Gout: a disease of humans or culture?

In medical school I was taught that gout was a condition caused by uric acid crystals that attack and inflame a joint. Thinking of these sharp crystals stabbing cells in joints such as the big toe still creates for me a mental image of extreme pain.

From Wikipedia

Uric acid is the end-product of purine metabolism.  Purines are organic compounds that are rich in foods such as meat (particularly kidneys, liver and brains) and alcohol.  Many people can have elevated uric acid levels without developing gout, but once the crystallization process begins, it is often a lifelong condition.  The primary cause, I was taught, was secondary to an under-excretion of uric acid by the kidneys, and the treatment was primarily to acutely decrease the pain and inflammation with medications such as colchicine, steroids, or non-steroidal anti-inflammatories, and then try to reduce the occurrence of gouty attacks with medications such as allopurinol.

Further, as it was more common with diets high in meat products, alcohol, obesity, insulin resistance and kidney disease, it was also advisable to treat these conditions as well.

And this is largely how I still treat gout.

However, I don't remember ever being taught (or myself asking) why we develop these uric acid crystals in the first place. In fact, humans are one of the very few organisms that develop uric acid crystals, or uric acid kidney stones or deposits of uric acid in joints, called typhi. Most other organisms have an enzyme called uricase, which destroys the uric acid, and thus they never have to worry about this condition.

In fact, this uricase enzyme in humans has been effectively disabled by genetic mutations. Why? Many scientists think that there may be many reasons for this.  Uric acid is a very strong anti-oxidant, and it may be beneficial in reducing reactive oxygen species (ROS) that can damage cells and cause premature aging.  It also offers neuroprotection.  Other scientists believe that at one time humans lived in a very low salt environment, and they adapted to this environment by disabling the uricase enzyme. This allowed humans to increase their production of uric acid, which allowed them to gently increase their blood pressure without the use of salt.

However, place these humans in areas with highly processed foods, high in calories and animal proteins, and environments prone to kidney disease (i.e., hypertension, diabetes, smoking), then they will under-excrete the uric acid. Indeed, gout was once referred to as the "disease of the kings" because only the rich could afford meals high in purines such as animal protein and alcohol, particularly wine.  Now, however, gout affects 4% of Americans and has doubled in incidence from the 1960s to the 1990s.  Further high uric acid levels (without actual gout) affect 20% of Americans.

Thus, maybe gout isn't a medical problem of the body, but rather ourselves and our culture not obeying the laws of the body. Maybe the body is trying to tell us to eat a low salt diet, drink plenty of water, and limit its intake of purine rich foods. Maybe we should listen to our body instead of constantly trying to "correct" its "mistakes."

What We Might Learn From Automobile Safety

One of the major advancements in public health has been the decrease in mortality from automobile accidents, as seen in this graph.

This achievement took action on part of engineers, behavioral psychologists, law enforcement, and countless other individuals working together to create a desired effect. For instance, below is a video from the National Highway Transportation Safety Administration (NHTSA) showing the result of a 1959 Bel Air automobile crashing into a 2009 Chevy Malibu. Although the Chevy Malibu is a smaller car, the passenger in the Malibu is much more likely to survive a crash than the passenger in the larger Bel Air. This occurred largely secondary to the impact of improved seat belts, improved crunch zones, and air bags.

Let’s break down how some of this achievement in decreasing automobile fatalities occurred. Here is a graph showing how seat belts (particularly shoulder-restraint rather than lap belts) saved lives, as well as the potential impact from air bags.

 

Further, behavioral modification changes such as greater criminalization of drunken driving have also decreased mortality.

We still have significant challenges, such as the increase in distracted driving by people texting or using their phone to search the internet, the potential increase in death rates from higher speed limits, the potential increase in marijuana-related accidents, and the challenge to decrease mortality from more fuel efficient cars that are often made with less steel. But these are seen as process-oriented problems with a hope for process-oriented solutions.

In short, this improvement in automobile fatalities occurred because many bright people from different fields worked together to help create a desired outcome.

But what would have happened if we just left the outcome to the individual buyer or driver of the car? Would the outcome have been as positive?  What if the buyer were given the option not to purchase that annoying beep when you don’t buckle your seat belt? Or if he/she could have paid a little less money not to have seat belts or air bags?

Yet when it comes to public health, we often state, “Well, it’s up to the individual.” Is this the best way to effect behavioral change? As a country, it is estimated that our obesity rate will be 42% to 50% by 2030. How will we pay for the increased health care costs that wlll result? If we have an outcome we desire as a population, for the individual and society, such as decreased obesity, why don’t we have thought leaders from many disciplines -– healthcare providers, industrial engineers, city planners, nutrition specialists, exercise physiologists, restaurateurs, farmers, basic scientists working on human homeostasis -- all work together to help generate the desired outcome?

Perhaps we may have better opportunity to effect the behavioral change desired if we create cities where people want to walk around, create communities that foster social interaction in healthy behaviors, create more nutritious fast food meals that are satisfying yet low in calories, and work together to decrease the burden for individuals and for society.

Help Your Provider, Help Yourself

I was eating dinner the other day with one of the healthiest appearing 62-year-old women I've ever met. She was vibrant, active and looked 15 years younger than her age. She said that she sees her doctor once a year and every year her doctor appears a little older, a little more harried, and little more distressed. She said, “I just want to give her a hug and tell her everything is going to be okay.”

The truth is that with decreasing reimbursements, liability concerns, office over-head expenses, personal debt concerns, more regulations, the need to see more patients in fewer hours, etc..., many providers feel quite frazzled. I believe some of this stress also occurs from the technological disruption which is occurring in the medical environment. Providers are not Luddites. Most providers I know love using their I-phone, and apps such as Epocrates which allows them to search medications or using web based resources such as E-medicine or Up-To-Date. However, many electronic medical records (EMRs) are not necessarily doctor-patient friendly. Rather, instead of the computer working for the patient and physician (as in the case of Epocrates and Up-To-Date), often providers feel they are working for the computer and they must adapt to it. For instance, here is a discharge note I received from an excellent cardiologist just last week. This is taken verbatim. “Please note that it is difficult to give the exact instructions of amiodarone on our electronic medical record system; but the fact that the patient will take 200 mg twice a day of amiodarone for 1 week followed by 200 mg daily has been explained to the patient and his family members.” It is not the fault of the drug or the physician, but the electronic medical record simply does not allow the input of such directions. Overall, it is a difficult transitions for many providers which I hope will work out for the best, particularly for the patient.

Lastly, new coding guidelines (called ICD-10) require such precision that in the future I am not sure how providers will be able to performs such tasks without either a medical scribe or a more enhanced artificial intelligence build into the medical record. To give an example, below I created a simple medical narrative and how it could be coded with the new ICD-10 guidelines. It could be funny, until you realize all the codes are real.

