Low fat recommendations have been the mainstream message from such esteemed organizations as the American heart Association, the AMA and the USDA (creators of the food pyramid) among others.  The logic behind this school of thought seems intuitive.  Since increased blood lipids were associated with cardiovascular disease, and, cholesterol is a major component of arterial plaque, reducing dietary intake of saturated fats and cholesterol should remedy the situation.  In addition, fat is more calorie dense than carbohydrates, so eliminating fats from the diet should reduce caloric intake and result in weight loss.   There are, in fact, some clinical studies supporting the benefits of low fat diets on blood cholesterol levels and regression of arterial plaque.  This philosophy has been questioned in recent years.  An 8 year study of postmenopausal women eating a reduced fat diet over 8 years derived no significant benefit relative to cardiovascular disease, stroke, and coronary heart disease or CVD risk factors.[i]  As logical as the low fat diet seemed intuitive is the question:  if low fat was all it was purported to be, why over the last 30 years of low fat promoted diets and low-fat food products of every stripe, have Americans become more obese than ever, and cardiovascular disease remains the leading killer?

 The answer is based more on indisputable physiology and nutrition science than intuition.  Excess carbohydrates cause obesity, lead to insulin resistance, and signals the body to make and store more fats.  High carbohydrate meals, particularly simple, easily absorbed carbs found in sugar, pasta, potatoes or anything made with white flour, stimulate the secretion of insulin.  That insulin causes the carbs to be taken up by cells for energy but if not needed immediately, stored as fat.  That rapid reduction in blood sugar causes hunger which leads to more carbohydrate ingestion and the cycle continues.  As a result, blood cholesterol and triglyceride levels go up, thereby increasing cardiovascular risk.  Earlier this month, a randomized comparative study of low carb and low fat diets concluded that weight loss was comparable between the two but only the low carb diet reduced cardiovascular risk parameters.[ii]  Generally speaking, the low-carb approach is more satisfying and sustainable since it does not require limiting calories.  The fat and protein content keep you feeling full longer obviating the need to count calories.

 Is it just as simple as eating low carb?  Of course not.  No diet strategy taken to an extreme is good.  Individauls metabolize food substrates differently.  The diet that has most consistently been shown to reduce the risk of chronic diseases is a Mediterranean-style diet.  It is not low fat nor strictly low carb.  At Alternity Healthcare we make our recommendations are individualized and based on an extensive diet analysis, a thorough metabolic assessment and nutritional consultation with our registered dietician, Dr. Cassandra Forsythe.  Here are some guidelines:

• Eat real food – something grown or has a parent.  Something your grandparents would recognize as food.
• Eat healthy fats, such as omega-3 fats found in fatty fish (salmon, sardines), olive oil, nuts.  Fats should comprise about 30% of calories.
• Consume most of your carbohydrates from colorful fruit and vegetables
• Eat lean grass-fed meats, free-range poultry and wild caught fish
• Avoid simple, refined carbohydrates, sugars and artificial sweeteners
• Avoid trans fats and processed foods

[ii] Foster G, Wyatt H, et al. Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet. A Randomized Trial. Annals IM August 3, 2010 vol. 153 no. 3 147-157

Cholesterol had become the indisputable villain for heart disease over the last several decades.  After all, it seemed intuitive that cholesterol was the cause of heart disease, since cholesterol made up a large portion of the vascular plaque that characterized atherosclerotic heart disease.  But as the understanding of cholesterol metabolism has become better delineated, the connection between cholesterol and the cause of heart disease has become considerably more tenuous, and the role of statin drugs questionable.

 Data from the landmark Framingham Heart Study revealed that the distribution of cholesterol levels among individuals that had a heart attack and those that did not essentially mirrored each other.  That means at any given cholesterol number, the chance is equally good that you will or will not have a heart attack.  In another very large study looking at the lipid numbers of more than 136,000 people admitted to hospitals across the country with coronary artery disease, more than 70% of those individuals had LDL (“bad”) cholesterol numbers in the “normal” range, and 50% had numbers considered in an “optimal” range.[i]

 Most heart attacks occur in people who have “normal” cholesterol.  So, using cholesterol as the predictor of a future heart attack is not even as good as flipping a coin.   This is borne out by the facts   There has been a concerted and aggressive focus on lowering cholesterol over the last two or three decades, yet heart disease remains the leading killer of people worldwide.  A number of studies have suggested that total cholesterol and LDL levels have been decreasing in the general US population.[ii]  In the United States, heart disease kills more people than the next five causes combined; including all cancers. Cholesterol, it seems, may be found at the scene of the crime but is not necessarily the guilty party.  Many factors go into the development of arterial plaque and heart disease.

 Cholesterol is carried in the blood in a variety of different proteins.  Each of these particles contains cholesterol, triglycerides and lipoproteins.  HDL cholesterol (“good”) has different lipoproteins than LDL cholesterol (“bad”).  Within each class, the particles differ in size and density.  Simply measuring LDL tells nothing about the particle size or number.  The ability of cholesterol to penetrate the arterial lining is dependent on the amount of inflammation present, type of lipoprotein carrying it, the particle size and number rather than on the total level of cholesterol in the blood.  Two of the most important sub-particles are Apolipoprotein (apo) B, a component of LDL and apo A-1, a component of HDL.  Several large prospective studies have clearly shown that Apo B/Apo AI ratio is a superior marker of CHD risk to all conventional markers.[iii]  These measurements can be made using one of several sub-particle tests; the most common being the VAP or LPP tests.

