Advice about diet is probably the most confusing.  Mainstream media seem to love telling us that whatever we thought we knew about eating is wrong.  The only thing they seem to like more is telling us that whatever they told us yesterday is wrong today.   The advice about osteoporosis is as confusing as anything else.  Is protein good for bones or bad?  Does taking calcium after menopause help or not?  What about red clover and soybeans?  Will soda leach calcium from my bones?  It is so easy to lose track of what is and what is not good for maintaining healthy, strong bones.

But what makes bones healthy?  You say, “calcium,” that is only part of the story.  Bones are living tissue.  Cells that maintain the bones are surrounded by non-living material.  The part outside the cells is called matrix and it is made of protein strengthened by calcium.  You can think of this matrix like reinforced concrete.  The minerals act like the concrete resisting compression and the protein strands act like rebar resisting bending and tension.

It surprises most people, but bones never stop growing, not completely.  They may stop getting longer and even shrink as we get older, but the body is constantly taking away old bone matrix and replacing it with new matrix.  This is called normal bone turnover.

Bones also heal after being broken or other damage.  The cells that take away old or damaged bone matrix are osteoclasts.  The cells that put down new matrix to replace or heal are osteoblasts.  When osteoblasts and osteoclasts are both working together, bone turnover is balanced and bones are healthy.  When one type of cell is either stimulated or suppressed, then bones will either grow too much or waste away.  The most common form of bone wasting is osteoporosis, which literally means “porous bones.”

Osteoporosis happens when the metabolism of bone turnover is disturbed.  The density of the bones is decreased and their structure deteriorates.  In both men and women, bones are strongest by the early 20’s and then are maintained at that level for approximately ten years.  After this, bone density declines by about 0.4% a year.  In men this decline is generally constant or slowly worsens.  Women experience a sharp decline after menopause, when bone loss increases to 3% to 5% a year.

Osteoporosis has a number of impacts on the skeleton.  Loss of bone strength at the neck of the femur makes a person vulnerable to hip fractures, which are very dangerous.  Other fractures also become more common, as does the risk of falling.  In addition to an increased fracture risk, loss of bone in the spine causes curvature and “dowager’s hump.”  In extreme cases, a person can lose so much height and strength that their lower ribs come to rest on their hip bones.

One consequence of osteoporosis is that people who have it often reduce their activity.  Whether from a fear of falling, pain from bone compression, or a general sense of fragility, osteoporosis makes people timid about movement.  The irony of this is that when the bones have to bear our weight, they generate a signal to increase the activity of the osteoblasts.  So if a person lets osteoporosis reduce their activity, they actually make the osteoporosis worse in a vicious spiral.

Instead of focusing on the negative things that can worsen osteoporosis, I want to focus on the positive things that can prevent or improve it.  Cutting through the confusion about diet is possible.  Adequate nutrient intake is, of course, important.  Not just calcium, but also other minerals such as phosphate, boron and magnesium.  Diet isn’t just a concern for women who have gone through menopause – it applies to men as well and throughout life.  One could even say it also applies even further back than each person’s life, back to the health of the mother.  Good maternal nutrition, not just in terms of vitamins and mineral but overall nutrition as well, increases bone growth in the child and lays a foundation that reduces fracture risk in later life[i].

Let’s look at the nutrients and foods that may help maintain bone health:

Calcium: You already know that calcium is vital for maintaining healthy bones, but you may not know the right amount or when it is most important.  Although the general recommended daily intake for men and women is 1,000mg[ii], an intake of 1,200mg is now considered “ideal” by many experts[iii].  Even more important is having a good base of calcium in early adulthood – in young women 1,300mg a day is not unreasonable.  Although supplements are one way of obtaining this level of calcium, calcium in food sources is more readily absorbed and used by the body, which means it is difficult to create a bone-healthy diet that does not include three servings of dairy a day[iv].  Obtaining dietary calcium from dairy products also means that you are also getting other important nutrients, like protein, potassium, and small amounts of vitamin D.

Vitamin D: While calcium is essential for building strong bones, vitamin D is vitally important for maintaining bone health.  For example, in women after menopause given calcium supplements there are minimal changes in osteoporosis, but vitamin D supplements have been shown to reduce fracture risk[v].  Vitamin D promotes absorption of calcium in food and also helps regulate metabolic use of calcium.   The recommended intake increases from 200IU (international units) between age 14 and 50 to 400IU for people 50 or older and 600IU over age 70[vi].  These recommendations were instituted to prevent rickets.  However, recent population studies have demonstrated the inadequacy of these recommendations, since nearly 85% of the US population is currently estimated to be vitamin D deficient.  Many experts now recommend 1000 to 2000IU daily and doses between 5000 and10,000IU have been used safely.

Other vitamins and minerals: Other vitamins that are necessary for healthy bones are vitamin K, vitamin C, and several B-vitamins[vii].  Vitamins K & C help cells make the protein that is part of the bone matrix.  B-complex vitamins are necessary for the health of connective tissue.  Minerals that are important include phosphate and magnesium.  Phosphate has long been known as part of the bone matrix with calcium.  Magnesium has recently been identified as increasing the number and activity of osteoblasts[viii].  A healthy, balanced diet should be able to provide all these nutrients in food, but most people can use the help of a multivitamin to ensure adequate levels.  Commercial farming technologies have stripped the soil of its natural minerals content resulting in a dramatic drop in the nutritional content of most fruits and vegetables.  According to USDA statistics, some vegetables have less than half the calcium and magnesium than they did in 1975[ix]

Alcohol: Long-term alcohol abuse has many negative effects, but in the last fifteen years we have been learning more about how it is a major risk factor for osteoporosis.  Heavy drinking, especially during late adolescence and early adulthood, significantly compromises bone quality.  As this is when we need to lay down as much bone strength as possible, this represents a loss of bone strength that can’t be made up for later[x].  Alcohol interferes with the metabolism of building bones and prevents proper formation of bone matrix, leading to higher fracture risk in later life[xi].  The body can compensate for moderate or occasional alcohol use, but chronic intake of large amounts of alcohol does not give the body the chance to repair the damage before more is done.