“John Doe drank a little and bet some money on the 2^nd Annual Llama and Camel Race at the Henderson Race Track. Unfortunately, he drank a little too much, tripped and fell on the driveway outside a local mobile home but was able to regain his balance before falling into a telephone pole and then, catching his balance, falling into it again. Undeterred, he decided to get on one of the llamas himself and ride off into the sunset, but was unfortunately hit by a 1994 Chevy Malibu. Thrown off the animal, he suffered a tri-malleolar fracture and appears to you dishelveled and slightly drunk.”

Now, CODE IT!

Y92024 Drive of mobile home as the place of occurrence of the external cause

W22.02XA Walked into lampost, initial encounter

W22.02XD Walked into lampost, subsequent encountered

V80.919 Hit by motor vehicle while riding an animal

S82.851A Initial encounter for closed fracture of tri-malleolar fracture

R46.1 Bizarre Personal Appearance

Such coding accuracy is often not taught in medical school or residency and requires a great deal of understanding and effort by the provider. Lastly, the simple basic medical narrative which tells of the patient's very real concernces and conditions can get lost.

So, in an effort to “do no evil” as Google might say, using Microsoft Word, my program director, Dr. Michael White, led a simple task force of myself and a college student to create a Microsoft Word template for an individual to construct his/her own medical summary. This can then be handed to the provider by the patient. It's a simple template which allows you to fill in your own medical history. Here is an example.

It can take a little while to accomplish depending upon your medical history but I believe it can be useful for both yourself and for the provider caring for you. One patient gave it to his doctor, and the physician actually started to cry because it was so useful for him and the medical record in general.

I do not know how to embed a formatable Microsoft Word document in Blogger, but if you would like to email me at delippman@yahoo.com with subject line, Medical Record, I will send you a copy for free.

Stress and Health

I am frequently asked if stress causes disease. Stress, I believe, has a huge psychological impact, and maladaptive behaviors in which we often engage in response to stress (such as smoking, overeating, excessive alcohol consumption, excessive rumination, etc...) can have extreme effects on one's physical health. Thus, potential treatment of stress may focus not only on reducing the stress-inducing events themselves, but also on one's response to such an event.

One of the organizations most interested in the physical and psychological impact of stress on the individual is the military. Military soldiers such as special operation forces who have a high probability of being behind enemy lines are often trained in intensely stressful situations with the hope of developing “stress inoculation.” Similar to vaccination theory, in which one is inoculated from a potential disease by vaccination with the virus and allowing one's immune system to fight it, stress inoculation hopes to build hardier soldiers to allow them to survive stressful situations associated with war.

One of the most stressful situations soldiers can experience is a course called Survival, Evasion, Resistance and Escape (SERE) at Fort Bragg's JFK Special Warfare Center. The SERE course is designed to simulate the evasion of an enemy, and if caught, to simulate a prisoner of war experience. Yale University's Dr Morgan, a researcher for the National Center for Post Traumatic Stress Disorder, studied 109 participants in the course.  Dr Morgan, et al. published their work with the title “Hormone Profiles in Humans Experiencing Military Survival Training” in 2000 in the Journal of Biological Psychiatry (2000:47: 891-901). They studied the salivary levels of cortisol and serum levels of testosterone at various stressful episodes of the training. Cortisol is a hormone released from the adrenal glands, which release carbohydrates for use by the brain. Testosterone is the primary male sex hormone.

In examining these individuals during stressful situations, researchers found that cortisol levels increased, while testosterone decreased. There was a change in the cortisol and testosterone during the escape and evasion, but the greatest changes in these hormones occurred when the soldiers were captured and underwent interrogation. During captivity and subsequent interrogation, testosterone levels could decrease to castration levels within 8 hours; the soldiers became effectively sterile during such episodes.

This study and others like it demonstrate that physical and psychological stress can have a profound biochemical effect on the body. It appears that this psychological impact is activated by a small walnut-sized organ in the middle of our brain called the amygdala. The amygdala analyzes for potential threats. If a threat is perceived, then messages are sent to the hypothalamus to release the fight or flight hormones.

From Wiki

It appears that there can be imprinting of a fearful event on the amygdala during a stressful situation. Thus, experiences that remind the amygdala (even unconsciously) of the stressful event can activate the amygdala to send a signal to the hypothalamus to release a cascade of fight/flight hormones. It is similar to someone who is having a panic attack. That person is convinced there is impending doom about to affect them. “Rationality” or “reason” are rarely effective during the acute attack, because one's body is currently being flooded by an activated amygdala subjecting oneself to a cascade of stress hormones.

People can respond to stressful events in different ways.  For instance, many smokers state that they smoke more in response to stress. Smoking releases dopamine, which is a “feel good” hormone. One can understand the desire for the cigarette in the effect that it has on dopamine release. However, when the dopamine wears off, the smoker often feels the need to smoke another cigarette to replenish the dopamine. This often creates a vicious cycle.

Are there other, more healthy means to decrease the impact of an activated amygdala? Actually, our frontal cortex is filled with inhibitory neurons, that, if activated, can calm an over-excited amygdala.  One activity that can help "turn down" the amygdala is meditation.  Meditation activates the inhibitory neurons from the prefrontal cortex and frontal cortex.  When functional MRIs (MRI scans that are performed with radioactive glucose that goes to areas of increased activity) are performed on skilled meditators, the activity in their frontal cortex and prefrontal cortex "light up."

There are various meditative techniques one can use to "silence the amygdala."  Often it is an attempt to decrease the constant inner voice chatter that occurs in our minds, most of which is negative, and allow a more contemplative, passive process.  Dr. Harold Benson, a cardiologist from Harvard, wrote The Relaxation Response in the mid-1970s and still has courses for physicians and other healthcare providers at Harvard.  His technique is at this website.  Christians may find Father Thomas Keating's Centering Prayer helpful; here is a website that offers PDFs that describe his process.  Thich Nhat Hanh, a Buddhist monk who has written extensively on meditation, has a short essay here on one of his simple, yet potentially powerful techniques.  

Center and Balance in Da Vinci's Vitruvian Man

Leonardo Da Vinci's Vitruvian Man has amazed me for at least the past 15 years.  Here is a little video I made to explain some of my reasons and perceptions, particularly from a functional anatomy point of view.

 

 

 

I am not the only individual to believe that there may be physical exercises within Da Vinci's drawings.  Michael Gelb has written several books, and this link has some of the exercises he has developed from the drawing.  http://www.signlanguageofthesoul.com/leonardo.html. 

 

My view is more static.  I simply ask the individual to stand in the "box" position for several minutes or lie down on the floor or the bed in the circular position for several minutes and to truly feel one's center of balance in the body.  Regardless of whether you engage in these exercises, Mr. Gelb's exercises, or simply a thought exercise, I hope the genius of Da Vinci shines through this little video.