 It has become increasingly clear that chronic silent inflammation plays a critical role in the development of atherosclerotic heart disease.  Markers of inflammation, such as C-reactive protein, homocysteine, interleukin-6 and tumor necrosis factor (TNF alpha) have been associated with an increased risk of heart disease.  According to the American Heart Association, “high-sensitivity C-reactive protein (hs-CRP) levels are an independent marker of cardiovascular disease risk.”[iv]  And, elevated homocysteine levels were associated with increased risk for mortality in patients with coronary artery disease.[v]

 Statin drugs were developed to treat high cholesterol and have been prescribed with alarming frequency to reduce cholesterol to ever lower and lower numbers.  It seems that the process to lower cholesterol has taken on a life of its own, even in the face of scientific reviews questioning the benefit of that approach.  Statin drugs are not without risk.  They frequently cause people taking them to feel fatigued and old.  They deplete coenzyme-Q10, which is central to cellular energy production and heart health.  They can also cause muscle pains and weakness, flu-like symptoms, liver dysfunction, peripheral neuropathy, cognitive impairments, total global amnesia and interfere with neuro-synaptic transmissions in the brain.

 Despite marketing efforts to the contrary, the results of recent cholesterol-lowering drug trials on decreasing morbidity and mortality among persons with or without coronary heart disease (CHD) have been consistently negative.[vi] [vii] [viii] [ix] [x]Although some statin drugs, most notably Lipitor, have been shown to lower heart attack risk and lower cholesterol, it is now believed that those are two independent effects.  The latest scientific information suggests that statins reduce heart attack risk by reducing silent inflammation; the same risk reduction mechanism attributed to fish oil, stress reduction and healthy lifestyles.  All of the latter do not carry the potential risk of statin side effects and are quite a bit less costly to implement.  Several studies comparing omega-3 fish oils to statins demonstrate significant reduction in all cause mortality in heart failure patients taking fish oil, but statins showed no effect on all cause mortality or cardiovascular admissions. 

 One drug, Zetia, illustrates this phenomenon.  It is not absorbed and lowers cholesterol by blocking its absorption in the gut.  It has no effect on blood vessels or systemic inflammation and has failed to demonstrate any effect on the progression of atherosclerosis.  Recent studies have shown participants taking Ezitimibe (active ingredient in Zetia and Vytorin) may actually have an increased risk for cardiovascular events by increasing carotid intima-media thickness.[xi]  So just lowering cholesterol alone has not shown any consistently demonstrated benefit for the prevention of atherosclerotic heart disease.

 Drilling down to the genetic level, carriers of a specific gene variant, KIF6 have been shown to be at significantly increased risk for cardiovascular events.[xii] [xiii]  That gene variant is present in about 60% of the population studied.  Interestingly, those without the KIF6 variant had no significant CHD event reduction with statin therapy.[xiv] [xv]

 One recent pharmaceutical-industry sponsored trial, the JUPITER trial, concluded that giving rosuvastatin (Crestor) to people with normal cholesterol reduced the risk of cardiovascular events by 50%.[xvi]  This reduction was attributed largely to the reduction of inflammation as measured by C-reactive protein.  This sounds impressive until one scrutinizes the raw data.  The study was flawed.  It turns out that the 50% percent risk reduction occurred in less than 3% of the study population.  In other words, there was no effect in more than 97% of participants.  Furthermore, a recent review concluded that “the results of the JUPITER trial are clinically inconsistent and therefore should not change medical practice or clinical guidelines. The results of the JUPITER trial support concerns that commercially sponsored clinical trials are at risk of poor quality and bias. Documentation of the failure of the JUPITER trial to demonstrate a protective effect of rosuvastatin is all the more important as it occurred in the context of the failure of more than 12 other cholesterol-lowering trials published in recent years and in various clinical settings… the time has come for a critical reappraisal of cholesterol-lowering and statin treatments for the prevention of CHD complications. The emphasis on pharmaceuticals for the prevention of CHD diverts individual and public health attention away from the proven efficacy of adopting a healthy lifestyle, including regular physical activity, not smoking, and a Mediterranean-style diet”[xvii]  I couldn’t have said it better myself.

[i] Sachdeva A, Cannon C, et al. Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J, Jan 2009 111-117

[ii] Carroll MD, Lacher DA, Sorlie PD, et al. Trends in serum lipids and lipoproteins of adults, 1960-2002. JAMA 2005;294:1773-81.

[iii] Kulkarni K, Tlwarl H, et al. A Novel Approach to Measure Apolipoprotein B/A1 Ratio Using the Vertical Auto Profile Method. Diabetes Vasc Dis Res 2007;4:266

[iv] Americna Heart Association Scientific Sessions, 2008

[v] Mager A, Orvid K, et al. Impact of Homocysteine-Lowering Vitamin Therapy on Long-Term Outcome of Patients With Coronary Artery Disease. Am J Card. Vol 104, (6), Pages 745-749 (15 September 2009)

[vi] Kastelein JJ, Akdim F, Stroes ES, et al; ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med. 2008;358 (14):1431-1443.

