As a former anesthesiologist whose practiced for close to 3 decades I am well aware of patients requiring surgical procedures following a fall. Many of such patients are over 65 years old and have co – morbid issues in their medical history making it challenging for the anesthesiologist to provide proper care for such patients. I myself have taken care of thousand of patients over the years some of which required hip surgery. My oldest was a woman that was 101 years old. Though she was a healthy woman it was challenging anesthetic to perform.
The American Academy of Orthopedic Surgeons and the Physicians weekly news letter site that the average cost to the patent is $26,912.00 for hip surgery. Forty percent of these patients re-quire post surgical nursing care costing roughly $200.00 per day. The statistics show that over 300,000 patients over the age of 65 sustain hip fractures and it is estimated by 2040 it will rise by 500,000 patients.
Many patients are not so lucky though. Some patients require and ICU stay after developing pneumonia or other complications. Sadly some never survive in their post-operative stay. Others require extensive painful rehabilitation in an in-patient rehabilitation hospital.
I decided to look at the causes of hip fractures and found that some of the leading causes were from pathologic fractures from cancer and from osteoporosis.
This article is a review of osteoporosis.
involves the porosity of bones and a decreased bone mass leading to increased risk of fractures.
Osteopenia : is the bone loss not severe enough to become osteoporosis
1/3 of woman will develop fractures
At menopause there is a loss of bone.
Risk Factors include :
Sedentary life styles
Excessive Consumption of Alcohol
Cushings Syndrome ( Excessive Cortisol )
Bisphosphonates : are the most class of drugs used to treat osteoporosis. These drugs have mul-tiple side effects including : esophageal ulcerations, atrial fibrillation, Femoral fractures, osteone-crosis of the jaw.
Other treatments include : Estrogens, Selective Estrogen Receptor Modulators and Calcitonin
Dietary Factors :
Refined sugars lead to low bone mineral density in men and women. There are various beliefs that sugar effects bone loss. These include :
Sugar lacks micronutrients i.e. : minerals and vitamins that are essential for bone health.
Large quantities of sugar ingestion leads to a transient increase of urinary calcium due to the mobilization of calcium from bone to urine
Sugars lead to an increase level of cortisol which leads to bone resorption
Carbonated Beverages :
Both young and older woman that consume large amounts of cola have a lower bone mineral density and suffer from an increased risk of fractures. It is believed that phosphoric acid in the soda cause calcium release from bone making it more porous and fragile. Remember how pour-ing soda on the car paint eats it away, think of what it does to bone.
A large consumption of caffeine resulted in a lower bone mineral density and more rapid bone loss and an increased risk of hip fractures.
Tea seems to have a beneficial effect in increasing bone mass density. Though tea does contain caffeine. It is believed that the Flavanoids has a beneficial effect at maintaining or increasing bone density.
There seems to be a conflict of milks benefit in relationship to calcium. However a large popula-tion of people have unrecognized allergies to cow milk proteins. This leads to Gastrointestinal inflammation, malabsorption and nutritional deficiencies.
Patients that consume large quantities of sodium “salt” have large increases of the excretion of calcium due to the loss of hydroxyproline in urine. This is correlative to bone resorption.
Celiac Disease :
is a malabsorption disorder without symptoms. Osteoporosis is a known part of the sequelae
of celiac disease. Loss of nutrients, micronutrients from malabsorption leads to bone loss. Pa-tients whom avoid gluten have an increase in bone mass density. Patients with unexplained os-teoporosis should be evaluated for celiac disease. Studies have shown that patients that have osteoporosis and celiac disease DONOT benefit from supplementation from exogenous calcium and Vitamin D. However patients whom supplement with magnesium in a dosage of 550 mg for 2 years had a higher bone mass density.
Food Allergy :
Chronic inflammatory intestinal diseases from food allergies may leas to lower bone mass densi-ty. The inflammation causes a loss of micronutrients and nutrients from absorption. Additionally due to the release of steroids from food allergenic food may lead to bone resorption.
