BONE HEALTH AND OSTEOPOROSIS


                                     THE SCOPE OF THE PROBLEM

           Over 50% of adult males and females over 50 years old have bone loss. Osteoporosis (OP) is responsible for millions of fractures annually, mostly involving the lumbar vertebrae, hips, and wrists. Fragility fractures of the ribs are also common in men.  Although more women than men (80% vs. 20%) suffer with osteoporosis, men are more likely to die from OP related fractures. OP related fractures can result in painful loss of mobility and can be life threatening: if people are bedridden as a result of their injuries, there is increased risks of pneumonia and thrombophlebitis (blood clots) and associated pulmonary embolisms. Hip fractures are responsible for the most serious consequences of OP. Hip fractures usually require surgery. The six-month mortality rate for people age 50 and above following a hip fracture is about 14%. The incidence of hip fractures increases each decade from the sixth through the ninth for both women and men for all populations. Vertebral fractures, while having a smaller impact on mortality, can lead to severe, chronic neuropathic pain as well as kyphosis (hunchback) deformities which can impair ventilation. OP is also associated with atherosclerosis, dementias, depression and cancers. OP fractures are associated with a  reduced quality of life.

                                               THE CAUSES OF OP

Bones are living tissue and not solid and static structures. Bones constantly change in response to environmental stresses.  Bones grow stronger or weaker as a function of movement, exercise and body weight changes. {For example, Astronauts in low gravity have to vigorously exercise in order to limit serious bone loss.} Bones perform four vital roles: 1) structural support, 2) organ protection, 3) production of blood cells, and 4) storage of minerals for on-demand use by other parts of the body. Blood levels of calcium are tightly regulated, perhaps one of the most strictly controlled processes in the body. The two processes of absorption (depositing calcium) and resorption (withdrawing calcium) are constantly changing the structure of the bone in a cycle called bone remodeling.

The underlying mechanism in all cases of OP is an imbalance between bone resorption and bone formation. Like a bank account, bones have counter-balancing cells that make deposits (osteoblasts) or withdrawals (osteoclasts). Osteoblasts produce an organic matrix which contains Type 1 collagen. Bone matrix is the mortar that captures and incorporates calcium and multiple other minerals into the network of interconnected collagen fibers to make the final product of hard bone tissue. In health, the process is kept in balance. With aging, especially because of a lack of supportive sex hormones, withdrawals exceed deposits resulting in reduced bone-mineral density, which results in osteoporosis and increased risks for fractures. The sex hormones estrogen and testosterone are critical for maintaining a healthy balance: they inhibit osteoclast activity (bone breakdown) and promote osteoblast activity (new bone formation).  {Demontiero, et. al., “Aging and Bone Loss: new insights for the clinician”, The Adv Musculoskeletal Dis., 2012; 4(2):61-76.}

Another major cause of osteoporosis is focal scurvy of the bones. Quite simply, scurvy (severe vitamin C deficiency), whether general or localized can be prevented, cured and reversed with appropriate dosing of vitamin C and other important nutrients. Vitamin C maintains a healthy osteoblast—osteoclast balance. In the absence of vitamin C, bone-making osteoblasts fail to form. At the same time, there is an unchecked increase in bone-dissolving osteoclasts, resulting in focal scurvy inside the bones, thus initiating the imbalance that results in a detrimental breakdown of the bone integrity, along with calcium loss. Also, a deficiency of vitamin C directly increases oxidative stress in the bones which attacks cellular structure causing damage and even death of the cells. And, vitamin C is essential for the synthesis of collagen and for creating the fibrous interconnecting collagen cross-linking strands required to optimize the physical strength and resilience of the cones. A vitamin C deficiency results in weaker bones.

Bone remodeling is constant: up to 10% of all bone mass may be undergoing remodeling at any point in time. Cortical bone is the hard outer shell of bones and the middle of long bones. Trabecular bone is the sponge-like bone in the ends of long bones and vertebrae where the marrow is located. Trabecular bone is more active with osteoblasts and osteoclasts, and more subject to remodeling. In OP, not only is bone density decreased, but the naturally weaker spicules of trabecular bone may break with stress and are replaced with an even weaker, disrupted bone micro-architecture. The most common areas of OP fractures have a relatively high trabecular to cortical bone ratio. With aging, women may lose as much as 50% of trabecular bone because of a reduction in their alpha-estrogen receptor activity, while men lose about 30%.

