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Natural bone loss after age 35! Three Steps to Prevent Osteoporosis with Calcium

By ＼Smile Pharmacist Pharmacy Liao Wei Ching, Pharmacist

It's common knowledge that people don't consume enough calcium and vitamin D, so they don't take advantage of their youth to save up their bone capital, and they often face the dilemma of osteoporosis after the age of 35, even increasing the risk of bone fracture. But do you know? The fact is that the medicines we take may also cause us to lose bone mass.

This week's excerpt looks at common osteoporosis-causing medications, and what details you must pay attention to when faced with a choice of calcium tablets.

First, the metabolism of bone

Bone this living tissue, rich in collagen and minerals, these substances will make the bones become elastic and have a strong supportive, the human body's bone from early childhood to puberty to pre-adulthood, these stages of bone storage is greater than the metabolism, to reach the peak is about 25 to 30 years.

But after the age of 40, both men and women, bone density will slowly go downhill, and the older you get, the more likely you are to have an imbalance in bone metabolism. After the loss of bone mass, it is easy for the bones to become fragile, have holes, and even progress into osteoporosis, which leads to fractures.

Bones are metabolized every day, and there are two main types of cells in the body's skeletal tissue: osteoclasts and osteoblasts. Osteoclasts are responsible for removing and resorbing old or injured bone; osteoblasts are responsible for making new bone.

Before the age of 35, osteoblasts operate more frequently than osteoclasts, so bones are healthy and strong with a lot of trabeculae and very few gaps. After 35, osteoclasts operate faster than osteoblasts to make bone, resulting in bone loss, fewer trabeculae, and more gaps. When combined with dietary habits, medications, and other factors, this can exacerbate the loss of bone mineral density and even lead to osteoporosis.

Osteoporosis can be categorized into primary and secondary

Primary osteoporosis can be divided into postmenopausal osteoporosis and senile osteoporosis, which is caused by an imbalance in the metabolism of bones.

Secondary osteoporosis is the result of many other conditions, such as hyperparathyroidism, liver disease, kidney disease, intestinal calcium malabsorption, and steroid use.

Currently, there are two common scoring systems for osteoporosis, the T-score and the Z-score. The DXA test is the most important predictor of an individual's future fracture risk. When the DXA results are compared to the optimal or peak bone density of a healthy 30-year-old adult, a comparative value is calculated, called the T score.

The WHO defines how osteoporosis is graded based on the T-score of bone mineral density (as shown in the table below), with a more negative T-score indicating lower bone mineral density, more severe osteoporosis, and a higher risk of future fractures.

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When an individual's measured bone density is compared to the average bone density of a person of the same age, rather than to a healthy 30-year-old adult, the result is a Z-score, which can help to detect bone loss due to an underlying disease.

Second, common osteoporosis-inducing medications

In addition to age, diet, and disease, osteoporosis can also be caused by medications. The following is a compilation of common osteoporosis-inducing drugs for your reference in the 2017 Journal of Pharmacy, Volume III, Issue 2:

1. Steroids

The most commonly associated drugs are steroids, and studies have shown that about 30?50% of patients who use steroids suffer fractures, and even with a low dosage (prednisone 3?10mg/day) there is still a tendency for them to break. Even at low doses (prednisone 3?10mg/day) there is still a risk of fracture.

Prednisolone at 7.5 mg/day was associated with a 5-fold higher risk of vertebral and hip fracture; at 10 mg/day for 90 days, the risk of fracture was even higher by a factor of 17, with a particularly large effect in women who had stopped menstruating and in the elderly. The risk of fracture returns to normal 1 or 2 years after stopping steroids.

Steroids have both direct and indirect effects on bone development. Their direct effects on osteoblast metabolism include prolonging osteoclast survival, over-activating bone resorption, prompting osteoblast apoptosis, decreasing the production of osteoclast precursors, and ultimately decreasing bone formation, and their indirect effects on bone turnover, decreasing calcium reabsorption, and suppressing growth hormones and sex hormones.

2. Proton pump inhibitors (PPIs)

Many large observational studies have suggested that PPIs may be associated with osteoporosis or fracture risk, and in 2010, the US FDA issued an alert suggesting that the generic version of PPIs should indicate that the use of PPIs may result in the loss of bone mass. In 2010, the FDA issued a warning that generic versions of PPIs should indicate that the use of PPIs may be associated with a risk of hip, spinal cord, or radial fractures.

The mechanism by which PPIs increase the risk of fracture is still unknown, and it is hypothesized that they may be related to the inhibition of gastric acid secretion, which reduces intestinal calcium absorption and leads to increased bone resorption. Interestingly, however, some studies have shown that PPI use increases fracture risk, but H2-blocker does not.

Many studies evaluating long-term use of PPIs for more than one year have confirmed an increased risk of hip fracture by 20?62% and vertebral fracture by 40?60%, whereas short-term use of PPIs was not associated with an increased risk of fracture, showing that the risk of fracture due to PPIs is related to the duration of the drug's use, but that the risk of fracture decreases when the drug is discontinued.