[vii] Cowell SJ, Newby DE, Prescott RJ, et al; Scottish Aortic Stenosis and Lipid Lowering Trial, Impact on Regression (SALTIRE) Investigators. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl JMed. 2005; 352(23):2389-2397.

[viii] Knopp RH, d’Emden M, Smilde JG, Pocock SJ. Efficacy and safety of atorvastatin in the prevention of cardiovascular end points in subjects with type 2 diabetes: the Atorvastatin Study for Prevention of Coronary Heart Disease Endpoints in Non–Insulin-Dependent Diabetes Mellitus (ASPEN). Diabetes Care. 2006; 29(7):1478-1485.

[ix] Tavazzi L, Maggioni AP, Marchioli R, et al; GISSI-HF Investigators. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomized, double-blind, placebo-controlled trial. Lancet. 2008;372(9645):1231-1239.

[x] Barter PJ, Caulfield M, Eriksson M, et al; ILLUMINATE Investigators. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med. 2007; 357(21):2109-2122.

[xi] Tatlor A, Villines C, et al. Extended-release Niacin or Ezitimibe and Carotid Intima-Media Thickness. NEJM Nov 26, 2009 (22) Volume 361:2113-2122

[xii] Bare, L, et. al. Five Common Gene Variants Identify Elevated Genetic Risk for CHD. Genetics in Medicine. 2007: 9(10); 682-689.

[xiii] Shiffman, D, et. al. Association of Gene Variants in Incident MI in the Cardiovascular Health Study. ATVB. 2008;28:173.

[xiv] Iakoubova, O, et al. Polymorphism in KIF6 Gene and Benefit from Statins after ACS. Results from the PROVE IT-TIMI22 Study. JACC. 2008; 51(4): 449-455.

[xv] Iakoubova, O, et al. Association of the Trp719Arg Polymorphism in KIF6 with MI and CHD in 2 Prospective Trials. The CARE and WOSCOPS Trials. JACC. 2008; 51(4): 435-443

[xvi] Ridker P, Danielson C, et al. Rosuvostatin to prevent vascular events in men and Women with Elevated CRP. NEJM Nov 20, 2008. (217) Volume 359:2195-2207

[xvii] Logoril M, Salen P, et al. Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER Controversy.  A Critical Reappraisal. Arch Intern Med. 2010;170(12):1032-1036

After a decade of hype surrounding the project that gave us the full sequence of our human genome, and the regular discovery of genes for killer diseases and complex traits, this unexpected result led many scientists to a stunning conclusion. The seesaw struggle between our genes (nature) and the environment (nurture) had swung sharply in favor of nurture. “We simply do not have enough genes for this idea of biological determinism to be right,” asserted Craig Venter, president of Celera Genomics, one of the two teams that cracked the human genome.

 Although some diseases are inherited through a single genetic mutation — cystic fibrosis and sickle cell anemia are examples — the classic “one gene, one disease” model doesn’t adequately explain the complex interplay between an individual’s unique genetic code and his or her personal history of environmental exposures.  Think of genetics as the “loaded gun” and your environment as “pulling the trigger.”  That is, if an individual with a predisposition to develop diabetes were put in an environment where they gained excess weight, they would likely become diabetic.  Conversely, if that same individual were put in a different environment where weight gain was difficult, they would be less likely to develop diabetes. 

Why is this important?  Obesity, or excess body fat, has been associated with a number of chronic diseases, including an increased risk of heart disease, high blood pressure, stroke, arthritis, depression and seven different cancers.  But of all the diseases associated with obesity, there is no stronger association than the one it has with diabetes.

 Over the last 20 years, there has been a frightening increase in the number of Americans that are obese or overweight.  The National Health and Nutrition Examination Survey has tracked the rise in obese and overweight adults since 1999.   Using Body Mass Index (BMI) data, the survey found that 32% of men and 35% of women were classified as obese, which meant their BMI exceeded 30.  This may be a conservative estimate, since BMI is an inexact measure and may actually underestimate the number of people at risk for adverse health outcomes such as cardiovascular disease, diabetes metabolic syndrome and certain cancers.  Some studies suggest that half of the people with a normal BMI (less than 25) may have an elevated body fat percentage.  Confirming this trend is a recent study by the Centers for Disease Control that estimated the body fat percentage of a typical American woman to be 40% and the typical American man at 28% based on a six year analysis of data.  These body fat measurements are nearly twice as high as what are considered ideal. 

 During that same time period, medical professionals have witnessed an alarming increase in the number of individuals diagnosed with type 2 diabetes.  During these past two decades, diabetes-related deaths climbed by 45% in contrast to declining death rates for cardiovascular disease and cancer.  An estimated 57 million Americans are at risk for diabetes, with another 24 million adults and children already diagnosed with the disease.