Marlboro, Portion Distortion and Marketing Magic

Marlboro.

 

Whether you smoke or not, what do you think of when you hear that word? Cowboys and the American West, right? I grew up in 1970s suburbia and have been on a horse once in my life. I have more to with the American West than Marlboro!

Where does Marlboro come from? Marlboro is owned by a British corporation, Philip Morris. The name comes from a street in London called Great Marlborough on which its factory was first situated.  It originally started as a cigarette for women in the 1920s, and was known with the tagline, Mild as May, because their first “smokeperson” was not the Marlboro Man, but rather the famous movie star Mae West.

As can be seen in the ad, smoking was considered a feminine activity and not considered “manly.” In the 1950s, Philip Morris wanted to change their marketing to men and worked with Leo Burnett of New York  to create the Marlboro Man to market to men. The cowboy was chosen and the rest is history. Instead of thinking of a street in London, England, we associate Marlboro with the American cowboys. That is the power of advertising and brand identification.

Marketing does not take place on a billboard, on a television station, or in a magazine. It takes place in one’s individual consciousness. It creates a mental image that the viewer identifies with or wants to identify with.

As Al Reis and Jack Trout state in Marketing_Warfare (p . 44) “Marketing battles are fought in a mean and ugly place. A place that’s dark and damp with much unexplored territory and deep pitfalls to trap the unwary. The mind is the battleground. A terrain that is tricky and difficult to understand. The entire battlefield is just 6 inches wide. This is where the marketing war takes place. You try to outmaneuver and outfight your competitors on a mental mountain about the size of a cantaloupe. A marketing war is a totally intellectual war with a battleground that no one has ever seen. It can only be imagined in the mind, which makes marketing warfare one of the most difficult disciplines to learn.”

It is the power of advertising to effect behavioral change in an individual and a society that most interests me. Personally, I believe advertising has led to some remarkable changes in American life in terms of one’s health. From my perspective we can see this in how it has changed our social norms.

For instance, I believe the greatest cause of increase in our calories as a country is related to increase in portion sizes. Supersized meals and supersized sodas now look normal. A “typical” (based on RDA values) individual serving size now appears small. This is not because the serving size has changed, but because how we perceive them has changed. A great deal of this was accomplished through very successful marketing by different organizations.  For instance, as detailed in Greg Crister's Fatland. David Wallerstein, who was a director at McDonald's corporation, was first to suggest to the founder, Ray Kroc, to introduce supersized fries.  He argued that it was a values proposition.  People felt (and bought) that they were getting an increased value for the extra money they spent on the larger fries.  The consumer thus doesn't feel they are suffering from gluttony but rather they convince themselves they are being "frugal" shoppers by paying a little more for a much larger portion.  Meanwhile the franchisee is able to spend just a few extra pennies to create the supersized meal, with the extra charge being  primarily pure profit.

This has had a caloric effect on the individual consumer.  From Fatland, p. 28: "By the end of the century, supersizing --the ultimate expression of the value meal revolution -- reigned.  As of 1996, some 25 percent of the $97 billion spent on fast food came from items promoted on the basis of either larger size or extra portions.  A serving of McDonald's French fries had ballooned from 200 calories (1960) to 320 calories (late 1970s) to 450 calories (mid 1990s) to 540 calories (late 1990s) to the present 610 calories (2003).  In fact, everything on the menu had exploded in size.  What was once a 590-calorie McDonald's meal was now...1550 calories.  By 1999 heavy users -- people who eat fast food more than twenty times a month -- accounted for $66  billion of the $110 billion spent on fast food...Kids had come to see bigger everything -- bigger sodas, bigger snacks, bigger candy, and even bigger doughnuts -- as the norm; there was no such thing as a fixed immutable size for anything, because anything could be a made a lot bigger for just a tad more."

We can see this change from  the National Institute of Health Portion Distortion website, regarding how portion sizes have changed over 20 years from 1984 to 2004

Just look at the first picture of the coffee.  I believe it is almost impossible to view the coffee on the left as "small."  However, if we went back 20 years, we may have looked at the coffee on the right as "huge."  The latter view is probably a more correct one from a caloric perspective.  Here are some more examples of portion distortion

 

 

 

 

 

 

 

But how do we go back?  Our appetite in a variety of ways has fundamentally changed, and we've entered a "new normal."  This blog is not a criticism of brand marketing. Rather it is to help us become aware of its impact. We often state how hard it is to effect behavioral change, yet many companies are quite effective at creating it and we may have something to learn from them.

Perhaps we can use similar marketing techniques to create a healthier society, but the question is, how?  This post may lead to more questions in this regard than answers; however, I think it may be beneficial to study how marketers can move products and in so doing effect behavioral change.  It often requires an understanding not of rational concerns, but emotional ones.  We must be able to connect with the individual -- understand and appreciate his/her anxieties, fears and desires.  Perhaps, if we are honest with ourselves, we can learn a great deal from this marketing warfare to truly effect a healthier society.

Is It Cholesterol or Is It Oxygen?

I am virtually a vegetarian. (I eat pizza, which has milk, and had a meatball in New York last summer). However, my cholesterol is high, and I take cholesterol-lowering medication. Cholesterol comes from the animal family, and I eat virtually no animal products, so why would my cholesterol be high?

Approximately 75% of our cholesterol comes from what our liver produces, NOT from what we eat.   An enzyme called the HMG-CoA reductase is used by the liver to create cholesterol.  Medications called statins, which act on this enzyme, can lower one's cholesterol by up to 60%.   By contrast, medications that block cholesterol absorption from our diet will only lower cholesterol approximately 10%.

What exactly is cholesterol, and why, for many of us, does the liver produce so much of it?

To understand cholesterol, we must go back to basic biology and discuss prokaryotes and eukaryotes. Prokaryotes are cellular organisms whose cells do not have a nucleus, and eukaryotes are cellular organisms whose cells have a nucleus and other membrane-bound organelles. Prokaryotes do not have cholesterol, while eukaryotes use cholesterol to form the nucleus and other membrane-bound organelles. The cholesterol allows a stiffness and organization to the cellular membranes. The cholesterol also acts as a means of intracellular transport within the membrane itself. We humans, as well as all mammalians, are eukaryotes. 

Konrad Emil Bloch received the Nobel Prize for Medicine for his work on the biological synthesis of cholesterol in 1964. He noted that the creation of cholesterol required a great deal of energy and oxygen. The creation of cholesterol requires approximately 27 separate processes. He hypothesized that the utilization of oxygen to create cell walls and cholesterol walls was a complex organism's response to an oxygen-rich environment.  From this theory, we understand that cholesterol formation is an ingenious process of using the oxygen for the organism's benefit.

As we age, this cholesterol production can contribute to atherosclerosis through the process of developing an atheroma, or an intracellular lipid accumulation. Here is a nice picture of it from Wikipedia.