                                               RISK FACTORS

1)  ***The PRIMARY RISK FACTOR for OP is age related SEX HORMONE DEFICIENCY.***  Consequently, the PRIMARYTREATMENT for osteoporosis is Bio-identical Hormone Replacement Therapy (BHRT). For men, Testosterone therapy is needed. For women, both Estrogen and Testosterone are the KEYS to optimizing therapy.  Estrogen and testosterone treatments also help to prevent periodontitis and tooth loss. If there are no contraindications, If there are no contraindications, it is never too late to start Estrogen and Testosterone therapy. However, it is important to consider the appropriate type of Estrogen to use and the route of administration.  {REMEMBER: always think of using Estrogen and Progesterone together as a single entity; for, Progesterone (but not a progestin like “Provera”) is always required to modulate the adverse effects of unopposed Estrogen stimulation and to enhance receptor functions. However, Progesterone therapy by itself doesn’t help OP.}

2)  Vitamin C Deficiency (Because It Prevents Bone Loss and Fractures):  Vitamin C creates bone-building osteoblasts; suppresses bone-dissolving osteoclasts; prevents bone-destroying oxidative stress; helps to synthesize collagen; and, helps in the formation of bone-strengthening collagen cross-links. {Also, supplemental vitamin C protects against dangerous calcifications, protects against calcium-laden kidney stones, and lowers all-cause mortality.} In the Framingham Osteoporosis study, the subjects with the highest intake of vitamin C had significantly fewer hip and non-vertebral fractures compared to those with the lowest intake. Intake of vitamin C limited to dietary sources alone had no statistically significant reduction of fractures; vitamin C supplementation was required to realize a decrease in risk. Supplementation with vitamin C is non-toxic and safe. Take at least 6 gm daily.

3)  An independent risk factor for both osteoporosis and vascular disease is elevated homocysteine levels. Women with a homocysteine level over 15 compared to women with a level less than 9 had 2.42 increased risk of hip fractures. Effective treatments for elevated homocysteine include:  vitamin B12 (1000 IU injections of methylcobalamin or sublingual therapy), vitamin B6 (50 mg daily), folic acid (800 mcg daily), and methylsulfonylmethane (MSM—1 gm twice daily). Even more effective are BETAINE AND CHOLINE– RECOMMENDED DOSES: Betaine: 500 mg/d up to 2,000 mg tid; and, Choline: 500-1,000 mg/d.

4)  Latitude: Areas of higher latitude, such as Northern Europe, receive less Vitamin D through sunlight compared to regions closer to the equator, and, consequently, have higher fracture rates.

5)  Genetics:  :  White European and Asian ancestry predisposes to OP. Those with a family history of fractures or OP have an increased risk of OP ranging between 25% to 80% increased risk, depending upon the study. At least 30 genes are associated with the development of OP. A small stature is another non-modifiable risk factor for OP.

6)  Modifiable risk factors include: excessive intake of alcohol; Vitamin D deficiency; tobacco smoking; malnutrition; physical inactivity; heavy metal toxicity, especially to cadmium and lead; medications, especially proton pump inhibitors; and, carbonated beverages.