Protein is necessary for the synthesis and maintenance of bone structure and formation. It ap-pears that excessive protein intake could be deleterious to bone density maintenance. This could be do to :
Amino acids that have sulfur in their composition that are metabolized to sulfate which creates an acid load.
Elevated levels of phosphorus impacts bone negatively by increasing parathyroid hormone.
Methionine increases homocysteine which also impacts bone.
The takeaway is that high protein intake is really beneficial to bone due to the intake of Vitamin D, Calcium and Potassium.
Vegetarian Diet :
There is conflicting studies related to bone health. However the most is the nutrients are building blocks for bone. Diets that are low in : zinc, vitamin B12, calcium and Vitamin D and high quality protein impact bone formation and health.
Dried Plums or Prunes :
Studies show that woman that are post-menopausal whom ingest 5-12 prunes daily have de-creased total bone loss. Plums or prunes are rich in Vitamin K, Boron, and Magnesium. These micronutrients are involved in promoting bone health.
Potassium Citrate :
30 meq/day increased bone mass in post menopausal women with osteopenia.
Nutritional Supplements :
Our traditional medical colleagues beat on two supplements : Vitamin D and Calcium. Unfortu-nately bone is a living tissue that requires its own nutritional requirements. In fact maintenance of soft tissue, repair of micro fractures and maintenance of bone requires hormonal balance along with the proper balance of nutrients and micronutrients.
The standard western diet is high in white flour, fat, refined sugar, processed food and canned foods. Along with environmental impacts, genetic factors, and other outside influences upon our own physiology during menopause leads to depletions in : calcium, magnesium, phosphorus, sili-ca, zinc and manganese.
Calcium supplementation ranging from 800 – 1500 mg has been shown to have beneficial ef-fects by slowing the age-related bone loss, and reduced the incidence of fractures. However studies seem to implicate that patients whom supplemented with calcium prior to the onset of menopause for long periods of time and were conscious of their diet had a better result. Addi-tionally as stated calcium should be taken with other minerals ( silicon, magnesium, zinc, phos-phorus, and manganese) as calcium depletes these in bone.
There are many formulations of calcium beneficial for osteoporosis. These include: calcium car-bonate, calcium citrate, calcium citrate malate and tricalcium phosphate. However in some stud-ies calcium citrate malate had a better performance ratio.
Vitamin D promotes the absorption and use of calcium. Vitamin D deficiency as you would ex-pect is common in patients with osteoporosis. Studies show that patents that supplement with 700-800 IU/ day reduced their incidence of fractures by 30%. One study showed that doses in the range of 100,000 IU of Vitamin D3 in a single dose every 4 months for 5 years has substan-tial beneficial effects.
Vitamin D has a protective effect against bone loss thus reducing fractures. Vitamin D also has influential properties in enhancing the muscle strength and balance in patients thus reducing the change of a fall and fracture. 800 IU unites daily seems to be the magic number by its effects in slowing bone loss along with preventing the fracture rate.
An additional interesting fact is that different racial and ethnic groups. Thus it should be tailored to the individual.
Calcium and Vitamin D:
Some studies show that the combination of calcium and Vitamin D worked synergistically in re-ducing the incidence of fractures. Therefore the literature shows that the use of both for prevent-ing and treating osteoporosis is evident.
Magnesium is a cofactor for enzymes to work in our body. Magnesium is necessary for bone mineralization. Women whom are depleted in magnesium showed decreased bone formation and a loss of bone mass and bone volume. Loss of magnesium absorption may be due to the western diet which has an abundance of refined and processed foods.
A dose ranging from 250-750 mg/day for 1-2 years increased bone density in post- menopausal women. Additionally woman with celiac disease benefited from Magnesium supplementation.
Vitamin K1 and Vitamin K2 are the naturally occurring forms of Vitamin K. Vitamin K1 is found in leafy vegetables while K2 is found in milk, meat, cheeses, eggs, and soybeans.