 Even as science searches for more clues about the causes of diabetes and medications to prevent it, the vast majority of new cases of the disease in older adults could be prevented by following a modestly healthier lifestyle, according to research led by scientists at the Harvard School of Public Health.  Their findings support the theory that diabetes really is a lifestyle disease. It is largely preventable by modifying five lifestyle factors:  physical activity, diet, smoking habits, alcohol use, and amount of body fat.  Although this study was conducted on adults over age 65, several studies have similarly linked these factors with diabetes risk on an individual basis.

 Two-thirds of diabetics will die prematurely from heart disease or stroke.  Nearly 70% of them will suffer nerve damage that can lead to pain and tingling in the hands and feet, sexual dysfunction, and digestive problems.  Diabetics are ten times more likely to have an amputation and diabetes is the leading cause of blindness and kidney failure.

What can be done about it?  We are not slaves to our genes; just because the gun may be loaded, the trigger never has to be pulled.  Adopting a healthier lifestyle could prevent the majority of type 2 diabetes cases.  It isn’t pure coincidence that the same healthy lifestyle modifications could prevent more than 80% of cardiovascular disease cases and virtually curtail the obesity epidemic.  It is a commitment and a forward-looking approach to living.  How you choose to live now will directly impact how you feel and function in the decades to come.  Start living better.

 We all would like to wrap up aging into one neat package for which a single curative pill or intervention could be discovered (the fountain of youth), but nature is usually not that simplistic.  Any explanation of the aging process must take into account the complexity of maintaining the integrity of genetic material (genome), managing energy production through the master metabolic regulators such as sirtuin genes[1], defending against oxidative stress from reactive oxygen species (free radicals), activation of tumor suppressor pathways and the state of the cytokine (chemical messengers) environment around the cells[2]

 The fundamental defining manifestation of aging is an overall decline in the functional capacity of various organs to maintain baseline tissue homeostasis and to respond adequately to physiological needs under stress.[3]   In most individuals, this decline is gradual over many years, only accelerating in later life.  Moreover, the decline differs among the various organ systems.  A typical element of that decline is a diminished response to physiological insults or stressors rendering the individual increasingly susceptible to disease.  Accordingly, age is the major risk factor for the development of chronic diseases and cancer.  Specifically, between ages 40 and 80, there is a rapid increase in cancer incidence that produces an overall lifetime cancer risk of nearly one in two individuals in industrialized nations. [4]

 In youth, and throughout most of our lives, we have a remarkable capacity for extensive tissue renewal mediated through reservoirs of tissue specific stem cells.[5]  Preserving an adequate pool of tissue stem cells with a robust potential for renewal is vital to maintaining organ function with advancing age.  Research has demonstrated an age-associated decline in functionally competent stem cells in multiple organ systems mediated though several molecular pathways and as a result of diminished mitochondrial function.

 Mitochondria are the cellular “power plants” responsible for converting dietary fats and carbohydrates into ATP; the essential source of energy for the cell.  ATP is analogous to the gasoline that fuels our cars. Without it, our metabolism grinds to a halt, and our cells rapidly die.  In order to achieve and maintain an attractive physique, low body fat, and an overall healthy body it is necessary to have an adequate supply of ATP. The more ATP we have available, the more efficient our cellular metabolism will be, and consequently the aging process slows.  The number and density of mitochondria is not fixed throughout life.  Exercise is the most proven method to improve the function of your existing mitochondria and to stimulate the production of additional mitochondria (called mitochondrial biogenesis), which in turn provides even more ATP for your cells.  Activating sirtuin genes through calorie restriction or resveratrol mimics the exercise effect on mitochondria.  Although creating ATP is essential to life, reactive oxygen species (ROS) or free radicals can and do form during this process, and are potentially harmful if they are produced in excess.[6]  Cells have several antioxidant systems to counteract the potentially harmful effects of ROS.  However, when the over production of ROS exceeds the capability to remove them, oxidative stress ensues, as it is frequently encountered in obesity, aging and many disease states.  The degree of oxidative stress impairs stem cell function and influences the rate of telomere attrition; that is, the rate that telomeres shorten.  This is a case where length really does matter.

 Telomeres are end-caps on your chromosomes that protect the integrity of the genetic material (see “Start Growing Younger”).  Telomeres shorten with each cell division.  In fact, you can judge the age of a cell by mea­suring telomere length. When the telo­mere gets sufficiently short, the cell enters a state of senescence and sometime dies.  So the telomere serves as a molecular counter, or clock, for the cell. But the telomere does more than just tell time. As the telomere shortens, it changes the behavior of the cell and makes the chromosome more susceptible to mutations; the very type of mutation that can lead to cancer. Cells with shorter telomeres begin to slow down. The signals that control hor­mone output and immune function be­come weaker. They start to act old.   We all are well aware that our bodies function less optimally and the incidence of chronic diseases and cancer are more common as we get older.  That is, unless we take an active role in preserving our health; which comes down to preserving mitochondrial function and telomere length.