Soda: People that drink soda have a higher risk of osteoporosis, but the reason has been unclear.  This has not stopped some authorities from telling women especially to avoid soda.  On one hand, young women especially that displace dairy or other nutritious beverages with soda are laying down a smaller base level of bone strength, but most sodas are not by themselves damaging to bones.  Colas, though, are definitely problematic because they have phosphoric acid and caffeine, both of which damage the ability of the body to put enough minerals into bone matrix[xii].

Soy and phytoestrogens: Japanese women have lower rates of breast cancer than Americans of European descent.  When Japanese women come to the United States, however, and adopt an American diet, their cancer rates match the rest of the population.  In Japan, most protein in the diet comes from soy products such as tofu instead of meat.  Researchers suspected there were compounds in soy that were preventing cancer from growing as it otherwise would.  They found a group of chemicals they named phytoestrogens (which means “plant estrogen”)[xiii].  Because estrogen in women helps protect bone before menopause, these phytoestrogens have also been suggested as remedies for osteoporosis.  Similar phytoestrogens are also found in some other plants, notably red clover.  A large number of studies about the effect of phytoestrogen on bone have been reported[xiv].  Generally positive effects have been seen in many of these studies[xv] but others show the extent of the effect is limited[xvi].  Clearly these chemicals do reduce bone loss, but the question seems to be whether this affects the risk of fractures or other negative consequences of osteoporosis[xvii].  Like the natural hormones they mimic, however, phytoestrogens have effects in many different systems, and we are just beginning to understand all of their effects.

Protein: As I said, the matrix of bone is protein that has been reinforced with minerals.  It would be logical, then, to think that high protein in the diet would be good for bones.  This has been disputed by some nutrition authorities.  The fear was that a diet high in protein created an excess of “acidic ions” in the blood, which would leach minerals from the bones.  Fortunately, recent studies have contradicted this idea[xviii], and there is no link between higher protein consumption and hip fractures[xix].  Elderly people who have higher protein intake have lower risks of hip fractures[xx].  People that do have hip fractures have more growth stimulation, greater bone density, and shorter recovery times when they take protein supplements during their recovery[xxi].

Vegetarianism: If protein is a good thing for bones, we would naturally wonder if a vegetarian diet would increase risk of osteoporosis and bone fractures.  The answer depends on the exact type of vegetarian diet followed.  The good news is that it is possible to have a well-balanced vegetarian diet that does not contribute to osteoporosis.  As long as adequate protein and mineral content, whatever the source, is part of the diet, even strict vegetarians have no worse bone health than meat-eaters[xxii].  People on a balanced vegetarian diet have similar bone density to people of the same age on a non-vegetarian diet[xxiii].  A diet high in protein from vegetable sources compares well with meat diets in preventing fractures[xxiv].  Vegan diets, buy reducing the protein and calcium intake, apparently lower bone density, although without increasing fracture risk[xxv].  Vegetarianism on some extreme diets do show lower bone density, but they maintain healthy bone turnover[xxvi].

Once again we return to the basics of preventive wellness: eating a balanced healthy diet, adding high quality nutritional supplements, engaging in regular weight-bearing exercises and insuring proper hormone balance.  Because there may be no symptoms associated with osteoporosis, far too many find out they have it after experiencing a fracture.  Early screening for evidence of bone loss or an altered bone metabolism can reduce the chance that you will suffer the tragic consequences from this disease.   For osteoporosis, like all chronic diseases, prevention is preferable to treatment.

[i]Session 2: Other diseases: Dietary management of osteoporosis throughout the life course. Earl S, Cole ZA, Holroyd C, et al. Proc Nutr Soc. 2010 Feb;69(1):25-33.

[ii] Dietary Supplement Fact Sheet: Calcium. Office of Dietary Supplements, National Institutes of Health, 2007 Oct 7, web resource at http://dietary-supplements.info.nih.gov/factsheets/calcium.asp accessed March 5, 2010

[iii] Nutritional therapies (including fosteum).Nieves JW. Curr Osteoporos Rep. 2009 Mar;7(1):5-11

[iv] Dairy and bone health. Heaney RP. J Am Coll Nutr. 2009 Feb;28 Suppl 1:82S-90S.

[v] Importance of calcium, vitamin D and vitamin K for osteoporosis prevention and treatment. Lanham-New SA. Proc Nutr Soc. 2008 May;67(2):163-76.

[vi] Dietary Supplement Fact Sheet: Vitamin D. Office of Dietary Supplements, National Institutes of Health, 2007 Nov 13, web resource at http://dietary-supplements.info.nih.gov/factsheets/vitamind.asp accessed March 5, 2010

[vii] Nieves 2009

[viii] Skeletal and hormonal effects of magnesium deficiency. Rude RK, Singer FR, Gruber HE. J Am Coll Nutr. 2009 Apr;28(2):131-41.

[ix] Vegetables without Vitamins.  Life Extension Magazine.  March 2001

[x] Alcohol and other factors affecting osteoporosis risk in women. Sampson HW. National Institute on Alcohol Abuse and Alcoholism Publications. 2003 June, web resource at http://pubs.niaaa.nih.gov/publications/arh26-4/292-298.htm accessed March 3, 2010

[xi] Skeletal turnover, bone mineral density, and fractures in male chronic abusers of alcohol. Santori C, Ceccanti M, Diacinti D, et al. J Endocrinol Invest. 2008 Apr;31(4):321-6.

[xii] Colas, but not other carbonated beverages, are associated with low bone mineral density in older women: The Framingham Osteoporosis Study. Tucker KL, Morita K, Qiao N, et al. Am J Clin Nutr. 2006 Oct;84(4):936-42

[xiii] Isoflavones–safe food additives or dangerous drugs? Wuttke W, Jarry H, Seidlová-Wuttke D. Ageing Res Rev. 2007 Aug;6(2):150-88

[xiv] Wuttke et al, 2007

[xv] Soy isoflavones and their bone protective effects. Zhang Y, Chen WF, Lai WP, Wong MS. Inflammopharmacology. 2008 Oct;16(5):213-5.

[xvi] The soy isoflavones for reducing bone loss (SIRBL) study: a 3-y randomized controlled trial in postmenopausal women. Alekel DL, Van Loan MD, Koehler KJ, et al. Am J Clin Nutr. 2010 Jan;91(1):218-30.