Cholesterol is insoluble in water and requires lipoproteins to transport it. Low Density Lipoproteins (LDL) deposit the cholesterol in plaques inside the arterial walls, while High Density Lipoproteins (HDL) act like scavengers and can help remove some of the plaques. The amount of LDL in the human organism is strongly related to cardiovascular risk.

However, it was discovered that it was not just LDL, but the degree of oxidized LDL that correlated with endovascular injury.  Oxidized LDL can damage the endothelial cells and allow cholesterol to build deposits in the subendothelial area (the space right below the endothelium lining the artery). This injury to the endothelial lining allows more cholesterol deposits to be created in the subendothelial area, creating more inflammation. White blood cells known as macrophages, which fight inflammation, try to repair the injury caused by oxidized LDL and consume them, causing “foamy macrophages.” This process is a very aggressive, angry, inflammatory process. If any of the area ruptures, then a blood clot can be formed, as stated in the prior post on coronary artery disease.

This process is known as “oxidative stress.” It is like rust on the bottom of an old car. Oxygen can be a very hungry molecule and has the ability to rip electrons off other nearby molecules. The molecules with the missing electrons are known as free radicals, and they can rip electrons off other nearby molecules, causing a free radical chain reaction.  As ferric oxide eats away at a car, so can this oxidative injury damage the endothelial lining of our cell walls.

As scientists understand more about this inflammatory, aggressive process, more unique treatments are being discovered. For instance, although powerful antioxidants such as Vitamin E and Vitamin C were not necessarily found to be beneficial for decreasing heart disease, other types called polyphenol antioxidants may be quite effective. In fact, in a study in the Journal of Clinical Nutrition, the use of pomegranate juice (a polyphenolic antioxidant) actually reduced atherosclerotic plaque in individuals with carotid artery stenosis. In a study in the journal Atherosclerosis, the addition of pomegranate extract to statins actually reduced macrophage foam cell formation and was felt to potentially decrease atherogenesis.

In short, cholesterol itself is amazing. It plays an essential role in the membranes of animal cell walls. It also is critical in the formation of molecules such as Vitamin D, steroid hormones and bile acids. But it appears intimately associated with oxygen.  Cholesterol may be created as a response to an oxygen-rich environment, and oxidative stress can impact the LDL receptors that carry it and contribute to the creation of atherosclerotic disease.  Perhaps in the future, we may become wiser about various lifestyles that may optimize the benefit of both oxygen and cholesterol without creating a disease process from them.

The Heart of the Matter

"And all of a sudden he just dropped dead. He ran and everything."

My friend told me as we drank in the bar, acknowledging with sorrow and fear the death of a male coworker. It was an acceptance of the toll of heart disease in our country, particularly among two 45-year-old men. According to the Centers for Disease Control, heart disease is responsible for approximately 1 out of 4 (600,000) of all American deaths and 1 out of 3 if you include stroke.  It is the leading cause of death for both men and women. Of these deaths the majority are from coronary artery disease (385,000). There are approximately 715,000 heart attacks a year, of which approximately 190,000 occur in individuals who have had one previously.

Although death from heart disease is a great burden on our population, it has decreased dramatically over the years.

Ford and Capewell, J Am Coll Cardiol. 2007; 50 (22):2128-2132

According to a 2011 article by Ford and Capewell in the Annual Review of Public Health, approximately 44%-76% of this decline appears to be because of prevention (such as smoking cessation) and the remaining from treatment such as coronary care units and rapid cardiac catherization during an acute heart attack.

Heart disease is a particularly sobering situation for men, as it affects us more than women. What man reading this post is as fit as Neil Reid was? He played college basketball for Indiana University in 1999. He died of a heart attack at age 36. Dana Carvey, the famous Saturday Night Live alum, had coronary artery bypass surgery at age 42. James Fixx, marathon runner, died of a heart attack at age 52. Former president Bill Clinton had coronary artery bypass surgery at age 57 and then had cardiac stents placed 6 years later. Personally, I think I will suffer a heart attack some time in my own life. Hopefully, it will just be later rather than sooner (at least from my perspective).

For me, the question is not why do we have so many heart attacks, but rather why don’t they occur even more frequently? There are only three main arteries around the heart (coronary arteries), and each is about the size of a piece of spaghetti. Considering how small these precious arteries are, it’s amazing they function as well as they do. The main arteries are the left anterior descending, the left circumflex and the right coronary artery. Smaller arteries arise from these larger arteries and provide blood flow to the whole heart.



From Wiki


Many people do not understand how most heart attacks occur. Many think that cholesterol clogs up a coronary artery by causing a cholesterol plaque (similar to a clogged pipe drain), leading to a heart attack. Actually, these plaques can often be very small and not cause much occlusion of the coronary artery. A heart attack usually occurs because a plaque int he coronary artery ruptures. The body then tries to repair this rupture. Just like when you cut yourself and your body forms a scab, the body tries to repair the damage caused by the rupture of the plaque by forming a blood clot inside the blood vessel. This blood clot prevents blood from flowing in the blood vessel, and therefore a heart attack occurs immediately.

This is the reason that the first medication given to heart attack victims in the emergency room is blood thinners to help increase blood flow (usually it begins with 4 baby aspirin which the patient chews) followed by a catherization to open up the blood clot, often with a stent, followed by more blood thinners such as Plavix.

Knowing one’s risk factors can help decrease the probability of heart disease. One of the largest public health undertakings to study heart disease began in Framingham, Massachusetts in 1948. The original study involved 5209 men and women and in 1971 it enrolled another 5,124 men and women to study the risk factors for heart disease. This large epidemiological study created the Framingham Risk Score, which allows an individual or a provider to calculate a 10-year risk score for an individual. You can find such a calculator here. The main risk factors are high blood pressure, high blood cholesterol, smoking, obesity, diabetes, and physical inactivity.

One critical element is that these risk factors are additive. Such that if a person smokes, has diabetes and has hypertension, they are at a much greater risk of future heart disease than if that person only had one risk factor.

Whatever one can do to limit the totality of risk factors, the more likely there is to be a favorable benefit.

Lastly, I want to emphasize again that, if at all possible, it is better to prevent heart disease than treat it, particularly in regards to coronary artery disease. If one is having a heart attack and has a stent put in (a wire mesh device that opens the artery), it can, and often is, life-saving and can prolong one’s life. Further, if one is having “unstable angina,” or pain from coronary artery disease that is changing in duration or severity, a stent can also be live-saving.

However, many cardiac stents are not placed for acute heart attacks or unstable angina, but rather for chest pain from stable angina. That is, the pain occurs at specified time and duration, (such as walking up the fourth flight of stairs). The primary purpose of such stents is to decrease pain, NOT to prolong life or prevent another heart attack. It is critically important to understand this, because too many people feel their artery is clogged and, like a plumber, the cardiologist has put in a stent which will open the coronary artery and prevent a future heart attack and prolong life.