Although Vitamin K is mainly involved in the clotting of blood. It is essential for the formation of osteocalcin which is a large protein in bones and involved in the formation of the bone minerali-zation. Thus Vitamin K is essential in bone formation and remodeling.
Several clinical trials in Japan showed that 45 mg/day of Vitamin K preserved or enhanced bone mass density and reduced the incidence of fractures in woman both post menopausal or elderly woman. This dose however far exceeds what is traditional in the U.S. Dosages of 180 ug/day were effective in preventing bone loss and fracture. Thus Vitamin K is needed in maintaining bone structure.
Vitamins B6,B12,Folic Acid and homocysteine :
Osteoporosis is found early in patients with genetic abnormalities of homocysteinuria. Homocys-teine interferes with collagen cross linking of connective tissue. Thus the strength and stability of bone could be interfered with. Therefore elevated homocysteine can cause a decrease in bone matrix density and bone quality. Folic acid, Vitamin B6 and Vitamin B12 are known to lower ho-mocysteine. Vitamin B12 has osteoblastic activity and Vitamin B6 is involved in bone formation and cartilage growth.
Copper is needed for cross-linking and stabilizes collagen in bone tissue along with osteoblastic activity. Children with deficiencies in Copper had developed spontaneous fractures.
The western diets and the grains that are consumed are depleted in copper and are substand-ard in our diet. A double blind study of woman taking 3mg/day of copper for 2 years provided a beneficial effect of bone formation.
Manganese is necessary for bone mineralization and the synthesis of connective tissue in bone and cartilage. A famous basketball player suffered multiple fractures do to osteoporosis. When a deep dive was performed on his mineral composition. Manganese was increased in his diet to a normal range. He was then able to return to playing sports.
Zinc is a co-factor for an enzyme “ alkaline phosphatase “ necessary for bone mineralization. A low zinc level was seen in men ranging from ages 46-68. It again appears that refined and pro-cessed foods maybe causative in low zinc
Boron is a trace mineral essential for plant life. Though apparently not essential for humans bo-ron is found in nuts fruits and vegetables. Boron has been associated with a decrease in prostate cancer.
Strontium is found in the human body in the amount of 320 mg. Strontium has 2 effects on bone and connective tissue. Firstly it is present in the crystal lattice of the bone and it stimulates bone formation, inhibits bone resorption and increases bone mass density. Dosages of 170-680mg/day for 2-5 years showed an increase in bone mass density of spine and hip reducing the fracture by 16-49% in post-menopausal women. This was apparently similar to men. However strontium is contraindicated in patents with cardiovascular diseases : which include is-chemic heart disease, peripheral vascular disease and cerebral vascular disease.
Strontium has some other deleterious effects in the formulation of ranelate. This is not available in the U.S. The citrate form of strontium is present in the US and has been to show no systemic effects or toxicity.
Silica or Silicon:
Silica in high concentrations are found in calcifications sites of growing bones. A higher dietary intake of silicon has shown to increase bone mass density. Foods that are processed lead to a decreased amount of silica. Bananas are high in silica or silicon. However the optimal dose is not known.
Phosphorous is essential for bone mineralization and hydroxyapatite formation of bone. Adding phosphorous accelerated the healing of fractures. The standard american diet is rich in foods containing phosphorous including ; meats, grains, dairy products, and additives in processed foods.
Vitamins C and A :
Vitamin C deficient patients may develop scurvy. It has been shown that providing additional Vit-amin C had a positive beneficial effect in osteoporosis patient.
Traditional Medicine advocates the use of Prolia.
I searched the internet for the official site for Prolia. Below are the contraindications of Prolia along with the side effects. You as the patient can choose which pathway to take as far as treatment modalities offered.
Prolia® is contraindicated in patients with hypocalcemia. Pre‐existing hypocalcemia must be corrected prior to initiating Prolia®. Prolia® is contraindicated in women who are pregnant and may cause fetal harm. In women of reproductive potential, pregnancy testing should be per-formed prior to initiating treatment with Prolia®. Prolia® is contraindicated in patients with a histo-ry of systemic hypersensitivity to any component of the product. Reactions have included ana-phylaxis, facial swelling and urticaria.