7)  MEDICAL DISORDERS: Our bodies regulate calcium balance with two pathways: one is signaled to turn on when blood calcium levels drop below normal, pulling calcium from bone reservoirs, and one is the pathway that is signaled when blood calcium levels are elevated. Many diseases and disorders influence one or both pathways, disturbing the calcium balance. THUS, it is imperative to have an accurate diagnosis for appropriate interventions. 1)  Immobilization: there is truth to the dictum– “use it or lose it.” Athletes with a high bone turn-over may experience localized osteoporosis after prolonged immobilization of a casted fractured limb. Also, people who are bedridden or who use wheelchairs may suffer similarly. 2)  Hypogonadal states:  such as various genetic disorders including Turner syndrome, Klinefelter syndrome, and Kallman syndrome. Other conditions such as anorexia nervosa, hyperprolactinemia, and hypothalamic amenorrhea affect the endocrine system and can also cause OP. Surgical bilateral oophorectomy and spontaneous premature ovarian failure cause deficient estrogen production. Surgical removal of the testes and andropause cause testosterone deficiency. 3)  Endocrine disorders:  Adrenal diseases such as Cushing’s syndrome (too much cortisol) and Addison’s disease (too little cortisol); thyroid diseases such as hyperthyroidism (too much thyroid hormone) and hypothyroidism (too little thyroid hormone); both Type 1 and Type 2 Diabetes; Pituitary gland diseases such as acromegaly; and, hyperparathyroidism. 4) Hematologic and Renal diseases can result in OP.: for example, renal insufficiency, sickle cell disease, hemophilia, thalassemia, multiple myeloma, lymphomas and leukemias. 5)  Malabsorption and malnutrition: inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis; surgeries including gastrectomy, intestinal bypass surgery, and, bowel resection; and, gluten enteropathy, lactose intolerance and milk allergy, bulimia, and cystic fibrosis. 6)  Rheumatological disorders:  (either as a part of the disease or frequent use of corticosteroids) include rheumatoid arthritis, systemic lupus, ankylosing spondylitis. 7)  Systemic disorders: such as sarcoidosis, amyloidosis, vitamin D, vitamin K and vitamin B12 deficiencies. Chronic Obstructive Pulmonary Disease (COPD) can also cause OP.  8)  Neurological conditions such as Parkinson’s disease and complex regional pain syndrome.

                                     PRESCRIPTION TREATMENTS

1)  FOR WOMEN:  Both oral and topical Estradiol improve OP. While Estriol can be especially helpful with vaginal dryness and hot flashes, it has no significant usefulness for OP nor Coronary Artery Disease (CAD). If a woman has been menopausal for >10 years and is not on BHRT, it is wise to only consider using a topical Estradiol, particularly if she has any CAD risk factors, in order to avoid vascular plaque rupture and blood clot formation. I will typically a use a compounded Estrogen cream: 2 mg to 3 mg of estrogen daily, {often as “Biest” with a mixture of 80% Estradiol and 20% Estriol}, or an Estrogen patch (such as Climara patches 0.0375 mg up to 0.1 mg once per week or Vivelle dots twice per week), or an Estrogen gel (such as Elestrin 0.06% –1 pump daily). NOTE: Estradiol needs to be used along with oral Progesterone: 100 mg to 600 mg daily.

          Testosterone cream also benefits OP. The standard dose is 20 mg/gm (2%) of a compounded cream: applying ¼ gm daily to the skin or to the vulvar mucous membranes. Women over 60 years old typically require a higher dose: a 40 mg/gm (4%) cream: applying ¼ gm daily to the skin or vulvar mucous membranes. The total and free Testosterone levels  are monitored. A vanishing cream will be used if the cream is to be applied to the vulva, and a lipoderm cream is used if it is to be applied to the thighs and buttocks skin.

2)  FOR MEN:  I use of a topical Testosterone cream or gel, or intramuscular injections of Testosterone is the treatment of choice.

3)  In addition to Estrogen/Progesterone and Testosterone helping to prevent and treat OP, BHRT has a direct effect upon the brain.  Particularly for elders, who have an increased OP risk for death and disability from falls with consequent hip and spinal fractures, BHRT helps to improve their stability and coordination, as well as helping with their memory and with their cognitive impairment.

4)  Be aware that treatment with Human Growth Hormone (HGH) can also be very beneficial. However, it is very expensive, requires nightly injections, and it is typically restricted in its use by State Medical Boards. Thus, I don’t use recombinant HGH. However, I may prescribe an amino acid non-peptide secretagogue, called “Secretropin”, which is used as a sub-lingual spray, if indicated, to help release one’s own HGH.

5)  Don’t be concerned about using Thyroid Hormones when they are monitored and used in balance with Estrogen, Progesterone and Testosterone. Inappropriate use of Thyroid Hormones, eg. for weight loss, may cause OP because it accelerates bone turnover. In both hyperthyroidism and hypothyroidism the risk of fractures is significantly increased. Treatment with thyroid hormone is best when thyroid stimulating hormone (TSH) is not overly suppressed because TSH has a direct bone-protecting effect, and, very low levels of TSH are associated with increased cardiovascular risk.

