These statistics are based on BMI; a notoriously inaccurate measure of body composition.  After all, it isn’t really weight that people want to lose, it is body fat.  We have just become accustomed to equating excess weight with excess fat.  But the two can be radically different.  BMI does not adequately take lean muscle mass into account and routinely underestimates the body fat percentage of individuals.  And it is excess body fat, particularly the deep visceral belly fat that is associated with an increased risk of diabetes, cardiovascular disease, high blood pressure, metabolic syndrome, breast cancer, colorectal cancer, gallbladder issues, dementia and more.  As if that was not enough, preliminary research from Boston University researchers has found a “significant” link between visceral fat and lower total brain volume[4].

The research looked at 733 healthy individuals that were part of the Framingham Offspring cohort with an average age of 60.  Seventy percent of the participants were women.  Researchers looked at the potential associations of body mass index (BMI), waist circumference, waist-to-hip ratio, and abdominal fat with the total brain volume.  Abdominal fat was measured by CT scan and could differentiate the deep visceral fat from the subcutaneous fat just under the skin surface.  While there was an association with BMI and waist circumference, the real culprit was visceral fat.  Subcutaneous fat was not [significantly] associated with any adverse effect on the brain volume, whereas visceral fat was clearly associated with smaller brain volume.  Smaller brain volume is associated with poor cognitive function on testing and a greater risk of dementia on follow-up.

 What can you do to reduce your body fat? 

•  Make the decision to make a change.  Resolutions won’t cut it.  The vast majority only last a couple of months, at best.  This change is for your lifetime.
• Exercise regularly.  You need to do both strength/resistance and aerobic activity.  Interval training is the best and most effective method of combining both.
• Low Glycemic nutrition.  Balance is key:  adequate protein, healthy fats and fewer carbohydrates.  Excess sugars and processed carbohydrates are the real enemies.  Not dietary fats.  Avoid man made trans-fats but you need to eat healthy fats in order to lose body fat. 
• Eat smaller frequent meals throughout the day of natural, nutrient-dense whole foods
• Hormonal assessment.  Check your hormone levels to determine options for balancing your endocrine system.

 The key message is pretty clear.  How you take care of yourself now will determine how well you can maintain both your physical and cognitive prowess as you age.  This concept is not new.  Don’t wait until it is too late.  There is no time better than now to start living better.

Testosterone is the primary male sex hormone, or androgen.  Circulating levels of testosterone increase at the time of puberty and peak in early adulthood for men.  Testosterone is responsible for men looking like men and feeling like men.  Following that peak is a gradual but steady decline in testosterone levels beginning in the mid-30’s. Declining testosterone levels cause a variety of symptoms including loss of muscle mass and strength, increased belly fat, impaired brain function, disrupted sleep, loss of libido, impaired sexual function and general fatigue.  But, because the loss of testosterone is gradual these symptoms typically occur little by little, and the impact on a man’s life may not be felt until his 40’s, 50’s or later.  This is sometimes referred to as andropause, or the male menopause.  This gradual decline in vitality, function and quality of life is too often attributed to “just getting old” when in reality, many of those symptoms can be reversed with proper treatment.

It is readily apparent to most that testosterone plays a crucial role in male sexual function. Sexual potency peaks along with the raging hormones of a teenager.  Similarly, testosterone is essential for building and maintaining muscle mass, youthful energy and strength.  Considering testosterone therapy to improve the way you look, feel and perform would be good enough for many.  In fact, testosterone therapy has resulted in improved libido and erectile function in middle aged men.[i]  However, recent scientific evidence has demonstrated significant adverse health implications for men with low and declining testosterone levels.  Numerous studies have now established a strong association between low testosterone and depression, metabolic syndrome, type-2 diabetes, osteoporosis and cardiovascular disease.  In one study men with low testosterone had a nearly 50% increase in mortality over a seven year period.[ii]   An unmistakable link has also been established between erectile dysfunction and the development of cardiovascular disease.