Same Active Ingredient
Prolia® contains the same active ingredient (denosumab) found in XGEVA®. Patients receiving Prolia® should not receive XGEVA®.
Clinically significant hypersensitivity including anaphylaxis has been reported with Prolia®. Symptoms have included hypotension, dyspnea, throat tightness, facial and upper airway ede-ma, pruritus, and urticaria. If an anaphylactic or other clinically significant allergic reaction oc-curs, initiate appropriate therapy and discontinue further use of Prolia®.
Hypocalcemia may worsen with the use of Prolia®, especially in patients with severe renal im-pairment. In patients predisposed to hypocalcemia and disturbances of mineral metabolism, in-cluding treatment with other calcium-lowering drugs, clinical monitoring of calcium and mineral levels is highly recommended within 14 days of Prolia® injection. Concomitant use of calcimi-metic drugs may worsen hypocalcemia risk and serum calcium should be closely monitored. Adequately supplement all patients with calcium and vitamin D.
Osteonecrosis of the Jaw (ONJ)
ONJ, which can occur spontaneously, is generally associated with tooth extraction and/or local infection with delayed healing, and has been reported in patients receiving Prolia®. An oral exam should be performed by the prescriber prior to initiation of Prolia®. A dental examination with ap-propriate preventive dentistry is recommended prior to treatment in patients with risk factors for ONJ such as invasive dental procedures, diagnosis of cancer, concomitant therapies (e.g., chemotherapy, corticosteroids, angiogenesis inhibitors), poor oral hygiene, and co-morbid disor-ders. Good oral hygiene practices should be maintained during treatment with Prolia®. The risk of ONJ may increase with duration of exposure to Prolia®.
For patients requiring invasive dental procedures, clinical judgment should guide the manage-ment plan of each patient. Patients who are suspected of having or who develop ONJ should receive care by a dentist or an oral surgeon. Extensive dental surgery to treat ONJ may exacer-bate the condition. Discontinuation of Prolia® should be considered based on individual benefit-risk assessment.
Atypical Femoral Fractures
Atypical low-energy, or low trauma fractures of the shaft have been reported in patients receiv-ing Prolia®. Causality has not been established as these fractures also occur in osteoporotic pa-tients who have not been treated with antiresorptive agents.
During Prolia® treatment, patients should be advised to report new or unusual thigh, hip, or groin pain. Any patient who presents with thigh or groin pain should be evaluated to rule out an incom-plete femur fracture. Interruption of Prolia® therapy should be considered, pending a risk/benefit assessment, on an individual basis.
Multiple Vertebral Fractures (MVF) Following Discontinuation of Prolia® Treatment
Following discontinuation of Prolia® treatment, fracture risk increases, including the risk of multi-ple vertebral fractures. New vertebral fractures occurred as early as 7 months (on average 19 months) after the last dose of Prolia®. Prior vertebral fracture was a predictor of multiple verte-bral fractures after Prolia® discontinuation. Evaluate an individual’s benefit/risk before initiating treatment with Prolia®. If Prolia® treatment is discontinued, consider transitioning to an alterna-tive antiresorptive therapy.
In a clinical trial (N=7808) in women with postmenopausal osteoporosis, serious infections lead-ing to hospitalization were reported more frequently in the Prolia® group than in the placebo group. Serious skin infections, as well as infections of the abdomen, urinary tract and ear were more frequent in patients treated with Prolia®.
Endocarditis was also reported more frequently in Prolia®-treated patients. The incidence of op-portunistic infections and the overall incidence of infections were similar between the treatment groups. Advise patients to seek prompt medical attention if they develop signs or symptoms of severe infection, including cellulitis.
Patients on concomitant immunosuppressant agents or with impaired immune systems may be at increased risk for serious infections. In patients who develop serious infections while on Pro-lia®, prescribers should assess the need for continued Prolia® therapy.