6)  BISPHOSPHONATES:  ***I generally choose NOT to prescribe Bisphosphonates because they poison osteoclasts (that remodel old, brittle bone) so that they can’t function.  Bisphosphonates are the most popular treatment for OP. They can be useful in decreasing the risk of fractures in people who have already sustained a fracture from OP. Fracture risk reduction is between 25 and 70%, depending on the bone involved.  HOWEVER, be very cautious if you are considering using them. Using them may make you think that you have stronger bones. Simply by preventing the necessary removal of the old brittle bone matrix, your DXA scan will look better. Although these medications will delay or stop bone loss, they don’t facilitate bone growth! The bone appears denser, but the “life has been snuffed out”. Consequently, Bisphosphonates are associated with osteonecrosis of the mandible (bone death of the jaw), spontaneous mid-shaft femur fractures, and an increased risk of esophageal inflammation and cancers. Also, there is often poor patient compliance because of the painful side-effects of esophagitis and stomach upset. Similar medications such as Raloxifene (Evista), and Calcitonin are also available, however, each have a very high side-effect profile and also a high cost. {I find it no surprise that in 2017 the American College of Physicians, endorsed by the AAFP, recommended that adults with OP and no known fragility fracture, limit treatment with bisphosphonates to 5 years. Women who used bisphosphonates for 10 to 13 years had a higher risk of clinical fractures than women who used them for 2 years.} For people with OP but who have not had a fracture, evidence does not support a fracture risk reduction by using bisphosphonates.

7)  I am intrigued by the medication Terparatide (Forteo), because it stimulates osteoblasts, thus, increasing the bone matrix along with producing a heterogeneous mineral content consistent with a younger bone age. However, it can stimulate a rare bone cancer called osteosarcoma. In addition to its expensive cost,  it has risks for lightheadedness—dizziness and hypotension, nausea, leg cramps, arthralgias and pains. It is administered as a 20 mcg subcutaneously injected dose once daily, with a 2 year maximum total lifetime treatment.

                                            MONITORING THERAPY

I monitor effective therapy by measuring serum Estrogen, Progesterone, and Testosterone levels, and by measuring a urine N-telopeptide/creatinine ratio (NTX), which helps to evaluates bone mineral metabolism. An NTX evaluates present bone metabolism.  NTX measures cross linked N-telopeptides of Type 1 collagen and is an indicator of bone resporption by osteoclasts. I prefer to measure the 2nd or later morning urine sample, to avoid over-night concentration. The LOWER the level, the better. The goal is to effect a change in the NTX so that it is less than or equal to 35. The urine can be monitored every 3 to 6 months until stable, and then yearly.  Levels higher than 35 indicate ongoing bone loss.

The U.S. Preventive Services Task Force recommend that all women 65 years of age or older be screened by bone mineral densitometry. They recommend screening younger women with risk factors. The International Society for Clinical Densitometry suggest bone mineral densitometry for men 70 years old. While bone mineral density X-ray scans (“DXA”, formerly called a “DEXA” scan) evaluate the results of past bone metabolism, it takes 2 to 4 years to see a change on the scan. (That’s why Medicare will only pay for a DXA scan every 2 years.) A DXA scan may look good, however, if the NTX is elevated, then bone loss is certain, and future DXA scans will become abnormal. Bone loss accelerates after menopause with the drop of Estrogen and Testosterone.

A DXA scan is reported as a T-score. 85% of young women have a normal T-score expressed as greater than or equal to -1.0. Osteopenia, or bone thinning, is defined as a T-score between -1.0 and -2.5, and affects about 14% of young women. Osteoporosis is defined by a T-score less than -2.5. Severe OP is defined by a T-score <-2.5 plus a fragility fracture.

***I STRONGLY ADVISE YOU TO AVOID USING CALCIUM SUPPLEMENTS!!  {From the introduction to “Death By Calcium” by Thomas E. Levy, 2013}***

At the time of Columbus, it was self-evident that the world was flat. Modern Medicine isn’t immune to a similar simplistic and wrong thinking. Regarding OP, since bones are brittle and largely made up of calcium, it is self-evident that calcium should be supplemented. However, this idea is very wrong!  “Osteoporosis involves a lack of calcium in the bones. It does not mean that there is a lack of calcium in the body or in the diet. Osteoporotic individuals have toxic excesses of calcium outside the bounds of bone tissue. The typical American menu is laden with calcium-saturated foods. A legitimate body-wide deficiency of calcium is virtually non-existent, but too much calcium is very common and highly toxic, and it reliably leads to great suffering and premature death. The real problem in osteoporosis is that the body is unable to synthesize a new structural bone matrix and to integrate calcium into it. Simply increasing the quantity of calcium in the body does not even begin to remedy this problem. The calcium simply deposits elsewhere in the body where there are no bone proteins. Excess calcium is a killer.