Several studies have shown that restoring testosterone to more youthful levels in middle-aged men improved insulin-sensitivity, reduced serum cholesterol, fat mass, waist circumference and inflammatory bio-markers associated with heart disease, diabetes, and metabolic syndrome.  One study concluded that “that testosterone treatment in men has potentially beneficial effects on virtually all of the coronary risk factors, as well as an independent anti-plaque forming action.”  In men with heart failure, testosterone therapy also improved functional capacity, or the ability to perform physical activity without constraint.[iii]

So why aren’t more men getting testosterone therapy?  Many physicians do not recognize the symptoms of low testosterone as a treatable condition. Traditionally, physicians have been reluctant to prescribe testosterone therapy in large part out of a misguided fear of increasing prostate cancer risk.  Recent evidence has called that conventional paradigm into question.  A large meta-analysis out of Harvard University[iv], as well as a collaborative review of 18 prospective studies[v] concluded that no significant association existed between higher testosterone levels and prostate cancer risk.  Conversely, studies have shown an increased risk of prostate cancer and aggressive prostate cancer in men with low testosterone levels.  In a group of middle-aged men treated with testosterone and followed for more than 5 years, there was no increase in the incidence of prostate cancer and PSA levels remained stable.[vi] 

 What is the bottom line?  Any man over 40 or 50 that feels off his game, run down or is experiencing any of the symptoms of low testosterone should have a thorough evaluation looking for cardiovascular disease, pre-diabetes, and osteoporosis among others.  I recommend seeking out a physician experienced in preventive health and hormone therapy for men.  At Alternity Healthcare, we utilize comprehensive evaluations and state-of-the-art diagnostics to form the basis of an individual preventive health program.  Rather than narrowly focusing on just your hormone levels, our comprehensive programs will expose your total health picture and help you to achieve renewed, long-term health and vitality.   

Although numerous studies have demonstrated substantial health benefits from physical exercise, there is debate about the optimal type, duration and intensity to achieve the most favorable result.  When you mention exercise to most people, it congers up images of tedious endurance training; that is, traditional “cardio” that many exercise gurus tell you to do.  But recent scientific studies are pointing to another, more efficient option to strengthen your heart, improve lung function and overall fitness.  Shorter bursts of vigorous exercise benefits heart health as much as tedious endurance training.

A small study done at McMaster University in Canada compared healthy men and women riding stationary bikes.  Some exercised five days per week doing 40-60 minutes of moderate-intensity cycling.  Others did four to six sets of 30-second sprints on the bike allowing 4-5 minutes of recovery between sets; with a total exercise time of 15-25 minutes just three days a week.  After six weeks, the researchers found that the intense sprint interval training improved the structure and function of arteries as much as traditional, longer endurance exercise.

A larger study, following 13,000 people for 15 years in the Harvard Health study found that people live longer if they do vigorous exercise, but not if they only do light or moderate exercise.[1]   Another study looking at the cardiovascular benefits of exercise in people following coronary artery bypass surgery (CABG) found that higher intensity interval training improved aerobic capacity (VO₂) significantly better than moderate intensity continuous training.  In fact, the study data showed that the 4 week improvement in VO₂ in the interval training group was greater than that achieved in the moderate continuous training group after 6 months.^[2]

What is VO₂?  There are a number of parameters that can be measured to assess your overall cardiovascular health but the one of the best is your aerobic capacity, otherwise known as your VO₂ max.  Measuring VO₂ max reveals how well your lungs can get oxygen into your blood, how efficiently your heart can pump that blood to your organs and exercising muscles and how well those muscles can utilize the oxygen for energy production.  The more oxygen your body can use, the better your body works.

Mitochondria are the power plants where fuel is burned, energy is produced and harmful free radicals are neutralized.  The number of mitochondria that you have in your cells determines your performance capacity.  But that number is not fixed.  There are several complex pathways that lead to an increased number of mitochondria.  The best known and most effective way to produce more mitochondria is with exercise.^[3]   Mitochondrial production increases in direct proportion to the amount of physical activity performed.^{[4] [5]}

I have previously reviewed in detail three nutritional supplements, Resveratrol, Alpha Lipoic Acid and L-arginine, which have been shown to augment mitochondrial production and thereby improve oxygen consumption.  Quercetin, a compound found in berries, onions grapes and red wine can also improve VO₂.  A study using elite cyclists demonstrated a 4% increase in VO2 over a six week trial [6], and a similar increase in healthy but untrained individuals given quercetin supplements over seven days.

Clearly, people that stay physically active throughout life reap substantial benefits from exercise.  But what about those getting a late start?  Can beginning an exercise program at any age make up for years of sedentary living?  The short answer is a resounding “yes”.