There was a large study called the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial in 2007 that enrolled 2,287 individuals, half of which received stents and half of which received medication for chronic stable angina. The follow-up was 4½ years. There was no statistical difference between death, nonfatal heart attack, or stroke (20% in the angioplasty group, versus 19.5% in the medical group). This is what Steve Nissen, a past president of the American College of Cardiology said about placing stents in individuals with chronic stable angina on the PBS Newshour “We know that stents do, in fact, help to relieve chest pain, but they really do not prolong life or reduce the risk of a heart attack in patients that are otherwise stable.”

This all points to the idea that coronary artery disease, like nearly all disease, is a process, not a static event. It is not treated by one pill, or one stent or one "magic bullet." Rather, try to curb the entire process by taking appropriate medications, lowering blood pressure, keeping one’s blood sugar down, and not smoking. And if you have chest pain that you think is coming from the heart, chew several baby aspirin (4 are usually given in the ER) and GET TO THE ER!

Type 2 Diabetes Mellitus -- A Primer

Insulin is a hormone produced by the pancreas; specifically, the beta cells of the pancreas, which are located in an area of the pancreas called the Islets of Langerhans. Insulin allows for the entry of sugar from the blood stream into cells of various organs such as the liver, skeletal muscles and fat tissues to be used as energy. Diabetes Mellitus simply means there is too much circulating sugar in the blood stream either because the pancreas does not produce enough insulin or because the cells stop responding to the insulin and thus glucose cannot enter the cells. Diabetes Mellitus is usually diagnosed by two fasting blood sugars of 126 or greater. It can also be diagnosed by a hemoglobin a1c (a blood test that measures the blood sugar over a 3 month time period) of 6.5 or greater or a glucose tolerance test greater than 200. A normal fasting blood sugar is less than 100. Pre-diabetes is diagnosed with a fasting blood sugar of 101-125. Diabetes Mellitus is the leading cause of blindness, kidney failure, and lower extremity amputations in America. There are two main types of Diabetes, Type 1 and Type 2.

Type 1 Diabetes Mellitus occurs when the islet cells of the pancreas that produce insulin are destroyed (usually by antibodies to attack a virus but which incidentally destroy the islet cells). If the islet cells are destroyed, then the individual cannot create insulin. Without insulin the individual will die, and therefore Type 1 diabetics require treatment with insulin in order to live.

Before Dr. Banting (and Best, and Collip and maybe Macleod) created an injectable form of insulin in 1921, Type 1 Diabetes was a virtual death sentence. Parents would often just watch their children wither away and die. Here for instance is a picture of a 3-year-old child before he was given insulin and 3 months after being on insulin.




From Lilly Archives

  It’s the SAME child, and the pictures are only 3 months apart. If you were this child’s parent, wouldn’t you feel that insulin was miraculous?

However, Type 1 diabetes (or the destruction of the pancreatic islet cells that create insulin) only accounts for approximately 5%-10% of diabetics in America. Most Americans with diabetes have Type 2 Diabetes.

Like obesity, Type 2 diabetes has increased dramatically in our country. Here is a nice graphical map from the Centers for Disease Control showing the increase in diabetes diagnoses and how it correlates with obesity.

The initiating insult in Type 2 Diabetes is usually insulin resistance. That means the cells that receive insulin are resistant to the insulin that the pancreas produces.

Some of the most insulin resistant cells of the human body are seen in the visceral fat. Visceral fat is the fat that surrounds the internal organs such as the heart, the liver, the pancreas and the kidneys. This visceral fat creates the central adiposity that can affect so many of us as we gain weight (“the beer belly”).

To counteract this insulin resistance, the pancreas initially produces more insulin in response. Thus early in the disease process (the pre-diabetic phase) the pancreas actually is producing too much insulin. This can occur 20-30 years before an individual is diagnosed with diabetes. The resistance of this visceral fat is often too great, and the pancreas eventually burns out, losing the ability to produce insulin. It’s like a car running out of gas. In fact, by the time most people are diagnosed with Type 2 Diabetes, the pancreas has already lost 50% of its ability to produce insulin.

One of the most effective ways to treat diabetes is likely to prevent it from occurring, particularly during this pre-diabetic phase.A large trial called the Diabetes Prevention Program, enrolled 3,234 individuals who were overweight and had pre-diabetes. The trial duration was nearly 3 years. Some participants received intensive dietary and lifestyle advice with a desire to exercise 150 minutes a week and lose 7% of their body weight, others received a diabetic drug called Metformin (850 mg twice a day) and a third group was the control group, receiving placebo pills and some basic literature on a healthy diet. Participants in the intensive lifestyle program reduced their risk of developing diabetes by 58% (and by 71% in those over 60 years of age). Approximately 5% of individuals in the intensive lifestyle group developed diabetes compared to 11% of the control group. Participants who used Metformin reduced their risk by 31% with 7.8% of individuals developing diabetes compared to 11% of the control group. Keep in mind that over 3 years the people in the Intensive Lifestyle group, only lost approximately 11 lbs.

Type 2 Diabetes Mellitus does not strike all people or groups equally. Individuals of certain races and nationalities often have increased incidence of diabetes. One of the groups with the greatest incidence of Type 2 diabetes is Native Americans that live in southern and central Arizona known as the Pima Indians. The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)  has studied this group for over 30 years. They have a dedicated section on the Pima Indians here.

A study by Schulz et. al compared adult Pima Indians who live in Arizona to the adult Pima Indians who live in Mexico.  These individuals have the same genetic heritage but a different lifestyle and different environment with a remarkably different effect on their health. 

Of the Pima Indians in America



(NIDDK)


63.8% of males are obese (average BMI of 33.3)
74.8% of females are obese (average BMI of 35.5)
34.2% of males have diabetes
40.8% of females have diabetes





Of the Pima Indians in Mexico

(NIDDK)

6.5% of males are obese (average BMI of 23.8)
19.8% of females are obese (average BMI of 26.3)
5.6% of males have diabetes
8.5% of females have diabetes







The striking difference in diabetes and obesity appears to be related to the different diet and energy activity among the different groups.  One could simply state that the Pima Indians in America eat poorly, don't exercise and get diabetes. Yet, there appears to be more.  Many different populations and groups may have similar body mass indexes to the Pima Indians in Arizona yet they don't have near the rate of diabetes.  In 1962, the geneticist James Neel proposed the "Thrifty Gene" theory.  That is, that certain populations are more apt to store energy.  When they are working and living in a hard and difficult climate, they need the ability to store energy.  This energy can be used during times of difficulty or famine.  However, if you place such individuals in an environment where there is little activity and great amounts of nutrient-poor calories, their body will respond by rapidly absorbing calories from the environment.