 Regularly, new studies are published demonstrating the correlation between telomere length and health.  In a recent analysis of a subset of the National Long Term Care Survey, telomere length was associated with disability, functional status, cardiovascular disease and cancer.[7]  A recent study found a correlation between telomere length and years of healthy life.[8] An intriguing connection has also been observed between telomere length and levels of psychological stress.[9]  This is particularly relevant since individuals subject to chronic psychological stress show a shortened lifespan and more rapid onset of diseases typically associated with aging. Researchers in Italy recently found a direct association with short telomeres and an increased risk of developing and dying from cancer.  The risk of dying was eleven times higher in those with the shortest telomeres.[10]

 So what can be done to age more youthfully?  Well, there is no magic bullet.  Regular exercise increases mitochondrial function, stimulates mitochondrial biogenesis and has been shown to upregulate telomerase, thereby increasing telomere reserves.  Exercise also reduces stress, improves mood and when combined with a healthy plant-based diet improves telomere maintenance.[11]  Obesity is associated with shorter telomeres and an increased risk of several degenerative diseases.  Reducing body fat also improves mitochondrial energy production. 

 How the various pathways are interconnected still remains to be conclusively determined.  Mitochondrial dysfunction and an inability to generate adequate amounts of ATP may be the underpinning of the frailty associated with aging.  Intact mitochondria are also crucial for the maintenance of stem cells for tissue regeneration.  But, there is compelling evidence from the study of a wide range of human degenerative diseases pointing to telomere length as the key element driving degenerative pathologies, increasing cancer risk and shortening lifespan.[12]   

How long are your telomeres?  Telomere length testing is available at Alternity Healthcare. 860-561-2294

171–176 (2008).

[2] Finkel, T., Serrano, M. & Blasco, M. A. The common biology of cancer and ageing. Nature

448, 767–774 (2007).

[3] Kirkwood, T. B. Understanding the odd science of aging. Cell 120, 437–447 (2005).

[4] DePinho, R. A. The age of cancer. Nature 408, 248–254 (2000)

[5] Sharpless, N. E. & DePinho, R. A. How stem cells age and why this makes us grow old.

Nature Rev. Mol. Cell Biol. 8, 703–713 (2007)

[6] Balaban RS, Nemoto S, Finkel T. Mitochondria, oxidants, and aging. Cell 2005; 120:483-495.

[7] Risques RA, Arbeev KG, Yashin AI, et al. Leukocyte telomere length is associated with disability in older US population. J Am Geriatr Soc. 2010 Jun 23. [Epub ahead of print]

[8] Njajou, O. T. et al. Association between telomere length, specific causes of death, and years of healthy life in health, aging, and body composition, a population-based cohort study. J. Gerontol. A 64, 860–864 (2009).

[9] Epel, E. S. et al. Accelerated telomere shortening in response to life stress. Proc. Natl Acad.Sci. USA 101, 17312–17315 (2004).

[10] Willeit J, Willeit P, Mayr A, et al. Telomere Length and Risk of Incident Cancer and Cancer Mortality.  JAMA. Vol 304 July 2010

[11] [8] Ornish D, Lin J, et al. Increased telomerase activity and comprehensive lifestyle changes: a pilot study. Lancet Oncol. 2008;9(11): 1048-1057.

[12] Sahin E, DePinho R. Linking Functional Decline of telomeres, mitochondria and stem cells during ageing. Nature. Vol 464, March 2010.

 All mammals have a fight-or-flight response when under stress.  This makes sense from an evolutionary sense – animals that didn’t react to danger didn’t leave behind descendents.  As Stanford University neuro-endocrinologist Robert Sapolsky says, “If you’re a normal mammal, what stress is about is three minutes of screaming terror on the savannah, after which either its over with or you’re over with.” 

 Humans, on the other hand, are not normal mammals.  We are nearly unique in that the fight-or-flight response isn’t only a response to immediate danger.  We experience stress for many more reasons and much more often.  Essentially, our fight-or-flight response is on a permanent hair trigger.  The health consequences of this are stress-related diseases, many of which are rare or even unknown in other mammals.  In fact, Sapolsky has written a book aptly titled, “Why Zebras Don’t Get Ulcers.”

 Whether you are a luckless zebra fleeing on the savannah or a luckless pawn fighting in the corporate jungle, when you perceive danger the brain floods your system with stress hormones like epinephrine, norepinephrine and dopamine.  This is the familiar “adrenaline rush” that makes you ready for whatever action is necessary to respond to the danger.  Cortisol production is increased to modulate how our bodies use various fuel sources.  Any process that is not needed right now for this response is downgraded in favor of those that are.   Testosterone and DHEA levels go down.  If, for example, a leopard appears on a rock above you, your reproductive or digestive systems are put on hold so that blood is sent to the skeletal muscles to fuel escape.  While this is useful in the short term, you can’t sustain these reactions indefinitely and remain healthy.

 The reactions that the fight-or-flight response triggers affect nearly every part of your body. These reactions are started by the release of stress hormones.  These hormones prime the brain, making you more alert and aware of your environment.  They also make more neurotransmitters available in your peripheral nerve system so that nerve impulses to your muscles are faster.  Stress hormones enter the circulation, where they travel to the rest of the body.  The heart beats faster and stronger, breathing goes into overdrive, the digestive system slows down, blood is re-routed from internal organs and other areas to the skeletal muscles, production of saliva and tears stops, the pupils dilate, reflexes are accelerated, and more. 