A study spanning 35 years in Sweden strongly suggests that starting to exercise at or after 50 years old is better than never starting at all.  Another British study traced men over 18 years, at an average age of 63.  This study revealed a strong link between exercise and survival.  A third study from Norway found that men who were physically fit enjoyed substantial protection from cardiovascular disease and early death.   Not to be outdone, a study of American veterans followed men over 25 years and noted a 38% lower mortality in men who were physically fit.  Just as important was the finding that men who were unfit at the start and improved their fitness had a 35% lower mortality than those who remained unfit.

So, improving your fitness level strengthens your heart, improves your vascular system, enhances lung function, reduces your risk for a myriad of chronic diseases and ultimately protects against premature death.  But exercise alone is not sufficient.  It should be part of an overall adoption of healthy lifestyle habits:  eating more fruits and vegetables, avoiding processed foods and added sweeteners, not carrying around excess body fat, not smoking, getting more sleep and managing stress.  If you are over 50 you should have a thorough medical evaluation prior to beginning an exercise program and seek guidance from an experienced trainer or exercise physiologist.  At Alternity Healthcare, we perform an extensive evaluation including VO₂ testing on all of our new patients.

 It is never too late or too early to start exercising.  You will feel better, look better and live better.  You could then spread the word to your children and younger friends who have become distressingly inactive, overweight and lazy.  Remember, leading by example is most effective.

 Ever since the term “male menopause” was first coined in 1949, there have been debates about whether men go though a psychological and physiological change that is similar to menopause in women.  The problem is that menopause literally means “the end of menses,” so it describes the loss of something that men never have.  Despite that, men do experience physical changes as they age that, like menopause, are caused by a decrease in hormone production.  Unlike menopause, this decrease in hormone production is drawn out over most of a man’s adult life.  This has lead to a series of attempts to find a better term to describe what is happening.  Many doctor use the term “andropause” to describe the age-related hormone changes in men.  Irritability, fatigue, depression, reduced libido and erection problems are hallmark signs of andropause.

 Andropause can be taken to mean “the end of male-ness.”  More accurately, it should be thought of as a reduction in the production of hormones called “androgens” that produce male sexual characteristics.  The chief androgen in humans is testosterone.  Testosterone is the hormone that makes men, men. 

 Testosterone production varies throughout a man’s life.  Before birth, testosterone and other androgens drive the differentiation of the embryo into a male baby.  In early infancy, testosterone levels rise and then retreat for reasons that are not well-understood.  Through childhood, testosterone is very low, but then it increases greatly in puberty.  Starting at about age 30, testosterone production drops approximately 1% to 3% a year and this decrease continues until the end of life.

 What principally distinguishes menopause from andropause, therefore, is the time scale and rate at which sex hormone production changes.  In women, menopause is a distinct life stage lasting 1-10 years.  Once menopause is complete, production of sex hormones remains at a steady lower level until the end of life.  By contrast, men normally experience no such abrupt change in sex hormone production and the decline of production continues throughout old age.

 Another way menopause is different from andropause is in how it changes fertility.  Although there are many women who mistake the appearance of menopause symptoms for the end of fertility, earlier at some point in the peri-menopause transition the ovaries will stop producing new eggs and she will no longer be able to become pregnant.  In men, however, the production of sperm can continue until very late in life at levels high enough to cause pregnancy. 

 Despite these differences in timing and fertility, however, there is a real biological change happening in men as they age.  While there is not yet any officially recognized diagnosis of andropause, researchers have been defining a wide range of ways the reduction in testosterone affects men, using terms like Symptomatic Late-Onset Hypogonadism (SLOH) and Androgen Deficiency in the Aging Male (ADAM).  These terms may be more accurate ways of describing testosterone deficiency that has dropped enough to produce recognizable symptoms. 

 Testosterone production varies not only with age but also daily and in response to stress.  Peak production occurs in the morning decreasing through the day to a valley in the evening.  Testosterone is produced by the testicles and adrenal glands and released into the blood stream where most is bound to proteins called sex-hormone binding globulin (SHBG) other proteins such as albumin.  The SHBG-bound portion is very tightly bound making it unavailable for use by the body, leaving approximately 2% “free” testosterone and 23% loosely-bound “bioavailable” testosterone[1].  When it reaches its target, a small portion of testosterone is converted into a more potent metabolite called dihydrotestosterone (DHT).

 Like menopause, testosterone deficiency is an endocrine condition that causes changes in a man’s metabolism with short and long-term effects in many different organs and systems.  The musculoskeletal system shows lower density in the bones and weaker muscles.  In the cardiovascular system, testosterone deficiency is associated with atherosclerosis, coronary artery disease, and other cardiovascular diseases[2].  In the nervous system, low testosterone shows up as decreased libido, increased rates of depression and cognitive difficulties.  It is also linked to erectile dysfunction, alterations of body hair and skin thickness, increased visceral fat, and infertility.