It is this excess of ingested calcium along with calcium chronically released from osteoporotic bone that poses the most dangerous threat to health and life as it moves in and around all of the cells of the body, promoting disease wherever it accumulates. This notably includes heart disease, hight blood pressure, strokes, and cancer. It fuels and accelerates all chronic degenerative diseases.

When a body-wide state of excess calcium already exists, any added calcium is too much as it promotes abnormal cellular, glandular, and bodily functions. That is why supplemental calcium needs to be stopped, excess dietary calcium needs to be curtailed, and all calcium-rich, vitamin D-fortified foods need to be avoided.

The excess calcium in non-bone tissues has been shown to increase mortality from all causes. You are 30% more likely to have a heart attack and 20% more likely to have a stroke if you take an extra 500 mg of calcium per day. Over one-third of Americans over the age of 45 have evidence of arterial calcification. This percentage rises drastically with greater age, literally skyrocketing in postmenopausal women as well as in testosterone-deficient men. The degree of calcium deficiency in osteoporotic bone is actually an indicator of the amount of excess calcium that has taken up residence in non-bone tissue. Not only does increasing calcium intake fail to improve bone strength, it fuels calcium excess everywhere in the body. Calcium supplementation does not prevent bone fractures. However, adequately dosed vitamin D supplementation does  decrease fracture risk.

Until you address your toxin exposures and your hormone deficiencies, you will not prevent or resolve osteoporosis regardless of whether you are ingesting appropriate or even elevated amounts of dietary  calcium. Calcium migration from the bone is not the cause of osteoporosis, but rather a symptom of it. Giving large amounts of calcium will eventually result in a small amount of it filling in pores in osteoporotic bones. However, it cannot be emphasized strongly enough that this approach is simply cosmetic. It will make the bones look somewhat better on a bone density test, but it does no more to improve bone strength than blowing finely ground chalk into the cracks of an earthquake-damaged building will to restore its structural integrity, or putting a fresh coat of paint on rotting wood.”


Note: much of the positive impact of these anti-osteoporosis agents results from the increased anti-oxidant impact they ultimately have in the bones and the rest of the body.