Personally, I find James Neel's theory appropriately elegant. This ability to store energy may have led to an advantage for the individual who is living in a difficult environment. It allows the individual to survive harsh environments and gives them the ability to store energy for times of famine. Thus, in some respects, the ability to develop diabetes may be a sign of the strong organism -- an organism that can very effectively store energy. This is not "a problem", or "a disease" of the individual. Rather, it almost becomes a measure of a disease of a culture that doesn't respect the individual organism's ability to effectively store energy.

Look at the desert environment in which the Pima Indians have lived for thousands of years. Over generations they have had to develop the ability to survive the harsh climate. To survive, they may have developed this "thrifty gene" to endure months of famine and hardship. However, if you place such an individual in an environment where there are plenty of low quality food choices, then the organism will adapt by rapidly storing this energy as visceral fat.

Perhaps the problem isn't with the individual who has diabetes, per se, but rather the culture or environment that the individual finds him/herself in. It is like taking a Lamborghini and instead of putting in 93-94 octane you put 87 octane mixed with sugar in the gas tank. The Lamborghini, which requires high octane fuel to keep the car at peak performance, may suffer even more from such a concoction than a Ford Pinto that runs on leaded gas. That doesn't mean the Lamborghini is a more "defective" car, it just means that it uses energy very effectively and requires higher quality fuel to run. If one respects the beauty and power of the Lamborghini, then one might try to optimize the fuel that is placed in it.

Other groups can develop Type 2 diabetes very easily. Individuals from South Asia can have very high rates of Type 2 diabetes, up to 4 times the rates of other ethnic groups. As stated in the last post, there is even a South Asian BMI calculator which defines "overweight" as a BMI of 23.1 to 25 and obese a BMI greater than 25. Again, it seems to be related to their ability to store and develop visceral fat that is resistant to insulin.

The risk for all Americans for developing diabetes in their lifetime is approximately 11% by the age 70. However, there are certain genetic traits that rapidly increase that risk. If an individual has a parent that has diabetes, lifetime risk is approximately 33%. If an individual has 2 parents with diabetes, the risk is close to 50%. Again, certain ethnicities have significantly greater rates of diabetes than other groups. But again, it doesn't seem to be simply genetic. There is a strong environmental element as well. The lack of physical activity coupled with often large portion sizes and calories of poor nutritional value can foster a dramatic increase in diabetes, particularly among certain groups. This has led some researchers to conclude that we live in a "diabetogenic culture," particularly for certain groups.

So where does that leave you, dear reader? Do you have diabetes? If not, what is your risk of developing diabetes? Perhaps if your risk is high or if you have pre-diabetes or diabetes, hopefully some of this information can be empowering. If one does have diabetes or is at a high risk, I think it might be best to view oneself as possibly inheriting a body that can store energy very effectively. To maximize its energy storage ability, it will likely be very beneficial to eat a highly nutritious diet and maintain or create an active lifestyle. This is not to say that this is necessarily an easy process. To effectively tap into the power of a body that effectively absorbs energy means that the individual will have to respect its power and often fight the easy temptation to eat a diet high in processed foods and empty calories.

The Weight of the Matter

The statistics are sobering. Over 1/3rd of us are obese. In 2012, The London School of Hygiene and Tropical Medicine calculated the average Body Mass Index for 177 countries, and America was in the top 5 with an average Body Mass Index of 27.82 (behind Tonga, Micronesia, Croatia and Greece).

From the Centers for Disease Control:
69.2% of adults over 20 years old are either overweight or obese
35.9% of adults over 20 years old are obese
41.8% of 60- to 74-year-old males are obese
36.9% of 60- to 74-year-old women are obese

According to the National Health and Nutrition Examination Survey (NHANES), the average male weighed 166.3 lbs in 1960, and by 2002 he weighed 191 lbs, an increase of nearly 25 lbs. The average female weighed 140 lbs in 1960, and by 2002 she weighed 164.3 lbs. Thus, we live in a country with heavy citizens and one in which, over the past half century, its citizens have become heavier. As they age, they become heavier still.

According to the CDC, obesity is associated with coronary heart disease, type 2 diabetes, hypertension, cancers of the endometrium, breast and colon, dyslipidemia, stroke, sleep apnea, liver and gallbladder disease and gynecological problems such as abnormal menses and infertility. It is associated with medical costs of $150 billion dollars, or 10% of the medical budget. The center has a good video segment on it here

Many Americans don’t realize they are overweight or obese. Harris Interactive performed a poll, and 30% of overweight individuals thought they were normal weight, and 70% of obese individuals felt they were simply overweight. As stated in an earlier blog post, from a medical perspective, obesity is defined by the body mass index (BMI). A BMI of 30 is obese, while a body mass index greater than 25 is overweight. The body mass index was created by Adolphe Quetelet in the 1800s, was advanced by the epidemiologist Ancel Keys in the 1970s, and has been used for population studies for decades.
A visual representation of the Body Mass Index is seen in this chart below:

To use this chart, find your height on the left and your weight on the top and then determine your body mass index. Determine your BMI with minimal clothes and no shoes. A healthy body mass index is considered from 18.5 to 24.9, overweight from 25 to 29.9 and obesity from 30 onwards. A BMI calculator is also located online from the National Heart Lung and Blood institute.

As a simple epidemiological tool, it can give a good deal of information about groups, as higher BMIs are associated with increasing risk of certain disease states, particularly diabetes.  The Harvard School Department of Public Health sent out screening questionnaires to over 51,529 U.S. male health care providers over a 5 year period of time. They also analyzed the data from over 114,000 female nurses.  As can be seen by the graph below, BMI strongly correlated with the risk of developing diabetes, particularly for women.  Even women in the "healthy BMI range" still had a substantially increased risk of developing diabetes if their body mass index was 24 instead of 21.

 Adapted from Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med 1995;122:481-486; and Chan JM, Rimm EB, Colditz GA, et al. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care 1994;17:961-969.

Other weight scales have been used in the past. For instance, in 1942 Louis Dublin, a statistician working with Metlife, examined the mortality and weight of 4 million Metlife subscribers and developed a Desirable Body Weight for men and women. He divided people up into Small, Medium and Large frame based on their skeletal structure. He determined the skeletal size based on the size of the elbow, but you could also estimate skeletal size by wrapping your right thumb and middle finger around your left wrist.  If your thumb overlaps your middle finger, you are small frame, if they just touch then you have a medium frame, and if they don't touch, you are large frame.  His scale was determined with his subjects wearing shoes and 3 lbs of clothes. For the most part, his desirable body weights seem thinner, around a BMI of 21-23. The major criticism of the Desirable Body Weight Scale came from a gentleman named Andres, who stated that it may be a good scale for individuals, but as people aged, more weight may actually be protective from a health standpoint.