 The modern human, however, doesn’t face many leopard attacks.  We face infuriating commutes, corporate reorganizations, tax returns, airport security, and a thousand other insults of life in the twenty-first century.  When we encounter one of these stressful situations, our body still reacts in the same way as if there was a leopard lurking above.  In this case, the fight-or-flight response turns from a helpful reaction that can possibly save your life into a negative reaction that can damage your health. 

 What’s more, that zebra on the savannah has to run from danger maybe once a day or even once a week or less.  We experience stress on a daily basis, and many times a day.  Our physiology is just not adapted to the constant demands we place on our bodies.   When we trigger production of stress hormones over a long period, we experience chronic stress. Both the fight-or-flight response and chronic stress are mediated by the same hormonal pathways.  In fact, another name for the fight-or-flight response is the acute stress response.  Although all animals have an acute stress reaction, only humans experience stress on an ongoing, purely psychological basis.   While animals do not normally harbor chronic stress like humans, when chronically exposed under experimental conditions, they get sick just like humans.

 When instead of immediate danger, the body experiences repeated or long-term physical or psychological stress, the hormones produced in the hypothalamus repeatedly or constantly trigger production of cortisol in the adrenal gland.  Chronically high cortisol levels affect a wide array of metabolic processes such as suppressing the immune system and increasing blood sugar.  High cortisol levels from chronic stress are linked to diabetes and obesity.  The combination of high cortisol and low testosterone leads to muscle wasting and can affect bone density.  Although recurrent stimulation of the fight-or-flight response can be one trigger for this type of stress response, it is not the only trigger.

 Acute stress from the fight-or-flight response causes a number of issues throughout the body differing from chronic stress associated with constantly high cortisol.  As Sapolsky says: “You need to turn off anything that’s not essential.  Growth, reproduction,…tissue repair,… do it later if there is a later.”  This is the compromise the fight-or-flight response imposes on your body. 

 Shunting resources from the digestive system, for example, slows down or stops digestion.  It’s not important to be properly digesting food if you’re about to become food, after all.  This can have some surprising effects.  By shutting down the intestines, however, we become more likely to suffer polyps, bowel cancer, diverticulitis, and more.  A bowel that moves is an all-around healthier bowel.  If we keep sending the signals that it should stop what it’s doing, then trouble can follow.

 Chronic stress also causes other conditions as the body attempts to adjust to the frequent stimulation of the fight-or-flight response.  Carnegie Mellon University psychologist Sheldon Cohen has found stress negatively contributes to the course of disease in conditions as diverse as depression, cardiovascular disease, and HIV/AIDS.

 Depression is perhaps the most clearly stress-linked disease.  Major clinical depression is the most common psychiatric disorder in the U.S, with between 32 and 35 million adults meeting the criteria for diagnosis at some point in their lifetime.  It also imposes a huge financial cost on society, with over 50% of cases requiring medical treatment and almost 60% resulting in severe or very severe impairment of ability to work or care for others.  In fact, depression causes more lost work days every year than substance abuse.

 Both the onset and the relapse of depression are associated with stress. Stress events, such as divorce and the death of a loved one, are among the biggest culprits in depression.  Depression also is common among people who have been diagnosed with a serious illness, because physical disease itself is a stressful event that can lead to depression.  In both such cases, the stress event or the diagnoses are treated as dangers and the fight-or-flight system is activated.  In one sense, this makes sense – the death of a loved one or being told you have an awful disease are definite threats to your emotional and physical health. 

 The problem is that you can’t run away from one of these events the way you can run away from our hypothetical leopard.  You still want to, and your body still tries, but there’s nowhere to run to.  So neither the stress nor the stress hormones dissipate and your brain metaphorically stews in a soup of stress hormones.  This interferes with normal neurotransmitter function and literally re-wires the brain.  In extreme cases, the constant psychological stress causes the brain to re-play the stressing event over and over, leading to post-traumatic stress disorder.  All this because your brain acts like a zebra’s.

 Cardiovascular disease is still the number one cause of death in the United States among adults.  Over a quarter of all deaths in the US every year is due to heart disease, and strokes account for another 5%.  The link between cardiovascular disease and stress is also well-established.  In one study, people who experience high levels of workplace stress had a 50% higher risk of cardiovascular disease.  In another, people that experienced physical, emotional, or sexual abuse as children also had higher risks of developing heart disease in later life. 

 The fight-or-flight response is related to these risks because psychological stress increases the physical stress on the heart.  In the fight-or-flight response, the heart rate and blood pressure both increase, and blood vessels constrict.  These reactions place a much higher burden on your entire cardiovascular system.  When these strains are continued for long periods, they can create dangerous changes in the heart, such as inflaming and weakening the heart muscle. 

 The fight-or-flight response also activates pathways that increase the inflammatory response and make coagulation happen faster.  In a true immediate life-or-death situation these prepare the body to deal with the damage that such a situation might inflict.  When these mechanisms are continually, chronically primed, they make blockages and clots in the arteries and veins more likely – possibly leading to strokes, heart attacks, or pulmonary emboli.