 Men with low testosterone levels have higher risks of osteoporosis and fractures.  As testosterone decreases, deposition of new bone also decreases, reducing bone strength and density.  Osteoporotic men given testosterone supplementation reduce the rate of bone degradation and increase bone density.  Fractures, especially hip fractures, in the elderly are very dangerous to both men and women.  Men are more likely to die following hip fracture than women.  The one year mortality rate following hip fracture for men is double that of women.[3] 

 As both men and women age, they lose muscle strength.  Testosterone is an anabolic steroid, which builds muscle, so it makes sense that reduced levels would reduce muscle mass and strength.  The loss of independence and increased overall frailness we associate with old age are partly a consequence of this decline of the anabolic effects of testosterone.  Older me with relatively low testosterone levels are at increased risk of frailty than those with higher levels.[4]   Elderly men that have higher testosterone levels have better physical capacity as measured by physical fitness tests.  They also are better able to carry out normal daily activities, like writing, eating, walking, and dressing. Men given testosterone supplementation have reduced body fat, increased lean muscle mass, and increased grip strength.  They also gain upper and lower body strength and aerobic endurance.

 It has been a long-standing belief in the medical community that higher levels of testosterone put men at increased risk for heart disease.  The exact opposite is in fact true – lowered amounts of testosterone increase the risk of heart disease over normal men.  Men that have coronary artery disease have lower levels of testosterone than men without blocked arteries.  No study so far, in fact, shows a relation between higher testosterone and coronary artery disease.  Neither does an increased testosterone level from supplementation lead to increased heart disease.  This overturns years of dogma and leads to the question whether testosterone supplementation can help men with cardiovascular disease?

Fortunately, men with decreased testosterone and coronary artery disease do show improvement when given testosterone supplementation.  Angina frequency and intensity are reduced, they tolerate exercise longer before experiencing chest pain, and have improved mood.

Mood and other emotional and cognitive disturbances are another group of symptoms that men and women share and may be related to hormonal changes.  The brain produces testosterone and receptors for testosterone are common in the brain.  We are just beginning to understand the effects on the brain of late-life testosterone deficiency. 

Elderly men in one study that had higher levels of bioavailabile testosterone did better on tests that are designed to find brain damage or dementia.  Declining testosterone also appears to reduce the type of thinking called “spatial cognition” – tasks that require attention to objects in three-dimensional space like visual perception, object perception, and visual memory.   Men with lower levels of testosterone also report greater levels of memory problems and other dementia symptoms as they age. Testosterone also appears to both help protect and heal nerve cells in the brain.  In laboratory studies, testosterone protects neurons from attack by a variety of possible toxins.  It also helps heal severed nerves and produces other chemicals that help nerves re-grow after injury.

 With all these effects on the brain, it is no surprise it is being looked at as a way to treat one of the worst diseases of aging, Alzheimer’s disease (AD).  AD is characterized by progressive loss of higher brain functions and the deposition of plaque in the brain.    Testosterone and other hormones appear to possibly impact this process and are being considered as therapies for AD.  In some laboratory studies, testosterone significantly reduced the impact of AD on memory loss and the production of these plaques.

Another effect of menopause is that declining sex hormone production reduces interest in sex.  Men also experience a decline in sexual desire with reduced testosterone levels.  In fact, decreased libido with no other cause is a standard symptom for clinically-significant decreased testosterone.  Men with decreased testosterone also have more trouble producing or maintaining an erection.  Several small studies have shown that testosterone supplementation in older men results in both increases in libido and in a higher sense of well-being and satisfaction.

Weight gain in elderly women is frequently blamed on the hormonal and metabolic changes caused by menopause.  Similarly, decreased testosterone is linked to increased body fat, especially “visceral” fat.  Visceral fat is also called abdominal fat or organ fat.  It is the fat that is located inside the abdomen instead of just under the skin where most fat deposits are located.  Packed in among and around the abdominal organs, visceral fat is associated with a much greater risk of cardiovascular disease, diabetes, hypertension, atherosclerosis and premature death. 