  1. a) ***Vitamin D3: 2,000 IU up to 10,000 IU daily. Monitor a 25-OH-Vitamin D level to keep the level 60- 100 ng/ml.
  2. b) ***Vitamin K (for those not on Coumadin)–{especially vitamin K2}– up to 1 mg daily. Vitamin K inhibits abnormal calcification outside of the bones; helps dissolve pre-existing abnormal calcifications; K2 lessens susceptibility to coronary artery disease; K1 may increase bone density and definitely decreases fracture risk; K2 as MK-4 prevents fractures, sustains bone density, and improves bone quality via increased collagen content and collagen cross-linking when administered in pharmacological doses; K2 as MK-4 can compensate for bone weakening induced by magnesium deficiency, can prevent and/or treat some forms of cancer, and,can augment positive bone effects of bisphosphonates; and, K2 decreases cardiac mortality as well as all-cause mortality.
  3. c) ***Boron: supplementation reduces urinary loss of calcium and magnesium and improves levels of Estradiol and Testosterone. Foods high in boron include (in descending order): raisins, almonds, hazel nuts, dried apricots, avocado, peanut butter, Brazil nuts, red kidney beans, cashews and dates. Or, supplement with 3 mg of boron daily.
  4. d) ***Magnesium is nature’s calcium channel blocker. Magnesium and calcium can largely be characterized as biological antagonists. Magnesium levels are strongly associated with the anabolic hormones testosterone and human growth hormone. Magnesium dissolves calcium deposits and keeps them in solution; decreases intracellular oxidative stress by decreasing elevated intracellular calcium levels; regulates active calcium transport; and, increases bone density and decreases fracture incidence. Magnesium is at the center of every chlorophyll molecule, thus, eating green leafy vegetables is a good dietary source for magnesium. Magnesium is also found in nuts, legumes, whole grains, fruits and fish. However, you cannot reliably expect to obtain consistent and sufficient amounts of magnesium by ingesting these foods. Magnesium content is vegetables has seen a huge decline since pre-1950 levels because of soil depletion. Additionally, many soils have too much potassium which competes for absorption of magnesium into the plant. Also, typical grain refining processes for bread and pasta removes 80%-95% of total magnesium. Start supplementing slowly and back off if diarrhea ensues. The mineral form, Magnesium Oxide 400 mg to 800 mg daily,  is the least expensive and works just fine if it is absorbed and if it doesn’t cause you diarrhea.  However, some people don’t absorb the mineral form of magnesium well.  A chelated form of magnesium is usually much better absorbed. The best gut tolerated form is magnesium glycinate 400 mg-500 mg or magnesium asporatate 400 mg to 500 mg daily. Magnesium L-Threonate 1,000 to 2,000 mg taken at bedtime can be very helpful with sleep management and for neurological conditions.  This form of magnesium most easily crosses the blood-brain barrier with comprehensive benefits for sleep, anxiety,  cognitive function, and migraines. {It can be obtained from}
  5. e) ***Lactoferrin 300 mg daily is a potent anabolic agent that stimulates bone growth and bone repair and can help to prevent osteoporosis. Additionally, it has well-documented anti-infective, immune strengthening, antioxidant, anti-inflammatory and anti-cancer effects. It can also benefit weight management.
  6. f) ***Vitamin C 6,000 mg daily can help to prevent bone loss and fractures.
  7. g) Strontium: 1 gm/day increased to 1 gm twice daily in 1 to 2 month: caution– it may cause diarrhea. Strontium accelerates the action of bone-building osteoblasts and slows the action of bone destroying osteoclasts, with a net positive result for bones.
  8. h) Ipriflavone: is a synthetic flavonoid derived from the soy isoflavone called daidzein. It promotes the incorporation of calcium into bone and inhibits bone breakdown, thus preventing and reversing osteoporosis. It works by slowing down the action of the osteoclasts, thus, allowing the osteoblasts to build up bone mass. A typical dose is 600 mg daily
  9. i) A proprietary product called “Ostinol” ( contains bone morphogenic proteins (BMPs) that stimulate osteoblasts to grow new bone and cartilage. There are no negative side effects. For people with normal bone density, it is recommended to use 150 mg daily. For osteopenia, the recommended dose is 350 mg once or twice daily. If there is associated arthritis, the dose recommendation is 2, 350 mg caps twice daily. For osteoporosis, the recommended dose is 450 mg daily. If the bone loss is rapid or if there is associated arthritis, the dose is 450 mg twice daily.
  10. j) Omega-3 Fatty Acids: help to combat calcium toxicity and to create stronger bones and decreased fracture risk. They increase osteoblast activity and reduce inflammation. Men with the top 20% of DHA concentrations have protection from loss of bone mineral density compared to all the other subject. Higher levels of DHA and EPA in the red blood cells was associated with less OP and greater bone mass. {Additionally, Omega-3 fatty acids help protect against the formation of kidney stones; prevent coronary events; decrease new breast cancers; and, lower all-cause mortality.} An upper dose is 0.3 g/kg body weight, meaning a 150-pound person can take 21 g daily (having a content of about 13 g EPA and DHA). Most people do well taking 1 to 3 gm daily.

                                 ADDITIONAL CONSIDERATIONS

1)  FALL PREVENTION:  The increased risk of falling associated with aging leads to fractures. The risk of falling is increased by impaired eyesight (eg. Glaucoma, macular degeneration), balance disorders (eg. Vertigo), movement disorders (eg. Parkinson’s Disease), sarcopenia (muscle weakness),  dementias (eg. Alzheimer’s Disease), cardiac dysrrhythmias, vasovagal syncope, postural (orthostatic) hypotension, and seizures. People with gait or balance disorders and who have had previous falls are most at risk. It is important to remove obstacles and loose carpets in the living areas. Using a cane or walker may also help.

2)  Regular weight bearing ENDURANCE EXERCISING is strongly encouragedAlso, aerobics and muscle resistance exercises help to maintain cognition and increase bone mineral density.