[xvii] Soy isoflavone intake increases bone mineral density in the spine of menopausal women: meta-analysis of randomized controlled trials. Ma DF, Qin LQ, Wang PY, Katoh R. Clin Nutr. 2008 Feb;27(1):57-64

[xviii] Phosphate decreases urine calcium and increases calcium balance: a meta-analysis of the osteoporosis acid-ash diet hypothesis. Fenton TR, Lyon AW, Eliasziw M, et al. Nutr J. 2009 Sep 15;8:41

[xix] Protein consumption and bone fractures in women. Feskanich D, Willett WC, Stampfer MJ, Colditz GA. Am J Epidemiol. 1996 Mar 1;143(5):472-9.

[xx] Dietary protein intake and risk of osteoporotic hip fracture in elderly residents of Utah. Wengreen HJ, Munger RG, West NA,et al. J Bone Miner Res. 2004 Apr;19(4):537-45

[xxi] Protein supplements increase serum insulin-like growth factor-I levels and attenuate proximal femur bone loss in patients with recent hip fracture. A randomized, double-blind, placebo-controlled trial. Schürch MA, Rizzoli R, Slosman D, et al. Ann Intern Med. 1998 May 15;128(10):801-9.

[xxii] Veganism, bone mineral density, and body composition: a study in Buddhist nuns.Ho-Pham LT, Nguyen PL, Le TT, Doan TA, Tran NT, Le TA, Nguyen TV. Osteoporos Int. 2009 Apr 7. [Epub ahead of print]

[xxiii] Bone mineral density of vegetarian and non-vegetarian adults in Taiwan. Wang YF, Chiu JS, Chuang MH, et al. Asia Pac J Clin Nutr. 2008;17(1):101-6.

[xxiv] Effects of meat consumption and vegetarian diet on risk of wrist fracture over 25 years in a cohort of peri- and postmenopausal women. Thorpe DL, Knutsen SF, Beeson WL, et al. Public Health Nutr. 2008 Jun;11(6):564-72.

[xxv] Effect of vegetarian diets on bone mineral density: a Bayesian meta-analysis .Ho-Pham LT, Nguyen ND, Nguyen TV. Am J Clin Nutr. 2009 Oct;90(4):943-50.

[xxvi] Low bone mass in subjects on a long-term raw vegetarian diet. Fontana L, Shew JL, Holloszy JO, Villareal DT. Arch Intern Med. 2005 Mar 28;165(6):684-9

Osteoporosis is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased risk of fractures.  While there is a belief that osteoporosis is a “women’s disease,” more than two million American men have osteoporosis with 12 million more at risk.  Osteoporosis is significantly under diagnosed and undertreated in men.  Osteoporosis in men is expected to increase nearly 50 percent in the next 15 years.  One third of men over the age of 50 will experience a fracture due to osteoporosis, and men are twice as likely to die after a hip fracture than a woman.   The National Osteoporosis Foundation has not established a standard screening procedure for men before age 70. In 2008, the American College of Physicians issued new clinical guidelines that recommended performing individualized risk assessment to determine who should be screened.  Testing is critical. In my practice, 63 percent of men screened over the age of 45 had osteopenia, the early stage of bone loss, and 12 percent had osteoporosis.

 What can men do to offset their risk for osteoporosis?

1.   Get enough Vitamin D, vitamin K, vitamin C and Vitamin B
2.  Eat calcium-rich foods or take calcium pills
3.  Eat adequate protein
4.  Avoid excessive alcohol consumption
5. Don’t smoke
6. Regularly perform weight-bearing, resistance Exercise
7. Check your medications – some medications are hard on bone density
8. Get tested – Osteoporosis is a preventable disease, but there are no symptoms. Testing is critical.

Osteoporosis results from a disturbance in bone metabolism.  Throughout our lives, there is a continual dance between the cells that lay down new bone (osteoblasts) and the cells that take away old bone (osteoclasts).  During childhood, more bone is produced than removed, so the skeleton grows in both size and strength. For most people, bone mass peaks during the late teens or early twenties. By this age, men typically have accumulated more bone mass than women. After this point, the amount of bone in the skeleton typically begins to decline slowly as removal of old bone exceeds formation of new bone.  Osteoporosis develops when bone is no longer replaced as quickly as it is removed.

Adequate hormone balance is intricately involved in bone metabolism and bone health.  Androgens (testosterone, DHEA and growth hormone) are vital to new bone formation. Estrogen is necessary to maintain normal bone mass.  The lack of estrogen enhances the ability of osteoclasts to absorb bone.  In women, progesterone improves osteoblast mediated new bone formation.  In men, the lack of testosterone and estrogen increases the rate of osteoporosis.[i]  As men and women age, their hormones decline and the risk of developing osteoporosis climbs dramatically.

Osteoporosis is generally thought of as a woman’s disease, with more than half of all women over age 50 in the US suffering a fracture as a result of this condition.[ii]  What is not as well known is that nearly a third of all men over age 50 will also experience a fracture due to osteoporosis in their lifetime.  It is projected that number will increase by nearly 50% during the next 15 years, with rates of hip fracture in men expected to double by 2040.[iii]  In fact, men are more likely to die following hip fractures than women, in part related to the fact that men tend to get osteoporosis about 10 years later then women.  It is well established that older adults are five to eight times as likely to die for any reason in the first 3 months following hip fracture.  The one year mortality rate following hip fracture for men is double that of women, and that excess mortality persists for up to 10 years.[iv]

Today, 2 million American men have osteoporosis, and another 12 million are at risk for this disease. Yet, despite the large number of men affected, osteoporosis in men remains underdiagnosed and underreported.[v]   Men begin losing testosterone in their mid to late 30’s at a rate of 2-3% yearly.  Although not below the normal range, by age 50 most men are relatively deficient in testosterone.  In my practice, 63% of men screened over age 45 had osteopenia, the early stage of bone loss, and 12% had osteoporosis.  All of them were surprised that they were affected.