 Any doctor that sees middle-aged men is asked: “Do men have male menopause?” or: “Does male menopause exist?”  Because of the very different ways that men and women’s bodies change the production and availability of sex hormones, these are really the wrong questions.  The question that we should ask is: “Should men be evaluated for sex-hormone changes in later life?”  This answer to this question is a very firm and unequivocal: “Yes.”

 Without proper evaluation of androgen levels, many treatable symptoms will go unaddressed.  With proper evaluation, men can be treated in ways that will improve general health, longevity, and quality of life. 

 Unfortunately, most clinicians either do not recognize the symptoms of testosterone deficiency or believe that these symptoms are “normal aging.”  When doctors miss addressing testosterone deficiency, they cheat their patients of powerful treatment options.

 Complicating evaluation and treatment of androgen deficiency, however, is the difficulty in measuring or defining what is an abnormally low level.  Men’s testosterone levels in later life are variable and poorly-defined.  Among the issues: there are multiple protocols for testing androgens, each with different reference values, there are different androgen fractions (free testosterone vs. bioavailabile testosterone, etc.) that can mask the amount actually available for use by the body, and the reference standards for the “normal” range are incredibly broad. 

 The biggest issue in simply using blood tests to determine if a man is testosterone deficient is that the blood levels will vary greatly form one day to the next.  Even if the test is drawn the same time of day on successive days, the blood levels of testosterone can be very different.  This is why a full evaluation that considers the combination of clinical symptoms and blood tests is so important.

 Just as with estrogen replacement therapy in women, however, there has been a great deal of controversy about possible hormone replacement therapy in men.  The chief concern has been worries that testosterone replacement could stimulate heart disease or prostate cancer.  Fortunately, the concerns for both negative side-effects appear to be overblown.  As said, there is growing evidence that testosterone can help protect the heart from cardiovascular disease. 

 The case of prostate cancer is a bit more complicated.  Many treatments for prostate cancer attempts to reduce testosterone to suppress tumor growth.  Obviously, giving testosterone to a man with a prostate tumor is therefore not an option.  The question has been: will testosterone supplements provoke prostate cancer?  Fortunately, the answer appears to be, “No.”[5]  Increased testosterone levels are not linked to higher rates of prostate cancer or more deaths from prostate cancer.  In fact, it is quite the opposite.  Men with higher amounts of testosterone show lower incidence and mortality for prostate cancer, as well as for cardiovascular disease and for all causes of death[6].

 The decline in late-life androgen production is a very real and very treatable phenomenon.  Unfortunately, 50 years of debate about whether there is such a thing as “male menopause” has obscured these hormonal changes.  There is a growing realization that proper evaluation and treatment of testosterone deficiency is both appropriate and beneficial for many men.  For optimal results, I recommend seeking out a physician experienced in bioidentical hormone replacement therapy within a broader program addressing overall lifestyle modification and enhancement.

[2] Liu PY, Death AK, Handelsman DJ. Androgens and cardiovascular disease. Endocrine Review. 2003 Jun;24(3):313-40.

[3] 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

[4] Hyde Z, Flicker L, Almeida OP, et al. Low Testosterone Tied to Frailty in Older Men.  J Clin Endocrinol Metab. Pub Online April 24, 2010; doi:10.1210/jc.2009-2754

[5] Eaton NE, Reeves GK, Appleby PN, Key TJ. Endogenous sex hormones and prostate cancer: a quantitative review of prospective studies. British Journal of Cancer. 1999 Jun;80(7):930-4

[6] Khaw, KT, Dowsett, M, Folkerd E, et al. Endogenous testosterone and mortality due to all causes, cardiovascular disease, and cancer in men: European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) prospective patient study. Circulation. 2007 Dec 4;116(23):2694-701.

 Do our hormones decline because we get old?  Or do we feel old because our hormones decline?  One of the most pronounced health issues facing boomer men is plummeting testosterone levels.  Beginning in their mid to late 30’s or early 40’s, men lose 1% – 3% of their testosterone per year.  There is no abrupt drop off like women in menopause, but the decline for men continues throughout the remainder of their lives.  Insufficient testosterone levels can lead to a number of debilitating conditions with signs and symptoms including erectile dysfunction, low libido, impaired physical performance and frailty, decreased vitality, reduced bone mass, decreased muscle mass and strength, unfavorable lipid profiles, increased fatigue, sleep disturbances, depression, anemia and impaired cognitive function.