3)  AVOID SOFT DRINKS!!!  The high phosphorus level, required for dissolving the sugar and for contributing to the taste, causes calcium to be pulled from bone storage in order to for the phosphorus level to be biologically balanced.

4)  Consider ALKALINIZING your dietary intake by eating a predominantly vegan vegetarian diet. BE AWARE: Meat, fish, dairy products, refined sugars and alcohol, coffee, tea and sodas all produce acidity in the body.  I encourage quitting smoking cigarettes, eliminating or minimizing alcohol and coffee intake, limiting a diet high in animal protein and milk products, reducing salt intake, and increasing the eating of fresh fruits, vegetables and whole grains. Calcium rich foods are necessary on a daily basis. Good sources of calcium include: green leafy vegetables (such as collards and spinach), Soy products such as Tofu, almonds, sesame seeds, poppy seeds, black-eyed peas, blackstrap molasses, figs, bok choy, broccoli and sardines.

5)  ***Olive oil increases serum concentrations of osteocalcin (for bone building) and procollagen type 1 N-terminal propeptide (P1NP) which has protective effects against osteoporosis by increasing bone collagen synthesis and bone formation rates. {J Clin Endocrinol Metab. 2012 Oct;97(10):3792-8.} Black Olives, especially a variety called Lucques olives, have a high quantity of “oleuropein”, which nudges mesenchymal stem cells (MSCs) to turn into bone cells instead of fat cells. It also increases osteoblast formation. A proprietary product called “Osteokol Plus” from combines oleuropein along with vitamin K2, magnesium, manganese and zinc. The recommended dose is 2 tabs twice per day with food.   


  1. a) Regular weight-bearing exercise helps to strengthen bones.
  2. b) Avoid smoking cigarettes.
  3. c) Limit drinking alcohol.
  4. d) Avoid drinking sodas in order to limit phosphorus intake.
  5. e) Eat a balanced diet with fresh fruits and vegetables, and calcium rich foods such as dark leafy vegetables, legumes, and whole grains. Use milk products (if at all) in moderation.
  6. f) Strongly consider BHRT from mid-life onward under medical supervision.
  7. g) Avoid Calcium Supplementation. But, be sure to have an optimal vitamin D3 level.
  8. h) TESTING: Get a DXA scan to evaluate your bone-mineral density. {Be aware that it can pick up blood vessel calcifications and arthritic changes and report them as bone density that doesn’t exist.} A quantitative computerized tomogram or QCT scan is  a better study, however, it is not widely available.  Since it takes about 2 years to notice any changes on these studies,  following a urine N-telopeptide/creatinine ratio: NTX Is the best way to evaluate potential bone loss.

                  COMMON MEDICATIONS can lead to OP

  1. a) Chemotherapeutics for fighting cancers can suppress the sex hormones. Anti-androgens, which suppress testosterone levels, and aromatase inhibitors which reduce estrogen activity contribute to bone loss and fractures.
  2. b) Corticosteroids (such as hydrocortisone, prednisone and dexamethasone) are associated with bone loss and increased risk of fractures.
  3. c) Anti-coagulants eg. Warfarin (coumadin) inhibits calcium incorporation into bone and increases calcium deposition in arterial walls.
  4. d) Proton Pump Inhibitors (PPIs) such as Nexium, Prilosec and Prevacid) suppress stomach acid and slow calcium absorption from the stomach. (Also, aluminum antacids can bind phosphate and interfere with calcium metabolism.)
  5. e) Anti-epileptics such as barbiturates and phenytoin (Dilantin) accelerate the metabolism of vitamin D.
  6. f) Anti-Depressants, especially Selective Serotonin Re-uptake Inhibitors (SSRIs) decrease bone mineral density and increase fracture risk.


The more advanced the OP, the more calcium has been released from the bones over time. Calcium goes from the bone to be deposited in the arterial walls. Calcium can also occur in cardiac heart valves leading to a decreased blood flow, cardiomegaly and CHF, and angina pectoris. There is a 5x increased risk of CAD in people who have OP. Also, women with CAD have a 73% increased risk of OP.  Vitamin K2 helps to facilitate eliminating calcium from the arteries and depositing it appropriately in the bones. {Kiel, et. al. “Bone loss and the progression of abdominal aortic calcification over a 25 year period: the Framingham Heart Study”, Calcifi. Tissue Int. 2001;68(5):271-6.}

Arterial stiffening creates a vicious cycle of degeneration and decline. Consequences include: hypertension, myocardial infarctions, strokes, cognitive decline, Alzheimer’s dementia, Parkinson’s disease, kidney failure, non-alcoholic fatty liver disease (NAFLD), and type 2 diabetes. A main contributor of arterial stiffness is calcification. Increased arterial stiffness is a death risk predictor.

