Rethinking osteoporosis

Rethinking “primary” osteoporosis: Isn’t all osteoporosis really just “secondary” osteoporosis?

Dr. Susan E. Brown, PhDby Dr. Susan E. Brown, PhD

In the medical literature, osteoporosis historically has been classified as either “primary” or “secondary.” Primary osteoporosis is held to be a bone disorder of relatively unknown origin that occurs with aging and accelerates at menopause. Authorities state that there is no direct or singular cause for primary osteoporosis. Secondary osteoporosis, on the other hand, is the type of osteoporosis that has a direct cause. This type of osteoporosis is “secondary to,” or caused by, something else. For example, osteoporosis caused by the use of prednisone is a very common form of secondary osteoporosis.

Is there really such a thing as “primary osteoporosis”?

In many years of researching bone health, however, we at the Center for Better Bones have come to challenge this distinction between primary and secondary osteoporosis. Our work leads us to suggest that all osteoporosis is indeed caused by something, and in this sense, all osteoporosis is secondary osteoporosis. For example, the American College of Rheumatology has estimated that 20% of all osteoporosis in the US is due to use of steroid medications. Other researchers have suggested that 20% of all hip fractures are related to smoking. The use of acid-blocking drugs has been shown to double fracture rates. Some studies suggest that almost 20% of those with osteoporosis have the disorder caused or worsened by an excessive loss of calcium in the urine. Vitamin D inadequacy could be causing half or more of all osteoporosis, and so forth.

In other words, the more we scratch the surface, the more we see that many of our current dietary and lifestyle behaviors directly limit bone health and encourage osteoporosis. Even the classic primary osteoporosis that is vaguely attributed to “aging” is now known to be caused by many concrete factors that affect older people, such as reduced kidney function, vitamin D deficiency, chronic low-grade metabolic acidosis, increased use of mood-altering drugs and other pharmacological agents, reduced nutrient intake, loss of muscle mass, and a reduction in physical activity.

It is also interesting to note that when osteoporosis is discovered in men, a great effort is generally made to uncover the causes of this osteoporosis. In fact, most male osteoporosis is considered to have a secondary cause. When women are found to have osteoporosis, however, there are fewer attempts to discover the causes of this bone weakening and more a tendency to explain that this is just “primary osteoporosis,” something that happens to women as they go through menopause into their senior years — as if it were normal to the female gender. But in other cultures, women don’t develop osteoporosis as a matter of course — and that says it’s not normal.

We at the Center for Better Bones, however, suggest that if you look carefully enough you will find secondary causes for almost all the osteoporosis among women just as in men. If we can’t find the cause, it is because our tools are not yet precise enough to catch the problem, not because there is no cause.

Below I list the disorders and conditions associated with the development of osteoporosis. These are recognized causes of “secondary osteoporosis.” Over time, I suspect you will see this list grow as we come to understand that all osteoporosis has a cause and is indeed secondary to something else.

Known secondary causes of osteoporosis

Table 1. Nutritional Factors

Nutrition Anti-nutrients Modern eating patterns
Chronic low-grade metabolic acidosis High caffeine intake High fat intake
Imbalance among the 20 key bone nutrients High salt intake High sugar intake
Inadequate intake of 20 key bone nutrients Excess alcohol consumption Processed and synthetic foods
Undereating or food restriction Colas and other sugar-sweetened drinks Eating on the run
Excessive protein intake Skipping and incomplete meals
Excess vitamin A
Parenteral nutrition

Table 2. Lifestyle Factors

Physical Activity/Exercise Other
Inadequate physical activity Smoking
Poor muscle development Significant weight loss
Sub-optimal strength Use of recreational drugs
Immobilization (prolonged bedrest) Use of medications (see Table 3 below)
Weightlessness (as occurs in space flight) Birth control methods such as tubal ligation
Other surgeries such as hysterectomy, bariatric, gastrointestinal, etc.
Emotions such as worry, unhappiness, fear
Response to stress (increased levels of cortisol, epinephrine norepinephrine)