Unlike women, there has not traditionally been any standard screening procedure for men before age 70; the age that the National Osteoporosis Foundation recommends screening men.  In 2008, the American College of Physicians issued new clinical guidelines for screening men for osteoporosis.   It recommends performing individualized risk assessments to determine who should be screened.  Although better than not having any specific recommendation, this guideline falls far short of the ideal.   Osteoporosis is a potentially preventable disease.  This guideline, much like the screening recommendations for women, is primarily designed to detect the disease in individuals considered “good candidates for [pharmaceutical] drug therapy”.  And, that typically means bisphosphonate therapy.

Bisphosphonates, such as Actonel, Boniva, Fosamax and Reclast, have been the standard recommended therapy to treat osteoporosis.  They work by poisoning osteoclasts, thereby inhibiting bone resorption, but do nothing to enhance bone formation.  It has been suspected for some time that this unnatural process could result in formation of relatively brittle bone.  Two studies reported at the conference of the American Academy of Orthopedic Surgeons in March of this year showed that the bones of some postmenopausal women taking bisphosphonates for more than four years stopped rejuvenating and became brittle, resulting in unusual hip (femur) fractures.[vi]  One of the researchers, Dr. Joseph Lane, chief of metabolic bone diseases at the Hospital for Special Surgery in New York commented “normally, bone is a distribution of young bone, middle-aged bone and old bone…when we look at these bones, it’s all old bone”.  Another researcher, Dr Melvin Rosenwasser of Columbia University Medical Center, found buckling potential in the femur area in similar patients.  This type of association was first reported in 2005.

A separate study, funded by the pharmaceutical companies Novartis and Merck, both makers of bisphosphonates, refute the association.[vii]  Bisphosphonates are among the nations top selling drugs, with annual sales exceeding $3.5 billion.[viii]  The FDA has weighed in only to say that there is “no conclusive proof” of the association between these fractures and bisphosphonate therapy.  Hmmm, haven’t we heard that before?

Preventing osteoporosis is preferable to treating it.  Eating a healthy diet including fruits, vegetables and adequate protein, along with sufficient intake of vitamin D, calcium, magnesium and vitamin K is essential.  Regular resistance and weight bearing exercises increase androgen levels, muscle strength and bone mass. Avoid excess alcohol consumption and smoking.  Maintain optimal hormone balance and consider early screening to look for evidence of bone loss or altered bone metabolism to reduce your risk of suffering the debilitating consequences of this preventable disease.

[i] Fink H, Ewing S, et al. Association of Testosterone and Estradiol Deficiency with Osteoporosis and Rapid Bone Loss in Older Men. J. Clin. Endocrinol. Metab., July 18, 2006; Vol. 91, No. 10 3908-3915

[ii] National Osteoporosis Foundation.  http://www.nof.org/women/

[iii] Quaseem A, Snow V, et al. Screening for Osteoporosis in Men: A Clinical Practice Guideline from the American College of Physicians. Ann Intern Med. 2008; 148:680-684, 685-701

[iv] Haentjens P, Magaziner J, et al. Meta-analysis: Excess Mortality After Hip Fracture Among Older Women and Men. Annals Intern Med 2010; 152:380-390

[v] National Osteoporosis Foundation.  http://www.nof.org/men/

[vi] Long-Term Bisphosphonate Use Linked to Abnormal Bone Formation. Amer Assoc Ortho Sur 2010 Annual Meeting

[vii] Black D, Kelly M, Genant H. Bisphosphonates and Fractures of the Subtrochanteric or Diaphyseal Femur. Published at www.nejm.org March 24, 2010 (10.1056/NEJMoa1001086)

[viii] IMS Health Incorporated

Globally, cardiovascular disease is the leading cause of death.  It is also the number one killer of Americans; killing more than the next 5 leading causes combined.  CVD is responsible for more than a third of all deaths in the United States, and is expected to cost our healthcare system over $500 billion this year.[ii]   The majority of cardiovascular events are the result of atherosclerosis.  Dysfunction of the endothelium, or vascular lining, is thought to be the earliest step in the process of developing atherosclerosis.[iii]  It has been observed in people with coronary atherosclerosis and in people with risk factors for CVD.[iv]  Therefore, a healthy endothelium is essential in preventing atherosclerosis.  Recent research has identified emerging risk factors that better assess endothelial function, such as arterial stiffness, carotid intima media thickness, and pulse wave velocity.

Osteoporosis is a disorder of normal bone metabolism.  Healthy bone results from a lifelong coordinated remolding process of bone resorption and formation that renews the skeleton while maintaining its structure.  Approximately 10 million Americans have osteoporosis and another 34 million are at increased risk due to low bone density, or osteopenia.  The vast majority (80%) of individuals with osteoporosis are women, with 1 out of every 2 women suffering a fracture due to the disease.  But there are also 2 million men with osteoporosis.  The risks for men over age 50 are underappreciated with 1 out of every 3.5 of them experiencing a fracture due to osteoporosis.[v]  The mortality rate for an individual with osteoporosis following a hip fracture approaches 20% in the first year, and is twice as high for men compared to women.

For both men and women, their risks of developing osteoporosis increases with age and declining hormone levels.  Estrogen deficiency in menopause is a major cause of osteoporosis in women. Estrogen acts to maintain the appropriate ratio between bone-forming cells (osteoblasts) and bone-resorbing cells (osteoclasts).  Testosterone deficiency in aging men (andropause) is the leading cause of osteoporosis in men.  Testosterone directly stimulates the bone-forming cells[vi] and inhibits the formation of bone-resorbing cells.[vii]  These hormones act in concert with cytokines (chemical messengers) to control effects of the bone-resorbing osteoclasts.