1986 Met Life Desirable Body Weight for Women

 

1986 Met Life Desirable Body Weight for Men

Overall, the BMI may be a useful tool to estimate an individual's or country's risk for certain disease states. However, there are potential limitations of the BMI. The BMI does not take into account several factors, such as one's gender, nationality, body composition (such as waist circumference or lean body mass). Not all fat appears to be equal. The visceral fat, the fat in the abdominal cavity around the inner organs (such as the liver, the pancreas, the kidneys) appears to harbor much greater risk in terms of insulin resistance and future cardiac morbidity. Here is an MRI of abdomens of the same waist circumference, yet some individuals have more muscle mass, and some have a great deal more intra-abdominal adipose (fat) tissue -- the white stuff instead of the dense grey muscles. 

(From Wikipedia)

In regards to identify individuals at greatest risk, efforts to determine body fat composition have been undertaken. 

The waist-hip circumference ratio is a bio-metric study to help determine this visceral adiposity. Here is a nice diagram from the International Chair on Cardiometabolic risk to measure one’s waist.

(They also have a good website at www.myhealthywaist.org) The size of the hips is usually determined with both feet together and using a measuring tape around the largest part of the hips. For men, the Waist to Hip ratio should be less than 0.9, and for women, less than 0.85. An absolute waist circumference of 40 inches for men and 35 inches for women also puts individuals at risk for cardiovascular events.

Writing in the American Journal of Epidemiology, researchers determined that waist circumference was more predictive of coronary heart disease among middle aged and older US Men than the BMI alone.

Another concern regarding the BMI is differences across nationalities. In Japan, for instance, a BMI of 25 is considered obese by the Japanese Society of Obesity, secondary to the increased risk of diabetes in Japanese over a BMI of 25. In 2008, Japan instituted a law for workplaces and governmental facilities to measure the waistlines of all adults aged 40 to 74. The cutoff was 33.5 inches for men and 35.4 inches for women. Honestly, how many white or black American males have waistlines less than 33.5 inches? In Silicon Valley, where many people are from South Asia, there is a South Asian Body Mass Calculator created by Sutter Health, which defines healthy weight as a BMI of 18.5 to 23, overweight as a BMI of 23.1 to 25, and obesity as a BMI of > 25. They recommend any South Asian with a BMI over 23.1 to get screened for diabetes, hypertension and hypercholesterolemia. One of the major concerns for the increased rate of disease states at lower BMIs among certain ethnic groups is that they may be more prone to create this visceral fat and thus place them at higher risk of disease. In such cases, a waist to hip ratio may be more accurate in defining risk.
For its own definition of obesity, the American Council of Exercise focuses on total body fat percentage. This is often determined with various measurements such as calipers or bioelectric impedance analysis, which sends a small current through the body to estimate total body fat. By their guidelines:

Description     Women        Men
Essential Fat   10-13%       2-5%
Athletes           14-20%       6-13%
Fitness            21-24%      14-17%
Acceptable      25-31%       18-24%
Obesity          >32%          >25%


So where does that leave us, dear reader? I truly think it depends on knowledge of your own risks. If you are from South Asia or India, a "normal" BMI may place you at significant risk for heart disease compared to a white American. If you are Denver Broncos Corner Back Tony Carter, you may have a BMI of 25.8, but your lean body mass is likely very high, so are you really overweight? While the average American male has gained nearly 25 lbs since 1960, he was much more likely to smoke in 1960, which makes it unlikely that the 1960s male was "healthier" than his counterpart in 2014. The weight we carry, in my opinion, requires awareness of our ethnicity, our waist-to-hip ratio, our waist circumference to help assess our own visceral adiposity and an honest assessment of our risks based on our blood sugar, cholesterol and blood pressure. And, honestly, most of us could stand to lose 5 to 10 lbs, and even such a small amount of weight loss can lead to reduced risks of many disease states.

If you like, you can even evaluate yourself on the London School of Hygiene and Tropical Medicine's Global Fat Scale.

Sources for blog that don't have links (since I can not figure out footnotes...)

http://www.cdc.gov/nchs/fastats/overwt.htm

http://www.cdc.gov/nchs/data/databriefs/db56.pdf

http://usgovinfo.about.com/od/healthcare/a/tallbutfat.htm

http://care.diabetesjournals.org/content/17/9/961.full.pdf+html  (good article...)

http://annals.org/article.aspx?articleid=708530

http://aje.oxfordjournals.org/content/141/12/1117.short

Anatomy of a Cigarette

My earlier posts introduced continuous quality improvement concepts, which can hopefully be used to effect behavioral change for healthier living. The next few posts will delve into various disease states and various agents that can promote disease states. This post deals with smoking.

According to the Centers for Disease Control, smoking cigarettes is responsible for nearly 90% of all lung cancer deaths in men and 80% of all lung cancer deaths in women. According to the Department of Health and Human Services, over 20% of all coronary heart disease deaths are attributable to cigarette smoking. According to the National Cancer Institute, among current smokers, over 50% of all deaths (both men and women) are attributable to smoking cigarettes. Most smokers know many of the health consequences of smoking, but they continue to smoke. Why? I hope this post may elucidate some of the possible reasons.

“The cigarette is ... among the most awe-inspiring examples of the ingenuity of man....The cigarette should be conceived not as a product but as a package. The product is nicotine....Smoke is beyond question the most optimized vehicle of nicotine and the cigarette the most optimized dispenser of smoke.”

To me, those few simple sentences speak volumes. They were written in 1972 by a Philip Morris senior researcher named William Dunn. Those words express why cigarettes fascinate me. I am an internal medicine physician with a strong interest in smoking cessation, but I find myself continually amazed by a simple cigarette.

I view cigarettes as exquisite nicotine delivery systems.

The middle of a lit cigarette can reach over 1,000 degrees Fahrenheit. This heat generates a smoke that allows almost instantaneous absorption of nicotine as it passes through the mucous membranes of the mouth. Further, the nicotinic effect of smoking can be auto-regulated at the will of the smoker -- that is, he can take short, frequent puffs or long, "satisfying" draws. He can extinguish it when he desires. What other drug can be so instantly regulated by the user?

Then there are the cigarette additives: ammonia, for example. Ammonia is a "base" substance. That is, it makes its environment less acidic and more basic. As smoke is inhaled, ammonium compounds neutralize the natural acidity of the mouth from a pH of around 6.8 to a pH of between 7 and 8. This increase in the mouth pH allows for more nicotine, which is also a basic substance, to be absorbed through the mucous membranes. Thus, by adding ammonium compounds, it is possible to "free the base" of nicotine, giving the smoker a much stronger "hit" of nicotine. With ammonium compounds, nicotine can be “free-based,” much the way cocaine is free-based with baking soda.

And ammonia is only one of hundreds of chemicals in a cigarette. There's menthol, which anesthetizes the back of the throat, allowing greater ease of smoking; cocoa, which opens up the lung airways and allows for deeper inspirations; and various sugars and sweeteners, which can soften and improve the taste of a cigarette.