 HIV/AIDS is fundamentally different from depression and cardiovascular disease in that no amount of stress will cause AIDS.  If a person has not been exposed to the HIV virus, there is no chance of developing AIDS.  Stress will; however, worsen the course of the disease in a person who has HIV infection.  One study found that for every moderately to severely stressful event experienced while infected with HIV, the risk of progressing to full-blown AIDS increased by 50% and the risk of developing an AIDS-related condition increased by 2.5 times.

 How is the stress response able to change how a virus attacks the immune system?  First of all, stressful events may increase progression of AIDS by taxing an already weakened immune system.  Secondly, stress can reduce compliance with the often-complex antiviral regimens that have been successful in recent years in keeping the disease in check.  Lastly, the fight-or-flight response directly impairs the immune system’s ability to respond.

 The link between stress and cancer is less clear than for these diseases, but still suggestive.  Part of the issue is that cancer is not one disease but many, with different causes affecting different tissues.  Despite this confusing situation, however, it is clear that stress mechanisms negatively impact cancer through affecting antiviral defenses, DNA repair, and cellular aging.  During the fight-or-flight response, these physiological processes are, like digestion, not immediately necessary and therefore downgraded. 

 Stress can also cause us to age prematurely.  Most of us have seen the effects of stress on someone’s physical appearance.  Telomeres are part of our chromosomes that protect the genetic material as the cells divide.  Telomeres are longer when we are young and progressively shorten as we age, with each cell division.  At any given age, the length of our telomeres is the most accurate measure of our biological age.  A study reported in the National Academy of Sciences found that women with the highest levels of perceived stress had telomere shortening consistent with an additional decade of aging.  Whew!

 Triggering the fight-or-flight reaction, of course, requires us to perceive danger in some form.  Perception is a combination of what you know and the signals received from your senses.  Where one person perceives a harmless garter snake, another person may perceive a threatening serpent.  Most of us have some irrational fear.  So the conditions that provoke the fight-or-flight response are not universal, but instead are particular to each individual.  This also implies, of course, that perception can be changed to reduce our susceptibility to having the fight-or-flight reaction triggered. 

 Sapolsky’s studies in the Serengeti have found that production of stress hormones in animals is affected by many of the same things that experts recommend to humans.  For instance, male baboons that spend time with non-fertile females and infants have lower stress hormone levels, while males that cannot tell the difference between displays and threats are twice as stressed.  In other words, males that have multiple social connections and that don’t panic in the face of a threat are better off than their fellow apes.

 This is not very surprising.  Multiple studies have found that people with serious illness do better if they have a deep and dependable support system.  Cancer patients have been best studied in this respect.  In both quality of life and in severity and progression of disease, those patients that have support networks do better.  It does not seem to matter whether this network is family, church, support groups, friends, or other types of support, just that the patient feels able to depend on them.  The support reduces stress, improving health in both sorts of primates.

 Stress reduction is not merely making sure you have friends, of course.  Coping skills, meditation, good diet, exercise, etc. can all reduce your stress.  Self-medication with drugs or alcohol, a high-fat/high-sugar diet, inactivity, smoking, coffee, social isolation, etc. are all poor ways of coping with stress that can worsen the impact of stress on your health.

 Another way of managing stress is through learning more about it.  Learning that a garter snake is not a dangerous, poisonous reptile that demands a panicked response is one example.  It also applies on a more-general level.  The “four A’s” of learning about stress are:

• Avoid the stressor. Learn your limits and stick to them. Learn the people and situations that cause you stress and find alternatives.  Learn what changes you can make to reduce the stress you inflict on yourself.
• Alter the stressor. If you can’t avoid the stressor, learn how to alter it.  It may mean expressing your feelings instead of repressing them or learning to better compromise to the situation.  It may mean learning better time-management or organizing strategies.
• Adapt to the stressor. If you can’t avoid or alter the stressor, you may need to adapt to it.  Learn to change yourself instead of the immovable situation.  Is the situation truly worth getting stressed about?  Are there positive aspects you haven’t focused on?
• Accept the stressor. Finally, there are sources of stress you can’t avoid, you can’t change, and you can’t adapt to.  Learn not to try to control the uncontrollable.  Learn to forgive the slings and arrows of outrageous fortune. 

 Management of stress has no magic wands.  No pill or simple treatment eliminates stress.  If the stressor is there, your body is going to react to it just like a life-or-death situation.  The stress response cannot be shut off completely.  Management is a multi-pronged approach, involving sound nutrition, regular physical activity, psychological support and medical interventions to balance hormones and neurotransmitters. 

 Another reality of stress management is that it is a long-term project.  You will have set backs.  No single setback is going to cause a heart attack or a sudden tumor.  Don’t be discouraged when you feel stressed.  Even the experts have trouble.  Sapolsky himself says: “The reality is that I’m unbelievably stressed and Type-A and poorly-coping.  Why else would I study this stuff eighty hours a week?”

 Sources:

Cohen S, Janicki-Deverts D, Miller GE. Psychological stress and disease. JAMA. 2007 Oct 10;298(14):1685-7.

Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA. 2003 Jun 18;289(23):3095-105.

Leutwyler K. Stress Management Tips from the Serengeti. Scientific American. 2001 Feb 20. 284(2)

National Alliance on Mental Illness, Mental Health In the Workplace. The High Costs of Cutting Mental Health. 2010 (Jan).