Cardiovascular disease and osteoporosis are both major health problems in the United States.  Although traditionally viewed as separate disease entities a growing body of literature has revealed an association between CVD and osteoporosis. In addition to declining hormones and advancing age, other risk factors for CVD such as dyslipidemia, oxidative stress, inflammation, smoking, hypertension, and diabetes have also been associated with increased risk of low bone mineral density.  Elevated LDL and low HDL cholesterol are associated with low bone density.  Altered lipid metabolism is associated with both bone remodeling and the atherosclerotic process, which might explain, in part, the co-existence of osteoporosis and atherosclerosis in patients with abnormal lipid profiles. Similarly, inflammation plays a pivotal role in both atherosclerosis and osteoporosis.[viii]   As bone mineral density decreases, coronary and aortic vascular calcifications increases.[ix]  And, in groups known to exhibit marked endothelial dysfunction, such as diabetics, accelerated bone loss is common.[x]   Investigations with post-menopausal women have observed a 1- 4 fold increase in cardiovascular death in women with osteoporosis.[xi] [xii]

Preventing osteoporosis and cardiovascular disease is preferable to treating them.  Eating a healthy diet including fruits, vegetables and adequate protein, along with sufficient intake of anti-oxidants, vitamin D, calcium, magnesium and vitamin K is essential.  Regular resistance and weight bearing exercises increase androgen (testosterone) levels, muscle strength, and bone mass. Avoid excess alcohol consumption and smoking.  Maintain optimal hormone balance and consider early screening to look for evidence of bone loss or altered bone metabolism.  Anyone with osteoporosis or osteopenia should have a thorough cardiovascular evaluation looking for evidence of atherosclerosis, increased arterial stiffness or endothelial dysfunction.  Being proactive can reduce your risk of dying prematurely or suffering the debilitating consequences of these preventable diseases.

[i] National Institutes of Health – National Heart Lung and Blood Institute Working Group, Sept 1999

[ii] Heart Disease and Stroke Statistics. American Heart Association, 2010 update

[iii] Grey E, Bratelli C, et al. Reduced small artery but not large artery elasticity is an independent risk marker for cardiovascular events. Am J Hypertens, 2003.  16: 265-9

[iv] Anderson TJ. Nitric oxide, atherosclerosis and the relevance of endothelial dysfunction.  Heart Fail Rev, 2003. 8:71-86

[v] National Osteoporosis Foundation statistics, www.nof.org

[vi] Chen Q, Kaji H, et al. Testosterone stimulates osteoprotegrin mRNA expressionin mouse osteoblast cells. Horm Metab Res 2004; 36(10): 674-678

[vii] Chen Q, Kaji H, et al. Testosterone inhibits osteoclast formation by parathyroid hormone through androgen receptor. FEBS Lett, 2001. 491: 91-3.

[viii] Koh JM, Kyang YH, et al. Higher circulating hsCRP levels are associated with lower bone mineral density in healthy pre- and postmenopausal women: evidence for a link between systemic inflammation and osteoporosis. Ostoeposrosis Int. October 2005. 16, 10:1263-71

[ix] Barengolts EI, Berman M, Kukreja SC, et al. Osteoporosis and coronary atherosclerosis in asymptomatic postmenopausal women. Calcif Tissue Int, 1998. 62:2013

[x] Schwartz AV, Sellmeyer DE, et al. Diabetes and bone loss at the hip in older black and white adults. J Bone Miner Res. 205, 20:596-603

[xi] Tanko LB, Christiansen C, Cox DA, et al. Relationship between osteoporosis and cardiovascular disease in postmenopausal women. J Bone Miner Res. 2005, 20:1912-20

[xii] Kado DM, Browner WS, Blackwell T, et al. Rate of bone loss is associated with mortality in older women: a prospective study. J Bone Miner Res. 2000, 15:1974-80

Your Y

Cardiometabolic disorders impact the heart and vascular system as well as type 2 diabetes.  Common risk factors among the variety of related disorders include high blood pressure, altered glucose metabolism, obesity and an abnormal lipid profile.  A recent meta-analysis found a significant association between high levels of vitamin D and a reduction on the risk of having cardiovascular disease (33% reduction compared to low levels of vitamin D), type 2 diabetes (55% reduction) and metabolic syndrome (51% reduction).[6]

Although the specific mechanisms underlying these associations remains unclear, some studies have suggested that vitamin D may directly modulate gene expression through activation of vitamin D receptors.[7]  Its effect on the regulation of intracellular and extracellular calcium may also play a role.

Recent data has demonstrated that nearly 80% of the US population is deficient in vitamin D, and that number is twice as many as were identified 10 years earlier in a previous survey.[8]  This finding was surprising since our bodies are able to produce sufficient vitamin D provided we get adequate sun exposure.  But most of us don’t get enough direct sunlight to fulfill our vitamin D requirements because of concerns about skin cancer and skin damage, less time spent outdoors and low light quality in winter in the northeast. Keep in mind that sunscreens greater than spf 8, cloudy days, clothing and glass block the sun’s ability to aid in the manufacture of vitamin D.  Things are compounded for older individuals and those with darker, pigmented skin.

Vitamin D deficiency has become so prevalent that everyone should consider themselves at risk.  A simple blood test can determine the amount of vitamin D circulating in your blood.  A more sophisticated test can determine the intracellular concentration of this essential nutrient.  It is, after all, the concentration within the cell that really matters.  This test, called Micronutrient Testing from Spectracell Labs, is available at Alternity Healthcare.

What should you do if your vitamin d level is low?   The best food sources of vitamin D are fatty fish like salmon, tuna mackerel or sardines.  Vitamin D supplements are probably a good idea for most.  My recommendation is 1000 – 2000 IU daily for maintenance.  Higher doses would be required to raise a deficient level into the optimal range.

[1] Wang T, Passina M, et al. Vitamin D Deficiency and Risk of Cardiovascular disease. Circulation. 2008;117:503-511.

[2] Pittas A, Lau S. The Role of Vitamin D and Calcium in Type 2 Diabetes. A Systematic Review and Meta-Analysis. The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 6 2017-2029

[3] Jenab et al. Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations:a nested case-control study. BMJ, 2010; 340 (jan21 3)

[4] Ramagopalan SV, Maugeri NJ, Handunnetthi L, Lincoln MR, Orton S-M, et al. “Expression of the Multiple Sclerosis-Associated MHC Class II Allele HLA-DRB1*1501 Is Regulated by Vitamin D.”  PLoS Genetics 2009, 5(2): e1000369

[5] Turner M, Hooten WM, et al. Inadequate Vitamin D Levels Linked To High Use Of Narcotic Medication By Patients In Chronic Pain. Mayo Clinic Proced March 209.