Table 3. Medical Conditions

Endocrine or Metabolic Causes Connective Tissue/Genetic Disorders Digestive Disorders / Dysfunction Rheumatological & Autoimmune Diseases Neurological Diseases
Acromegaly Cystic fibrosis Celiac disease Ankylosing spondylitis Epilepsy
Adrenal disorders,
including:
Adrenal insufficiency
Cushing’s syndrome
Hyperadrenocorticism 		Ehlers-Danlos syndrome Chronic hepatic disease Lupus Parkinson’s disease
Diabetes mellitus
(Types I and II) 		Glycogen storage diseases Gastrectomy Multiple sclerosis Polio, history of
Gaucher’s disease Hemophilia Gastric bypass (Bariatric surgery) or other GI surgery Rheumatoid arthritis Spinal cord injury
Hemochromatosis Homocystinuria Inflammatory bowel disease Bone, Bone Marrow, and Blood Diseases Psychiatric Disorders
Hyperparathyroidism Hypophosphatasia Malabsorption syndrome (celiac disease and IBD, such as Crohn’s disease or ulcerative colitis) Leukemia and lymphomas Depression
Hyperthyroidism (Graves Disease) Idiopathic hypercalciuria Malnutrition Mastocytosis Anorexia nervosa and bulimia
Hypogonadism
(sex hormone deficiency), including:
Androgen insensitivity Athletic amenorrhea Estrogen deficiency Hyperprolactinemia Klinefelter’s syndrome Premature menopause Turner’s syndrome 		Marfan syndrome Pancreatic disease Multiple myeloma Other health factors
Hypopituitarism Menkes steely hair syndrome Primary biliary cirrhosis Plasma cell dyscrasias Alcoholism
Hyperpituitarism Muscular dystrophy Renal Diseases Post-transplant bone disease Amyloidosis
Thyrotoxicosis Osteogenesis imperfecta Chronic kidney disease Sickle cell disease Congestive heart failure
Pulmonary Diseases Panhypopituitarism End stage renal disease Idiopathic scoliosis
Chronic obstructive pulmonary disease (COPD) Pseudoglioma Renal tubular acidosis Parental history of hip fracture
Emphysema Porphyria Premature ovarian failure
Riley-Day syndrome Prior fracture as an adult
Thalassemia Sarcoidosis

Medications*

*(Not all drugs in each category affect bone health, so be sure to ask your physician to consider one that is less harmful to bone.)

Aluminum-containing antacids: interfere with the intestinal absorption of calcium.
Anticoagulants (heparin): used to prevent blood clotting. Vitamin K is one of several vitamins that play a role in bone metabolism. Since some oral anticoagulants interfere with vitamin K, their long-term use may increase the risk of osteoporosis, particularly of the spine and ribs.
Anticonvulsants: interfere with vitamin D metabolism, thereby lowering the availability of calcium for bone mineralization. The two widely used anti-epileptic drugs phenytoin (Dilantin®) and carbamazepine (Tegretol®) are recognized to have direct effects on bone cells.
Anti-depressants: daily use of SSRIs (selective serotonin reuptake inhibitors), a popular anti-depressant, may lead to increased risk for fragility fracture in older adults. Daily use of SSRIs is associated with a reduction in bone density in the hip and spine and with an increased risk of falling. Examples of drugs in this class include Prozac®, Paxil® and Zoloft®.
Anti-neoplastics (cancer treatments): used to treat a variety of cancers, immune disorders and resistant arthritic conditions. Cancer treatment-induced bone loss (CTIBL) is most common in breast (including aromatase inhibitors) or prostate cancer patients undergoing therapies resulting in low levels of sex hormones.
Antipsychotic drugs
Antiretroviral drugs
Aromatase inhibitors
Barbiturates
Cimetidine
Corticosteroids
Conception control agents: reports suggest that women who use Depo-Provera® (Depo-medroxyprogesterone) may lose significant bone mineral density, possibly because of the low estrogen that it induces.
Cyclosporine A and tacrolimus
Cytotoxic drugs
Furosemide
Glucocorticoids (≥ 5 mg/d of prednisone or equivalent for ≥ 3 mo)
Gonadotropin-releasing hormone (GnRH) analogues: used in the long-term treatment of endometriosis and uterine fibroids. GnRH therapy decreases production of the hormone estrogen to the levels women have after menopause. GnRH analogues are used in the treatment of breast cancer in women to suppress estrogen levels, and in prostate cancer in men to suppress testosterone levels.
Heartburn and ulcer medication: proton pump inhibitors that reduce stomach acid production have been associated with an increased fracture risk, perhaps because calcium absorption from food is less efficient in the absence of stomach acid.
Immunosuppressives: used in organ transplants and for the treatment of some diseases of the immune system.
Lithium
Loop diuretics
Methotrexate (Rheumatrex)
Phenolbarbitol
Phenothiazines
Thiazolidinediones (diabetes medication): a study found a higher risk of fractures among women who take the drug rosiglitazone (Avandia®), possibly because the drug increases the activity of the cells that absorb bone in the bone remodeling process. Also, clinical trials have shown that female patients treated with pioglitazone (ACTOS®) for type 2 diabetes mellitus were at an increased risk of fracture, particularly of the forearm, hand and wrist, and foot, ankle, fibula and tibia. No increased risk of fracture was identified in men.
Thyroid hormone therapy: sufficient levels of thyroid hormones are necessary for normal bone development; excessive amounts, however, can cause bone loss over time.

Our Personal Program is a great place to start

At the Center for Better Bones we promote an all-natural approach to bone regeneration and repair that includes nutrition, diet, exercise, and lifestyle guidance. Our Personal Program is a convenient, at-home version of this approach.

Questions about the Personal Program for Better Bones? Call toll-free at 1-877-200-1269.

 

Original Publication Date: 01/20/2010
Last Modified: 04/07/2010
Principal Author: Dr. Susan E. Brown, PhD