Dermatologic Adverse Reactions
In the same clinical trial in women with postmenopausal osteoporosis, epidermal and dermal ad-verse events such as dermatitis, eczema and rashes occurred at a significantly higher rate with Prolia® compared to placebo. Most of these events were not specific to the injection site. Con-sider discontinuing Prolia® if severe symptoms develop.
Severe and occasionally incapacitating bone, joint, and/or muscle pain has been reported in pa-tients taking Prolia®. Consider discontinuing use if severe symptoms develop.
Suppression of Bone Turnover
In clinical trials in women with postmenopausal osteoporosis, Prolia® resulted in significant sup-pression of bone remodeling as evidenced by markers of bone turnover and bone histomor-phometry. The significance of these findings and the effect of long-term treatment are unknown. Monitor patients for these consequences, including ONJ, atypical fractures, and delayed fracture healing.
The most common adverse reactions (>5% and more common than placebo) in women with postmenopausal osteoporosis are back pain, pain in extremity, musculoskeletal pain, hypercho-lesterolemia, and cystitis. The most common adverse reactions (>5% and more common than placebo) in men with osteoporosis are back pain, arthralgia, and nasopharyngitis. Pancreatitis has been reported with Prolia®.
In women with postmenopausal osteoporosis, the overall incidence of new malignancies was 4.3% in the placebo group and 4.8% in the Prolia® group. In men with osteoporosis, new malig-nancies were reported in no patients in the placebo group and 4 (3.3%) patients in the Prolia® group. A causal relationship to drug exposure has not been established.
The most common adverse reactions (>3% and more common than active-control group) in pa-tients with glucocorticoid-induced osteoporosis are back pain, hypertension, bronchitis, and headache.
The most common (per patient incidence ≥10%) adverse reactions reported with Prolia® in pa-tients with bone loss receiving ADT for prostate cancer or adjuvant AI therapy for breast cancer are arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials. Additionally, in Prolia®‐treated men with nonmetastatic prostate cancer receiv-ing ADT, a greater incidence of cataracts was observed.
Denosumab is a human monoclonal antibody. As with all therapeutic proteins, there is potential for immunogenicity.
In Functional and Integrative Medicine we look at finding the root cause of the disease process and attempting to prevent or reverse this process. Above in this article I sighted various causes that impact the development of osteoporosis.
Exercise is important to maintain bone health. Both aerobic and strength training should be per-formed on a daily basis. There should be an altering of this exercise routine. Studies have shown also that swimming on a dally basis has impacted patients with osteoporosis in a positive way gaining bone formation, health and strength.
Below are recommendations of nutraceuticals that have benefit in preventing and treating the osteoporosis. Remember supplements that are taking should be of the highest quality. Sadly these are not found in local supermarkets, drug stores, or stores that state they sell such items.
1. Avoid refined sugars, caffeine, cola and sodium chloride.
2. Patients that have unexplained osteoporosis should be tested for celiac disease.
3. Minimize exposes to : lead, aluminum, cadmium and tin.
4. Be checked for food allergies
5. Eat dried prunes!!!!
6. Ingest calcium ranging from 600-1200 mg daily
7. Take in magnesium : 300 -600 mg/day
8. Obtain Vitamin D and ingest 800-1200 IU/day
9. Get a mix of Vitamin K1 and Vitamin K2 ranging from 100- 1000 ug/day of K1 and 45mg/day of menaquinone-4
10. take folic acid 0.4-5.0 mg, stress B vitamins which include Vitamin B6 (10-25 mg), B12 ( 20-1000 ug), vitamin C 100-500 mg, strontium 2-6 mg, manganese 3-20 mg, silicon 1-5 mg, boron 1-3 mg, copper 1-3 mg
11. Hormone replacement therapy.
Your can find out more information by visiting our website; antiagingim.com or contacting our office in Melbourne FL at 321-421-7111 for a consultation.