It is also worth mentioning that studies have shown that if a patient is already taking bisphosphonates (bisphosphonates, drugs for osteoporosis), then additional use of PPIs will increase the risk of osteoporosis, so it is recommended to try to shorten the duration of use or change to H2-blocker.

3. Antiepileptic drugs

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Antiepileptic drugs have a strong association with bone mineral density, especially in postmenopausal women and men over 65 years of age, whereas phenytoin has been seen in younger patients. Many antiepileptic drugs such as phenobarbital, phenytoin, and carbamazepine induce cytochrome P-450 (c-P450) enzyme activity, which breaks down vit D into inactive metabolites, thereby decreasing the absorption of calcium, resulting in an increase in blood PTH, and accelerating the loss of bone mass.

Valproic acids are non-c-P450 enzyme inducers, but they have been shown to accelerate bone loss and risk osteoporosis and fractures. Studies have shown that antiepileptic drugs increase the risk of fracture in relation to the cumulative dose of the drug and the duration of use. Among the antiepileptic drugs, Levetiracetam is less likely to cause bone loss.

Long-term use of antiepileptic drugs, in addition to adequate calcium supplementation, and attention to vitamin D intake, it is recommended that people taking non-enzyme-inducing antiepileptic drugs, supplementation of vitamin D 1000-1200 IU per day; if you take an enzyme-inducing antiepileptic drugs, it is recommended that vitamin D supplementation 2000-4000 IU per day.

4.Medroxyproline is the most effective antiepileptic drug. strong> 4. Medroxyprogesterone acetate (MPA)

Low-dose MPA (5?10mg/day) is often used in combination with estrogen as a postmenopausal hormone supplementation therapy, and estrogen has no effect on the prevention of bone loss; however, high-dose MPA is used in the treatment of gynecological diseases and contraception. However, high doses of MPA used to treat gynecologic conditions and for contraception may increase bone loss.

Dopt MPA (DMPA) is injected quarterly intramuscularly or subcutaneously to inhibit gonadotropin secretion and ovulation, resulting in a 2?8% drop in BMD due to decreased estrogen production. Bone loss occurs most rapidly in the first 2 years of drug use, and most studies have shown that osteoporosis caused by DMPA is reversible and can be recovered when the drug is discontinued.

5. Aromatase inhibitors (AIs)

AIs (e.g., exemestane, anastrozole, letrozole) may be useful in the treatment of postmenopausal breast cancer with estrogen receptor (+). AIs inhibit cytochromeP-450 (CYP-19) enzymes and block the conversion of peripheral androgens to estrogens, resulting in a decrease in estrogen concentration and bone loss.

6. Gonadotropin-releasing hormone agonists (GnRHs)

GnRHs are used in the treatment of polycystic ovary syndrome (PCOS), endometriosis, uterine fibroids, pre-menopausal breast cancer and prostate cancer. GnRHs inhibit gonadotropin (gonadotropin) and cause hypogonadism. GnRHs bind to GnRHs receptors in the pituitary gland and down-regulate the secretion of LH (luteinizing hormone) and FSH (folliclestimulating hormone), which leads to the inhibition of ovarian function and a decrease in estrogen production. The result is the suppression of ovarian function, the reduction of estrogen production, and finally the loss of bone mass.

Androgen-deprivation therapy (ADT) used to treat metastatic prostate cancer can be effective in increasing survival, but in the first year of ADT, the patient's BMD decreases by 2?5%; after five years of use, the risk of bone fracture increases by 20?50%.

7. Selective serotonin reuptake inhibitors (SSRIs) versus serotonin norepinephrine reuptake inhibitors (SNRIs)

SSRIs （Both SSRIs (e.g. fluroxetine, sertarline, paroxetine, fluvoxamine, citalopram) and SNRIs (e.g. duloxetine) have been studied for their potential to contribute to bone loss, and there are serotonin receptors on osteoblasts and osteoclasts that are mediated by endocrine, The SSRIs have serotonin receptors on osteoblasts and osteoclasts, which are regulated by endocrine, autocrine, paracrine, etc. However, since the BMD of patients with fractures caused by SSRIs did not decrease, the SSRIs may have other effects on the mechanism of bone loss that are still unclear, and the dosage and duration of the drug use is related to the risk of fracture.

8. Thiazolidinediones (TZDs)

TZDs are insulin sensitizers, and PPARγ (peroxisome proliferator-activated receptor γ) can be used as a sensitizer. PPARγ (peroxisome proliferator-activated receptor γ) controls energy metabolism in fat, liver, and muscle. These proteins also control metabolic transformation and cell differentiation in bone.

The effects of activated PPARγ on bone are currently considered to be: (i) decreased osteogenesis and increased bone resorption; (ii) decreased osteoblasts and increased adipocytes; and (iii) increased osteoclast neogenesis.

There is no proven strategy to reduce the risk of fracture caused by TZDs, and it is recommended that the risk of fracture should be assessed prior to the use of TZDs, and that they should be avoided in patients with pre-existing osteoporosis.