National Geographic Television & Stanford University. Stress; Portrait of a Killer. Web resource at http://killerstress.stanford.edu/ Accessed on 5/4/2010

 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

Q. You have brought the SphygmoCor CP system, a new cardiovascular test, to your practice at Alternity Healthcare in West Hartford. What is it and why should people care about it?

A. The SphygmoCor CP system is a painless and non-invasive test that measures critical cardiovascular system parameters that are not available with traditional brachial blood pressure cuff measurements. The CP system allows the non-invasive measurement of the pressure that the heart, brain and kidneys actually experience. Through a complex algorithm, the pressure wave at the ascending aorta is derived from an external measurement of the patient’s radial artery at the wrist. This identifies the central aortic pressure, determines the portion of the pressure attributable to diseased or stiffened arteries, the relative workload of the heart, and the ratio between the heart’s demand for oxygen and the available supply.

These central blood pressure measurements have been shown to be a superior predictor of cardiovascular events. Traditional peripheral brachial blood pressure cuff measurements do not accurately reflect central pressures due to pressure amplification. And, medications have different effects on central blood pressure despite similar reductions in brachial blood pressure.

Incorporating this technology into the cutting edge cardiovascular screening already available at Alternity Healthcare helps me to correctly answer two questions for my patients: (1) Do I have cardiovascular disease that puts me at risk for a heart attack or stroke? (2) If so, what can I do about it?

Q. Is this procedure covered by insurance? How accurate is it? Have long-term results been done on it?

A. The SphygmoCor CP system is an FDA-approved device. Coverage varies with individual insurance policies and carriers. Unfortunately, despite much talk about preventive medicine and the benefits of catching disease at an early stage to reduce overall costs, our healthcare system, and health insurance system, is mostly reactive; focused on treatment of disease rather than prevention. Often people must pay out of pocket for some of the best screening tests to protect their health. There is a difference between the best care for an individual and cost effective care for a population. After all, who is it that suffers the consequences of an undetected disease? Not the insurer.

In clinical studies, it has been favorably compared to pressure measurements with a catheter inside the ascending aorta. The CP system measurements are within a negligible 0.7 mmHg of the internal catheter measurements.

The SphygmoCor CP system has been featured in hundreds of published studies and is used in leading medical centers worldwide, including the Mayo Clinic and Cleveland Clinic, and in pharmaceutical and device clinical trials.

Q. How long has this test been around and why is it now just coming to Greater Hartford? It seems as if a test of this nature might do better in a suburban environment without the vast medical services offered in a major urban center like New York or Boston.

A. Historically, central blood pressure measurements have been used to monitor and treat critically ill patients. It just wasn’t practical to use for everyone because it required an invasive procedure to place a catheter into the heart or aorta. The SphygmoCor CP system uses noninvasive applanation tonometry to capture the central aortic pulse waveform. This technology was developed in 1988 and was FDA approved in 2002.

Change comes very slowly to medical practice. Medicine has developed a lot of conventions that become ingrained beliefs or modes of operation and in many instances continue unchanged even in the face of scientific advancements.

I do not follow your logic regarding location as a determinant of the value of this technology. If anything, this technology may be more available in an urban setting as it is already in use at leading medical centers, and the density of innovative medical practices is likely to be greater. Irrespective of location, measuring central blood pressure is crucial.

At the risk of sounding self-serving, this technology is coming to Greater Hartford now because I recognized its value in the context of my practice philosophy. A year ago I brought another cutting-edge technology to this area; the HeartSmart IMT plus. That CIMT test measures the thickness of the carotid intima media, the innermost layer of the carotid artery where atherosclerosis begins. I was the first physician in CT to make this available in a clinical setting.

Q. Your practice focuses on preventive medicine with what seems to be an emphasis on hormonal deficiencies and the silent inflammations associated with heart disease. Does your practice use traditional health care methods or does it embrace more homeopathic medical treatments?

A. I try to avoid labels, because people tend to have preconceived notions about what any particular label means. I am a conventionally trained, board-certified internist with nearly 25 years of experience treating patients. Over the years, I became increasing disenchanted with the direction of conventional medicine, the focus on elaborate and frequently toxic treatment rather than prevention and the growing gap between the science of medicine and the practice of medicine. Alternity Healthcare is an integrative blending of traditional western medicine with elements of holistic practice.

Prevention of chronic diseases and enhancing quality of life are the core tenets by which I practice. The latest scientific evidence clearly implicates chronic inflammation as a root cause of most chronic diseases, including heart disease, and influences the rate and manner in which we age. Much of the inflammatory response can be managed through appropriate lifestyle modifications. Similarly, hormonal imbalances, not necessarily deficiencies, directly influence the risk for chronic diseases, the expression of those diseases and the quality of life we enjoy. Typically, when hormones are mentioned, most think only about sex hormones; estrogen for women and testosterone for men, or the abuse of growth hormone by elite athletes. There is much more to hormones than that oversimplification. Hormones are the chemical messengers that facilitate communication between our various organ systems. It is the overall balance of our endocrine system that is a key to better health.

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.