[6] Parker J, Hashmi O, et al. Levels of vitamin D and cardiometabolic disorders: Systematic review and meta-analysis. Maturitis, vol 63, issue 3, Pages 225-236 (March 2010)

[7] ScienceDaily. Study Shines More Light On Benefit Of Vitamin D In Fighting Cancer. Retrieved April 18, 2010, from http://www.sciencedaily.com­ /releases/2007/08/070821163248.htm

[8] Ginde A, Liu M, Camargo C, et al. Demographic Differences and Trends of Vitamin D insufficiency in the US Population, 1988 – 2004. Arch Intern Med. 2009;169(6):626-632

Estrogen, progesterone and testosterone are the three major sex hormones in both men and women, with the ratios and levels varying according to gender.  Estrogen and progesterone are the predominant hormones in women.  Any discussion of one must include the other, although this article will focus primarily on estrogen.

Estrogen is made in the ovaries, the corpus luteum, adrenal glands, breast and fat cells.

Estrogen is a generic term referring to a group of molecules. In humans, the three main identified estrogen molecules are estriol (E3), estradiol (E2), and estrone (E1).  A proper balance of estrogen enhances sensuality, improves the appearance of skin, moisturizes eyes, lubricates the vagina, preserves mental clarity, plumps up the breasts, and protects the bones and cardiovascular system.

When the scientific and lay communities refer to estrogen, they typically refer to its three components as one. At times, this oversimplification leads to errors in separating the individual function of the estrogens, particularly when discussing the differences between estrogen preparations used as hormone-replacement therapy available on the market. Although their actions are perceived and often recorded as one, the component molecules of estrogen have different potencies and effects.

Types of Internal Estrogens

Estradiol is the most powerful, abundant and active form of estrogen.  Prior to menopause, it is made mainly by the ovaries.  Post menopausal production occurs in individual cells throughout the body, particularly fat cells and stromal cells in the breast. Estradiol directly affects a wide range of cellular functions, as estrogen receptors are ubiquitous.

Estriol is the weakest of the estrogens. Estriol is primarily manufactured during pregnancy by the placenta. It attaches to cell receptors affecting hair, nails, and skin.  Recorded data on estriol’s function demonstrate that estriol’s effects are limited mainly to the vaginal walls with little effect on the heart and bones in non-pregnant women. In the non-pregnant, young, and premenopausal woman, estriol is made in the liver in small doses. Studies have shown it to have a protective effect against breast cancer.

Estrone is manufactured in fat cells after menopause primarily from testosterone derivatives (androstenedione). Estrone levels tend to rise after menopause and the increase in estrone has been implicated in an increased incidence of breast tumors but most data have been obtained from animal studies. Overweight older women have high circulating levels of estrone.

External Estrogens

Your hormonal health can also be affected by external estrogens and estrogen-like compounds introduced into your body.  These include bioidentical estrogens, synthetic estrogens, xenoestrogens, and phytoestrogens.  Bioidentical hormones are hormones manufactured with a molecular structure identical to that naturally found in the human body.  They are made from a plant source, frequently soy or yams, and are ideal for use in hormone replacement therapy.  “Bioidentical hormones” is not a marketing term. The term has been used for more than a decade in the inserts to all FDA-approved commercial hormone preparations that contain hormones molecularly identical to human hormones.  Bioidentical estrogen preparations include: 17-Beta estradiol (Alora, Climara, Estrace), 17-Beta estradiol patches (Vivelle-Dot, Vivelle, Estraderm), Estradiol transdermal spray (Evamist) and combinations of estradiol, estriol and estrone in compounded formulations (Biest, Triest).  In recent studies, bioidentical estrogens have demonstrated an ability to reduce degradation of telomere length.  Telomeres are protective end-caps on chromosomes, the length of which is correlated with biological age.

Synthetic estrogens are chemically manipulated and are molecularly very different from human estrogens.  These are the most common formulations used for hormone replacement therapy in the United States.  Synthetic estrogens are derived from the urine of pregnant mares, as the name Premarin implies.  The most popular preparations are conjugated equine estrogen (Premarin), esterified estrogen (Estaratab), and ethynil estradiol (Estynil).

Xenoestrogens are produced as by-products of the chemical pollution in our society and are very hazardous to your health.  They can be absorbed through your skin, inhaled when you breathe and ingested with your food.  Examples include dioxins, polychlorinated biphenyls (PCB), and dichlorodiphenal-trichoroethane (DDT), among others.  They can be stored in fat cells for long periods of time and although relatively weak, they can act in combination to increase your risk for certain cancers.

Phytoestrogens are abundant in nature and can weakly interact with estrogen receptors.  These compounds include lignans found in cereals, vegetables, green tea, legumes and flax; isoflavones in soy, beer, chickpeas, beans and lentils; and coumestrol present in grapes (resveratrol), alfalfa and clover.  In moderate doses, phytoestrogens have been shown to exert a protective effect on breast cancer by inhibiting the production of estrogen.

Estrogen Metabolism

The various metabolites of estrogen must also be considered in evaluating the overall hormonal milieu in your body.  These metabolites are 2-hydroxyestrogen (2OH), 4-hydroxyestrogen (4OH) and 16alpha-hydroxyestrogen (16OH).  The 2-hydroxyestrogen metabolite is considered a “good” estrogen because it has anti-cancer properties.  It does not exert proliferative effects on other cells and antagonizes the effects of other estrogens.  This metabolite also reaches very high levels during pregnancy, suggesting a protective effect against high hormone elevations.  Synthetic estrogens can reduce the formation of 2-hydroxyestrogens.  A competing pathway results in the production of 16alpha-hydroxyestrogen which has a high affinity for the estrogen receptor and strongly stimulates cell proliferation leading to cancerous changes in estrogen sensitive tissues.  Studies have shown this 16 alpha metabolite to be important for preservation of bone tissue.  It is, therefore, important to maintain an optimal ratio of 2-hydroxy:16alpha-hydroxy metabolites. The ratio can be measured by a urine or blood test.  A low ratio may put you at increased risk for breast, uterine and ovarian cancer.  A minor pathway leads to the production of the 4-hydroxyestrogen metabolite.  This metabolite also promotes cancerous changes but doesn’t bind to an estrogen receptor, rather it works by directly damaging cellar DNA.  Synthetic estrogens are metabolized to 4-hydroxy products; another compelling reason to avoid them.