 With studies like the recent Massachusetts Male Aging Study[1] demonstrating an overall reduction in average testosterone levels for American men over the last 30 years, and studies linking lower testosterone to increased risk for cardiovascular disease, obesity, type-2 diabetes, metabolic syndrome, osteoporosis and premature death, there is renewed interest in testosterone therapy for men to improve quality of life.  The Health in Men Study published this April found that older men with relatively low testosterone levels were more likely to be frail or to become frail over the next several years than men with normal testosterone levels.[2]

 The National Institutes of Health and the National Institute on Aging have undertaken a new study called the Testosterone Trial.[3]  This study began in 2009 and seeks to determine if testosterone treatment for one year compared to placebo will be associated with improved walking speed, improvement in sexual activity, improvement on the vitality scale and verbal memory test, and anemia correction.  It will include 800 men aged 65 or older with low testosterone and one or more of these symptoms: impaired walking or physical function, low vitality, cognitive dysfunction, low sexual function, or anemia.

 It is estimated that more than 4 million men over age 45 in the United States have low testosterone, and only a small percentage are receiving treatment.  Many physicians hesitate to offer testosterone replacement to men with the misguided belief that testosterone causes or fuels prostate cancer.  Unfortunately this misconception has been perpetuated in medicine for so long that it had come to be accepted as true.  It certainly seems counterintuitive to link the two when the incidence of prostate cancer increases with age, while testosterone levels decrease.  Several extensive reviews of the medical literature, including an analysis out of Harvard University have revealed no such association.   Lack of consensus about the diagnostic criteria also causes confusion.  Many doctors will not treat men with all of the symptoms of low testosterone, even if they are near the rock bottom of the normal range, because it is still within that range. Another factor causing apprehension is the abuse of steroid hormones at unnaturally high levels by professional athletes for performance enhancement.

 What is the bottom line?  Any man over 40 or 50 that feels off his game, run down or is experiencing any of the symptoms of low testosterone should have a thorough evaluation.  I recommend seeking out a physician experienced in preventive health and hormone therapy for men.  Rather than narrowly focusing on just your hormone levels, a comprehensive program will expose your total health picture and help you move toward achieving optimal health. 

[1] O’Donnell AB, Araujo AB, McKinlay JB. The health of normally aging men: The Massachusetts Male Aging Study.  Exp Gerontol. 2004 Jul;39(7):975-84.

[2] Hyde Z, Flicker L, et al. Low Testosterone Predicts Frailty in Older Men: The Health in Men Study.  J Clin Endocrinol Metab, April 2010

[3] http://clinicaltrials.gov/ct2/show/NCT00799617

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

Many magazine articles, trainers, coaches, and even the recommended heart charts on exercise equipment all suggest that you should exercise at a moderate intensity for long durations.  Conventional wisdom has said that this is the best intensity for two reasons: because you burn more fat at this intensity and because it avoids the dreaded lactic acid buildup.  This conventional prescription, however, is based on outdated ideas about how the body responds to exercise.

Your body can utilize several different fuel sources; carbohydrates, fat and proteins, and varies the proportion of each depending on the intensity and duration of an activity.  For the first couple of minutes of exercise, your body uses something called ATP – the most readily available source of energy.  But your supplies of ATP are limited. After 2 to 3 minutes, your body switches to carbohydrates stored in muscle tissue. This lasts for 15 to 20 minutes before you switch to fat.  Claims that moderately intense exercise burns more fat are based on studies that showed increased consumption of calories from fat over long workout periods.   The idea was to favor “long and slow” exercise, like a marathoner, instead of “short and fast” exercise, like a sprinter.

Research in recent years, however, is showing that the assumptions behind this recommendation are not entirely correct.  To the extent that a person exercising in this range is burning a greater proportion, the effect is small.  But burning fat during exercise is not the way to achieve long term changes in body composition and become leaner.

Moderate intensity durational exercise just doesn’t stress the energy-supplying systems efficiently.  The body has two paths to turn stored energy into work: the aerobic and anaerobic systems.  The aerobic system uses oxygen to break sugars, fats and protein into energy.  Anaerobic system works when not enough oxygen is reaching muscle cells.  You can get a very high-energy output from this system but not for very long.  When you are using your anaerobic system, you are building up reserve capacity in your heart, expanding your lung volume, triggering the production of growth hormone and melting away fat.  Moderate-intensity aerobic training improves aerobic power without changing anaerobic capacity, but high-intensity training improves both anaerobic and aerobic systems significantly[i].

