent early posttransplant bone loss should be instituted immediately following transplantation. Most pharmacologic agents available for therapy of osteoporosis have not been subject to prospective controlled studies in organ transplant recipients. However, antiresorptive drugs, such as biphosphonates, appear to hold therapeutic promise.

  • Bonjour JP et al. Peak bone mass. Osteoporosis International, 1994, 1:S7–S13.
  • Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Report of a WHO Study Group. Geneva, World Health Organization, 1994 (WHO Technical Report Series, No. 843).
  • Rodine, M, Shane, E, Excerpta Medica, 1998 (459-469)