          Vitamin K2 activates matrix Gla-protein, which inhibits calcium from depositing in arteries. Vitamin K1 (phylloquinone) is found in plants. Some is converted to K2. Vitamin K2 (MK-4) is found in meat, eggs and dairy and is rapidly absorbed and metabolized. It helps to preserve bone health. Vitamin K2 (MK-7) is found in fermented soy beans and fermented cheeses. It remains active for >24 hours. This is significant, because in the absence of vitamin K2, matrix Gla-proteins are quickly inactivated. Processed foods are nearly devoid of vitamin K. Supplementing with vitamin K helps to prevent and reduce arterial stiffness. Arterial elasticity dampens pulse pressure waves, thus, allowing blood to flow smoothly through capillaries without big pressure fluctuations. Arterial stiffening creates pressure induced capillary damage. Thus, hypertension becomes a vicious cycle resulting in end-organ damage.


          Sarcopenia is a decline in muscle mass that begins in the 4th decade of life. Age related sarcopenia increases the risk for falls, fractures, loss of independence, and, consequently, loss of life. As muscle mass falls, the risk of disability, hospitalization rates and nursing home placements greatly increases. There is an estimated 8% loss of muscle mass per decade after age 40, which increases to 15% per decade after age 70. A vicious cycle is triggered: decreased muscle mass and strength leads to decreased physical activity which leads to further muscle loss.

1)  Resistance training EXERCISE is an important component to help maintain adequate muscle strength.

2)  Another useful component is Beta-hydroxy beta-methylbutyrate or HMB which is a metabolic product of the amino acid leucine. As with bone health, there is a balance between muscle breakdown (catabolism) and muscle build-up or restoration (anabolism). HMB helps to maintain this balance. With aging, HMB declines with a consequent drop in lean muscle mass. Supplementation with HMB helps to preserve and to enhance lean body mass, and promotes improved muscle function. HMB helps to build up muscle and also to prevent its breakdown. HMB also promotes the growth of new nerve branches, and helps to maintain functional connections between nerves and muscles.  A typical dose is 1.5 gm twice per day. {Vukovich MD, et. al., 2001, J Nutr; 131(7):2049-52, and Sanz-Paris, A, et. al. , 2018, J Nutr Health Aging; 22(6):664-75.}   A proprietary product called “Muscle Strength & Restore Formula” is available from containing HMG and Vitamin D3.

3)  VITAMIN D3 can complement this by enhancing muscle contractile strength and performance, and one’s balance and coordination. Vitamin D3 also improves mitochondrial dysfunction, and has potent immunomodulatory properties linked to improvement in inflammatory markers. Dosage is guided by serum 25-hydroxy Vitamin D3 levels to achieve an optimal serum level 60 to 100 ng/ml.  {Beaudart C, et. al., 2014, J Clin Endocrinol Metab; 99(11):4336-45; Cangussu LM, et. al., 2015, Osteoporos Int; 26(10):2413-21; Gama ZA, et. al., 2008, Rev Saude Publica; 42(5):946-56; and, Girgis Cm, et. al., 2013, Endocr Rev; 34(1):33-83.}

4)  OMEGA-3 FATTY ACIDS contribute to brain health and neuromuscular function. Higher levels are associated with improved muscle size and strength. A typical dose is 6 to 8 gm daily. {Rodacki CL, et. al., 2012, Am J Clin Nutr; 95(2):428-36; Smith GI, et. al., 2015, Am J Clin Nutr; 102(1):115-22.}

5)  The amino acid derivative CREATINE helps with mitochondrial cellular energy by recycling ATP, and benefits both the nervous system and the muscles. Supplementation with creatine helps to prevent muscle loss and to improve strength and endurance. A typical dose is 5 gm daily. {Kougias DG, et. al., 2018, Nutr Res; 53:1-14.}




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