Other drawbacks with this durational exercise method are numerous.  On a psychological level, this type of moderate exercise is monotonous.  This is important because boredom is one reason that people often give for quitting exercise programs.  If the workout is boring, is it any wonder most people consider going to the gym an unpleasant chore?  Higher intensity effort is more challenging and achieves exercise goals in less time.  More intense efforts also require more concentration, creating more interest in the workout.

The most important limitation is that, like crash dieting, “long and slow” exercise can have a counter-productive effect.  Drawing preferentially from fat stores tells your body you need that fat.  The body replenishes these “necessary” fuel stores the next time you eat, and becomes more efficient at both using and maintaining fat.  Top-level endurance athletes expend enough total calories to overcome this handicap, but most of us find ourselves fighting an uphill battle.  Significantly, although they may not accumulate fat, it has been noted that the muscles of marathon runners actually shrink. When the muscle biopsies of marathon runners were analyzed, researchers found their muscle fiber size had decreased and atrophied.[ii]  One has only to look at elite marathon runners to see the paucity of their muscle mass, which can accelerate some negative effects of aging.

We see patients actually gain weight in many long duration, moderate-intensity exercise programs.  Short bursts of exercise tell your body that storing energy as fat is inefficient, since you never exercise long enough to utilize the fat during each session.  Carbohydrates, which are stored in muscle rather than fat, burn energy at high rates. Exercising for short periods will use these carbohydrates and burn much more fat after exercising while you replenish the carbohydrate stores. Short interval exercise maximizes fat “after burn.”  High-intensity exercise stresses both the aerobic and anaerobic systems[iii].  By doing so, it forces the body to recover and rebuild once the effort ends. In fact, studies show that high-intensity short duration exercise increases fat oxidation long after the exercise is done[iv].   The most important effects of exercise occur after, not during, your exercise session.  If done correctly, it can affect your metabolism for several days afterward.

Prolonged endurance exercise causes inflammation and generates free radicals, which cause damage to cells and possibly accelerate aging.   Excess free radicals are especially damaging because they directly attack DNA, which can cause mutations, cell death, or cancer.  Free radicals also cause other unwanted reactions leading to cell damage, such as breaking down cell walls, interfering in protein synthesis, and more.  In such ways free radical damage, also called “oxidative stress” is involved in diseases like atherosclerosis[v] and liver disease[vi]. Free radicals produced by “long and slow” exercise, such as a marathon, can also damage “good” cholesterol (HDL) for up to 4 days after the exercise is over, further increasing heart disease risk[vii].  It is not uncommon for a marathon runner to collapse and die suddenly at an endurance event.

Other unwanted effects of prolonged moderate intensity exercise include things like destruction of bone mass.  Male long-distance runners have lower bone mass and higher bone turnover than control groups, which indicates bone loss[viii].  Another study of male long-distance runners showed that they had lower levels of testosterone and higher levels of the stress hormone cortisol, and that these levels did not return to normal after a break in training[ix].

With all these dire effects, it may be easy to conclude that exercise can do almost as much harm as good.  That isn’t the case at all, of course.  The right exercise for the right person is still an effective part of the lifestyle changes that will help your overall health.  What each person making such changes needs is an exercise program that treats them as an individual.  Books, health magazine articles, etc. give recommendations based on what works for large groups, but what if you do not conform to the “average” person?

The pros and cons of different interventions, and combinations of interventions, should be weighed and balanced.  What we need, in essence, is an exercise prescription.

Fortunately, there are professionals that can help cut through this morass of information.     Once a plan is in place, committing to long-term changes is a key attitudinal adjustment.  By focusing on making changes to the way we treat food and exercise instead of “going on a diet” we are much more likely to be successful.

[i] Tabata I. Nishimura K. Kouzaki M. et al.        Effects of moderate-intensity endurance and high-intensity intermittent training on anaerobic capacity and VO2max. Med Sci Sports Exerc. 1996 Oct;28(10):1327-30.

[ii] Trappe S, Harber M, et al. Single muscle fiber adaptations with marathon training. J Appl Physiol, 101:721-727, 2006.

[iii] Tabata I. Irisawa K. Kouzaki M.     Metabolic profile of high intensity intermittent exercises. Med Sci Sports Exerc. 1997 Mar;29(3):390-5.

[iv] Lee YS. Ha MS. Lee YJ. The effects of various intensities and durations of exercise with and without glucose in milk ingestion on postexercise oxygen consumption.J Sports Med Phys Fitness. 1999 Dec;39(4):341-7.