Estrogen and progesterone are antagonists. Their actions are designed to balance each other and keep each other in check. We cannot live in a healthy state without hormonal balance.  Hormones do not act independently, under normal circumstances, in healthy bodies.

Progesterone

Progesterone is manufactured primarily by the corpus luteum (the follicle transformed after ovulation) and also to a small degree by the  arenals. In the ovary, progesterone production is activated at ovulation (15 days before the next menstruation), stimulated by the release of luteinizing hormone from the pituitary gland and is crucial to the survival of the ovum once fertilized. When pregnancy occurs, progesterone production increases rapidly and its manufacture is taken over by the placenta. If a woman does not get pregnant, the corpus luteum involutes and progesterone production diminishes and eventually disappears in parallel with estrogen production, heralding menstruation.

Progesterone is a precursor to most sex hormones, including estrogen in the ovaries, testosterone, all androgens, and other adrenal hormones, making it an extremely important hormone for reasons far beyond its role as a sex hormone.  Progesterone in the breast and uterus counteracts the stimulation of cell growth, which is a direct action of estrogen. It accomplishes this action by activating the progesterone receptor, which in turn, down-regulates the estrogen receptor. Because progesterone suppresses estrogen-driven cell proliferation, progesterone in the natural state helps keep breast cell growth in healthy balance.

Commercially and compounded bioidentical hormone preparations containing progesterone include:  Progesterone in peanut oil capsule (Prometrium), progesterone vaginal gel (Crinone), micronized progesterone in various compounded forms (capsules, troches, transdermal creams, vaginal suppositories), combinations of estradiol and progesterone in compounded formulations.

Beyond the commercial bioidentical hormone formulations, individually compounded preparations of bioidentical estrogens, progesterone and testosterone are prepared in compounding pharmacies or laboratories (some are FDA approved; all are regulated by the state they operate in) on an individualized basis as prescribed by a physician. These products contain the same active estrogens, progesterone, and testosterone as those found in the commercial preparations listed above. The difference is that they are individually mixed in tablet, capsule, troches, gels, or creams to the specifications of the prescribing physician for the individual patient.

The synthetic, non-human progestin found in Provera is medroxyprogesterone (MPA).  It has very different biologic effects than natural human progesterone.  Provera reduces the beneficial effects of estrogen on plasma lipoproteins, can lead to vascular spasms, opposes the beneficial effects of estrogen on the brain and has been shown to enhance the estrogen-induced proliferation of pre-existing breast cancer cells;  the opposite effects of bioidentical or natural progesterone.

Among the lay public as well as within the scientific and medical communities, there remains considerable confusion surrounding estrogen and progesterone formulations.  The confusion comes from the lack of clear distinction between their molecular formulas, the lack of focus on their different effects in the human body, and the use of nonspecific nomenclature when referring to estrogen and progesterone regardless of their actual differences in chemical structure or activity.

Hormone Replacement Therapy

Scientific studies on the effects of hormone replacement therapy after menopause have had conflicting results and conclusions.  As early as 1976, scientific data demonstrating the safety of bioidentical hormones appeared in the conventional medical literature from the American College of Obstetrics and Gynecology. Reports of increased risk of endometrial and breast carcinoma among users of synthetic conjugated estrogens also appeared in the scientific literature around the same time  As early as 1980 and continuing into the recent literature, untoward side effects of synthetic progestins, such as thrombotic phenomena; breast tissue cell hyperplastic changes;  cardiovascular symptoms, headaches, elevated blood pressure, and changes in cholesterol, carbohydrate, and lipid metabolism prompted more research into bioidentical (micronized) progesterone as a safer option.  A double-blind study comparing transdermal estradiol and Premarin reported in the American Journal of Obstetrics and Gynecology as early as 1985 suggested that  bioidentical hormones were superior in relieving postmenopausal symptoms without side effects.

Womens Health Initiative

Most recently, the Women’s Health Initiative (WHI) has been the source of confusing and sensationalized reports indicting all hormone replacement for causing breast cancer and heart disease.  The goal of the study was to evaluate the long-term effect of hormone-replacement therapy (HRT) versus placebo in the prevention of heart disease, osteoporosis, cancer, and strokes in postmenopausal women. The only form of hormone-replacement therapy used in the study was synthetic conjugated equine estrogens (Premarin) and synthetic progestins (Provera). Unfortunately, the WHI did not include a bioidentical arm even though bioidentical hormone usage and statistically significant studies consistently demonstrated positive results and sustainable safety and efficacy records.  The WHI was supposed to definitively answer questions about the efficacy and benefits of HRT but only created confusion and concern.  There were three treatment arms in WHI:  the first used a combination of synthetic hormones, Premarin plus Provera, called PremPro; a second arm used only a conjugated equine estrogen (CEE), Premarin and a third arm evaluated the effects of calcium and vitamin D on fracture risk. Subjects in the PrePro combined synthetic hormone arm were reported to have an increased risk of breast cancer, stroke and coronary artery disease.  The results from the Premarin only group were less publicized but demonstrated a reduced relative risk for both breast cancer and heart disease; the risk of thrombophlebitis was increased.  Initial news reports on the calcium and vitamin D arm suggested no benefit from taking those supplements.  Subsequent analysis has determined that the study was poorly designed and the initial analysis faulty.

Concerns with the WHI study design include the type of hormone used, dosing pattern, route of administration, timing of hormone usage, mean age of the participants, and prior health status of the participants.  The WHI used only synthetic hormones taken orally and at a relatively high, fixed dose.  The participants were, on average, 63 years old and more than ten years beyond menopause; the crucial time to mitigate the pro-inflammatory effects of the postmenopause transition.  Studies have demonstrated estrogen’s ability to block chronic inflammatory mediators, including interleukin-6, tumor necrosis factor alpha and prostaglandin E2.  Estrogen has also been found to have significant antioxidant effects.