9. Calcineurin inhibitors

Calcineurin inhibitors, including cyclosporine, tacrolimus immunosuppressants, have been widely used in the prevention of transplant rejection and autoimmune diseases. This class of drugs can bone loss while increasing the risk of fracture, but although the exact mechanism is not known.

However, studies have shown that this class of drugs indirectly affects the metabolism of osteoprotegerin and vitamin D, which can lead to bone loss secondary to hyperparathyroidism. The increased risk of fracture is related to the dose of the drug and the duration of its use.

10. Anticoagulants

Needle anticoagulants - Heparin causes bone loss by decreasing bone formation and increasing bone resorption, and long-term use of heparin decreases BMD, low molecular weight heparin is less likely to affect BMD than conventional heparin (unfractionated heparin). Low molecular weight heparin is less likely to affect bone loss than traditional heparin (unfractionated heparin), but will inhibit osteoblast differentiation and its function, resulting in decreased bone formation.

Many studies have shown that heparin treatment in about 30% of pregnant women decreases BMD by 2.2?3.6%, and long-term use in non-pregnant women results in a 15% incidence of spinal fractures, which are common within 6 months of initiating treatment; Heparin-induced osteoporosis is dose-dependent, and is almost completely reversible after discontinuation of the drug.

The oral anticoagulant warfarin decreases BMD and increases fracture risk by decreasing gamma-carboxylation and osteocalcin. Since the primary population of long-term use of heparin is pregnant women, there are no studies or recommendations to guide the prevention or treatment of bone loss due to heparin or warfarin, as bisphosphonates may cause fetal bone growth defects. For patients at high risk of osteoporosis, only calcium and vitamin D supplementation are available, and heparin can be replaced with LMWH or fondaparinux.

How to buy calcium supplements

There are many types of calcium tablets on the market, including calcium carbonate, calcium citrate, calcium lactate, and calcium amino acid chelate, and we don't know how to choose them, but it's not that complicated.

Step 1: Look at the calcium content

The same 500mg calcium supplements are labeled as calcium ion content, many calcium supplements are labeled as "calcium compounds" rather than "calcium ions" dosage, and calcium compounds will contain different ratios of calcium ions along with molecular weight size.

For example, Calcium Carbonate contains 40% calcium ions, Calcium Citrate contains only 21%, Calcium Amino Acid Chelate contains about 15?18% calcium ions, Calcium Lactate contains 13% calcium ions, and Calcium Gluconate contains only 9% calcium. Only 9%.

For example, 500 mg of calcium citrate actually contains 105 mg of calcium ions, while 300 mg of calcium carbonate actually contains about 120 mg of calcium ions. So when you buy a calcium supplement, it's important to look at the amount of calcium ions in the supplement.

As for the previous issue of calcium absorption, except for calcium amino acid (80%) and calcium citrate (35%), the absorption rate of other calcium supplements falls between 25 and 29%.

Calcium Amino Acid Sting, which has a high absorption rate of 80%, contains only 15-18% of calcium ions in 100 molecules. If the same calcium carbonate and calcium amino acid sting are taken with 500mg of calcium carbonate, the actual calcium ions absorbed will be 54mg and 72mg respectively.

Considering the balance between the economic benefits and the health benefits, the need to spend a high amount of money on a product that only claims to have a high absorption rate is still an issue.

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Step 2. Avoid calcium carbonate for those who take stomach medication and are prone to flatulence

Calcium carbonate requires the action of stomach acid to break down the ionic calcium. So for those who don't have enough stomach acid to produce a good meal, or who use stomach acid inhibitors or stomach medication, it is recommended that you choose a calcium preparation that is not carbonated. Because of the carbonate, it is easy to produce precipitation with many ions, so it is easier to produce constipation.

On the other hand, calcium carbonate is prone to produce carbon dioxide in an acidic environment because of carbonic acid, so some people feel bloated, burping, or flatulence after taking calcium tablets, and these are all due to carbonic acid, so it is also recommended that you take it after a meal, or switch to non-carbonated calcium preparations.

Step 3: Don't take more than 500mg in a single dose

The human body's peak absorption of calcium is about 500mg, more than 500mg, the intestinal absorption of calcium will decline, so don't take more than 500mg in a single dose of calcium tablets (the main factor is that the intestinal tract is limited in area, and the small intestine has a certain degree of absorption of calcium). The main factor is the limited area of the intestine, the small intestine itself on the absorption of calcium has a certain degree of saturation, so more than 500 mg dose, absorption saturation, of course, the absorption will begin to decline, but does not mean that more than 500 mg dose will not be absorbed Oh).

The recommended daily intake of calcium for adults is about 1000mg per day, with an upper limit of 2500mg (dietary intake + supplement intake).

Consuming too much calcium will slow down bowel movements, and on the other hand, it will make the colon absorb more water, which can easily lead to constipation. So in addition to calcium carbonate, excessive intake of other calcium preparations will also have the risk of constipation!

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