[v] Victor VM. Rocha M. Solá E. et al. Oxidative stress, endothelial dysfunction and atherosclerosis. Curr Pharm Des. 2009;15(26):2988-3002.

[vi] Muriel P. Role of free radicals in liver diseases. Hepatol Int. 2009 Nov 26. [Epub ahead of print]

[vii] Liu ML. Bergholm R. Mäkimattila S. et al. A marathon run increases the susceptibility of LDL to oxidation in vitro and modifies plasma antioxidants. Am J Physiol. 1999 Jun;276(6 Pt 1):E1083-91.

[viii] Hetland ML. Haarbo J. Christiansen C. Low bone mass and high bone turnover in male long distance runners. J Clin Endocrinol Metab. 1993 Sep;77(3):770-5.

[ix] Houmard JA. Costill DL. Mitchell JB. et al. Testosterone, cortisol, and creatine kinase levels in male distance runners during reduced training. Int J Sports Med. 1990 Feb;11(1):41-5.

New findings from the Massachusetts Male Aging Study confirm that ED may be a warning sign of a future cardiovascular event.[5] These results come from a collaborative study between New England Research Institutes, the Division of Cardiology, San Francisco General Hospital and the University of California, San Francisco which tested whether ED can be used to reclassify patients according to their future risk of developing cardiovascular disease beyond traditional risk factors (such as smoking, high blood pressure, high cholesterol, obesity, diabetes and physical inactivity).  After following 1507 men, aged 40-70, who had complete risk factor data available for more than 10 years, it was determined that ED predicted the development of cardiovascular disease (CVD) independent of age, traditional risk factors and Framingham risk score.   Men with ED had a 40% higher risk of developing cardiovascular disease than men without ED.

Looking at the Framingham risk score, which provides a 10-year estimated probability of a cardiovascular event, more than double the study participants with ED were in the highest risk category compared to men without ED.  In general, the men with ED were older than men without ED (59 years compared to 53 years), and had higher rates of smoking.  Men with ED also had higher body mass index, lower total and HDL cholesterol and higher blood pressure. All of the study participants were free of cardiovascular disease or diabetes at the start of the study.

Despite the statistical significance of the association between ED and CVD, in this study, ED was no better a predictor of CVD than traditional risk factors.  Although not improving the prediction of cardiovascular disease, the researchers reiterated that the results confirm the hypothesis that ED is a sentinel marker for cardiovascular disease, and these data should help put ED on the minds of physicians and patients.

Men with erectile dysfunction should be examined for testosterone deficiency and the metabolic syndrome, because these conditions commonly occur together.[6] Smokers are significantly more likely to experience ED than non-smokers; twice as likely in some studies.[7] Many risk factor can contribute to ED, including high blood pressure, diabetes, vascular disease, obesity, prescription medications, neurological diseases, depression, stress, physical injury, conflict with your partner and prolonged bicycling.

Other than reducing or eliminating any risk factor for ED, another solution may be found in a recent Finnish study: “Regular intercourse has an important role in preserving erectile function among elderly men…Continued sexual activity decreases the incidence of erectile dysfunction in direct proportion to coital frequency.”[8] Halleluiah!

[2] Thompson IM, Tangen CM, Goodman PJ, Probstfield JL, Moinpour CM, Coltman CA. Erectile dysfunction and subsequent cardiovascular disease. JAMA 2005;294:2996 –3002.

[3] Araujo AB, Travison TG, Ganz PA, et al. Erectile dysfunction and mortality. J Sex Med 2009;6:2445–54.

[4]Inman B, Sauver J, et al.  A Population-Based, Longitudinal Study of Erectile Dysfunction and Future Coronary Artery Disease. Mayo Clinic Proceedings February 2009 vol. 84 no. 2. 108-113

[5] Araujo A, Hall S, et al. Does Erectile Dysfunction Contribute to Cardiovascular Disease Risk Prediction Beyond the Framingham Risk Score?   J Am Coll Cardiol, 2010; 55:350-356

[6]Yassin A.  Low Testosterone May Cause Health Problems That Lead To Erectile Dysfunction.  The endocrine Society. June 2008

[7] He J. Erectile Dysfunction Linked To Smoking.  American Journal of Epidemiology. August 2007.

[8] Koskimäki et al. Regular Intercourse Protects Against Erectile Dysfunction: Tampere Aging Male Urologic Study. The American Journal of Medicine, 2008; 121 (7): 592