Participants in the WHI were not adequately prescreened for breast cancer or subclinical atherosclerotic heart disease, and it was reported in JAMA, the Journal of the American Medical Association in 2002 that a substantial portion of the participants had prior health histories which included obesity, hyperlipidemia, angina, strokes and smoking.  The adverse outcomes WHI attributed to hormone therapy, especially cardiovascular, could very well be linked to age and pre-existing risk factors.  A reanalysis by Rossouw et al  published in JAMA in 2007 separated WHI participants by age and found a reduced risk for coronary heart disease in all women taking hormone therapy 10 or fewer years from menopause.  The only statistically significant increase in cardiac events occurred in women 20 plus years postmenopause.  Furthermore, the results of the WHI Coronary-Artery Calcium Score Study performed after the conclusion of the WHI, demonstrated a 61% reduction in coronary artery calcification in women taking estrogen.  This translates into a reduced incidence of subclinical coronary artery disease in women receiving estrogen.  Although breast cancer may be the greater fear for women, 10 times more women die from cardiovascular disease every year than breast cancer.

As mentioned above, the WHI used only synthetic hormones.  Synthetic estrogens are metabolized to 4OH estrogen, which has been found to be thirty-times more toxic to cellular DNA than bioidentical estrogens.  Synthetic progestins appear to attenuate most beneficial effects of estrogens and enhance estrogen’s proliferative effects.  That may explain any increased risk of breast cancer noted after 10 or more years of synthetic hormone replacement therapy.

The synthetic hormones used in WHI, Premarin and PremPro are administered orally.  They are subjected to first pass through the liver resulting in increased production of clotting proteins and inflammatory markers, C-reactive protein.  Orally administered estrogen preparations have long been associated with an increased risk of venous thromboembolism (VTE), or blood clots.  In each of the two hormone therapy arms of the WHI, an increase in VTE was reported.   Transdermal estrogen has been shown to eliminate the thromboembolic effects noted by orally administered estrogens.   Two studies published in Circulation, the Journal of the American Heart Association, in 2005 and 2007 showed that transdermal estrogens did not increase the risk for blood clots, even when combined with micronized progesterone.

Breast Cancer

Public perception that all hormone preparations cause breast cancer was fueled by the notoriety gained in the media from the results of the combined estrogen-progestin arm of the WHI that ostensibly revealed an increased risk of invasive breast cancer among hormone users.  Those erroneous conclusions of so-called experts have been refuted by subsequent analyses. When corrected for multiple breast cancer risk factors, the results were no longer considered statistically significant.  Additionally, the combined WHI arm was discontinued after 5 years, and most cancer researchers agree it takes 7-10 years of dividing for a breast cancer cell to become a detectable lesion.  This further suggests that hormone replacement was not the cause of breast cancer.  A large review of studies prior to WHI published in the New England Journal of Medicine, 1997 demonstrated a 24% reduction of breast cancer deaths among women during the first ten years of hormone replacement.

Beginning hormone replacement therapy at the onset of menopause and continuing for  10 years significantly reduced the incidence of Alzheimer’s disease in the Cache Cohort Study published in 2002.  Women who began HRT ten years or later had an increased incidence of Alzheimer’s.  Similar results were reported in the journal, Menopause, in 2005:  replacing hormones early in menopause and continuing them for several years protected against cognitive decline and that benefit persisted for up to 15 years later.

Although the controversy surrounding the use of hormone replacement therapy is far from resolved, there is mounting evidence of its benefits for most women.  A recent study in Menopause reported that a “significant proportion of obstetrician-gynecologists continue to express skepticism regarding the WHI results”. The medical and scientific community will probably not reach any consensus until a definitive randomized trial directly comparing synthetic hormones with bioidentical hormones, while taking into account age, risk factors, timing and route of administration, and differing biologic activity during the crucial first ten years of menopause.

That being said, there is ample evidence to recommend hormone replacement for most women.  Bioidentical hormone therapy should be initiated at menopause or during perimenopause to provide protection for the cardiovascular system, maintain adequate bone mass and body composition, enhance sexual desire and responsiveness, preserve cognitive function, and minimize the unpleasant symptoms associated with the menopausal transition.  Women would be best served to seek out a physician specializing in bioidentical hormone therapy.  The most effective hormone balancing is achieved within a broader program addressing lifestyle modificatons, proper nutrition and nutritional modulation of hormone metabolites, high quality nutritional supplements, liver-gut detoxification, regular exercise, stress management and adequate sleep.   Remember, aging is inevitable, but how you age is up to you.

Most Americans are vitamin D deficient due to inadequate dietary intake and insufficient sun exposure (UVB rays).  The predominant dietary form of vitamin D is D2.  That is also the form typically found in OTC vitamin supplements. The preferred, and more potent, form is vitamin D3 which is synthesized  in the skin from sun exposure.  

For more information on sources of high quality vitamin D3 supplements, contact Alternity Healthcare 860.748.4064 or visit our website: AlternityHealthcare.com

Osteoporosis is defined by a reduction in bone mass, bone quality or the presence of a fragility fracture. It contributes to nearly 1.5 million fractures per year in the US.

One out of every two women will experience an osteoporotic fracture in her lifetime. For men, the number is one in four. Common fracture sites include the hip, spine, wrist and rib. For anyone with an osteoporotic fracture, the one year mortality approaches 20%

Bone is a living tissue balanced by the actions of osteoblasts that lay down new bone and osteoclasts responsible for bone resorption. Bone mineral density is a measure of the adequacy of mineralization of bone. Peak bone mass occurs before age 30. The gold standard test is a DEXA bone densitomitry scan.

Recent scientific information implicates chronic inflammation, oxidative cell damage and advanced glycosalated end products (AGE’s) as contributors to the development of osteoporosis. Bone loss is also correlated with vasclar calcifications and the development of cardiovascular disease.

Risk factors for the development of osteoporosis include:

• low estrogen in women and low testosterone in men
• low body weight (<127 lbs)
• smoking
• lack of exercise
• excessive alcohol
• deficiency in calcium and/or vitamin D
• excess phosporous intake (soda)
• high protein diet (acidic)
• diabetes, thyroid disease, celiac disease, inflammatory bowel disease, arthritis

To reduce your risk of osteoporosis be sure to eat a healthy diet that includes colorful fruits and vegetables, regularly engage in aerobic and resistance exercise, take adequate calcium, vitamin D and omega-3 fatty acid supplements.

Every woman over 40 and man over 50 should consider having their bone mineral density checked. Preventing osteoporosis is better than treating it; especially after an osteoporotic fracture.