Further, nicotine is incredibly addictive. In fact, according to the National Institutes of Drug Abuse, nicotine is more addictive than heroin or cocaine. This can make "breaking the habit" much harder than it seems.

I think an understanding of some basic pharmacology can help the smoker who decides to quit. Nicotine lasts in the body for six weeks. That is why nicotine patches use step-down approaches over a six-week period of time. And that is one reason why six weeks is considered a critical time-period to be smoke free, because by that time all the nicotine is effectively out of one’s system.

And that’s just the power of nicotine.

But, although the physical addiction to cigarettes can be very strong, the psychological addiction can be even stronger. Most people don’t just "smoke" cigarettes. Rather, they are smokers. Smoking changes their identity. And, I feel, this is why many people who desire to quit can break the incredible physiological addiction and be smoke-free for six to 12 weeks, but find it much more difficult to be smoke-free for a year or a lifetime. Ultimately, the smoker has to see herself a non-smoker. This is really a change in self-identity.

The ex-smoker not only has to resist the urge of a cigarette for the rest of her life, she also has to resist the thought of seeing herself as ever smoking a cigarette again, not after a satisfying meal, not after a stressful experience, and not even after a loved one passes away. Stopping smoking is a life-changing event.

And that’s why I ask smokers not only to set a quit date, but also to set a freedom date. Freedom from the cigarettes that don’t really offer stress relief or pleasure or satisfaction, but really only offer heart attacks, lung cancer, throat cancer and emphysema. In my opinion, one does not quit smoking; rather one sets himself free from it.

The CDC has a five-step plan to become smoke-free:

1. Get ready.
2. Get support.
3. Learn new skills and behaviors.
4. Get medication and use it correctly.
5. Be prepared for relapse or difficult situations.

1. Get Ready
Set a Quit Date and KEEP IT. Make yourself a diploma. Plan for your quit date by getting rid of all cigarettes and ashtrays, and don’t let people smoke in your home. Then, once you quit, don’t smoke –- NOT EVEN A PUFF!

2. Get Support and Encouragement
Tell your friends and family members that you have quit. This creates a positive peer pressure force to remain smoke free. Further, contact local agencies such as the local Health Department. Find a “stop smoking buddy.”

3. Learn New Skills and Behaviors
Develop action strategies to stop smoking. You may need to distract yourself. Talk, walk, exercise, drink water, but DON’T OVEREAT! If you associate smoking with certain activities, then change your routine –- take a different route to work, eat breakfast in a different place, eat a mint instead of using cigarettes. If you smoke for stress relief, find different activities to supplant this role (a hot bath, exercise, reading, etc.) CELEBRATE your daily successes with at least one enjoyable activity every day.

4. Get Medication and Use It Correctly
Nicotine replacement products, Buproprion SR (Zyban®) or Chantix can double your chances of success. Ask a physician if one of these products is right for you.

5. Be Prepared for Relapse or Difficult Situations
Most people relapse before they quit. Most relapses occur within the first three months after quitting, so be especially vigilant during this time. Avoid alcohol and other smokers. Accept a few extra pounds (most gain less than 10). Finally, accept stressful situations as challenges to see if you can find other means of stress relief besides getting a cigarette.

I have posted an 8 minute youtube video on smoking which you may find informative.

Lastly, for a little personal plug -- I do have a trademarked anti-smoking cartoon character named Jack Jackass. Check the Smoking Mule Fool out at www.JackJackass.com

Your Own Root Cause Analysis

A Root Cause Analysis is a problem-solving method to determine a primary cause of a causal chain which can lead to operating events.

For our purpose, we will define your Root Cause as current aspects of your behavior which impact your health. The more brutally honest you are with yourself, the greater opportunity you will have to induce meaningful change in your own life. The next questions are an overview to help you determine your own root cause of disease processes. These questions are simply an overview and may not be as in-depth as required for your own individual situation.

#1) How healthy are your parents and your siblings?
Your family tree is part of your genetic heritage. As you the share the DNA of your family, if you partake in the same environment and share similar behavioral activities, there is a fair likelihood that you will share similar health care-related events. Looking at organisms to which you are most similar can give you a clue as to a potential causal chain of events which may impact your own future health.

#2) Do you smoke?
This does not have a follow-up question, such as “If so, how much?” Smoking, according to the Centers for Disease Control, is the leading cause of preventable death in America. Smoking is so noxious to individual and public health that the only true treatment for this addiction is cessation.

#3) Are you obese? Are you overweight?
Obesity is defined by the Body Mass Index (BMI), a determination created by Belgian statistician Adolphe Quetelet in the 1800s. It came to fame from the work of the epidemiologist Ancel Keys in 1972 and has become used to determine obesity rates for different societies and countries by the World Health Organization. You can also use an online calculator from the National Heart Lung and Blood Institute. Some fault the BMI because it does not take into account several factors such as visceral adiposity (the belly fat around the organs) or total body fat percentage, but it has been studied and used for so many years, it is helpful to identify one’s own BMI. It is often surprising to realize how little weight is required to be obese or overweight. For instance, a 5 foot 8 inch individual is considered obese with a weight of 197 lbs, and overweight at a weight of 165 lbs.

#4) Do you have hypertension, and/or elevated cholesterol?
The Joint National Committee on the Prevention, Detection and Treatment of High Blood Pressure is a committee which determines blood pressure guidelines. Their latest (JNC 8) was just released in December, 2013 but primarily focused on treatment guidelines for specific blood pressure readings. The prior report, the JNC 7 which was released 10 years earlier in 2003, had the following guidelines.

Normal: <120 systolic (top number) AND < 80 diastolic (bottom number) Prehypertension: 120-139 systolic OR 80-89 diastolic
Stage 1 Hypertension: 140-159 systolic OR 90-99 diastolic
Stage 2 Hypertension: >160 systolic OR > 100 diastolic

Regarding cholesterol results, there are various recommendations on cholesterol lowering medications, yet studies have consistently shown that often the lower the total cholesterol and bad cholesterol (LDL), the lower the risk of cardiovascular disease. As a corollary, an elevated good cholesterol (HDL) can reduce the risk of heart disease. However, merely taking medications to raise the good cholesterol has not shown cardiac protection. Rather, it appears to be much more cardio protective if one can raise the good cholesterol with exercise and activity. A low cholesterol diet to also decrease the total cholesterol and LDL cholesterol also seems to be a good choice for cardio protection.

#5) Do you have heart disease?
Have you had a heart attack, angina (chest pain related to heart disease), a heart rhythm problem or an enlarged heart? The greatest risk factor for a future heart disease is a personal history of a prior cardiac event. In short, if you have had a heart attack, you have a much higher risk of developing future heart disease. For instance, Bill Clinton had coronary artery bypass surgery at age 57 (2004) but then had cardiac stent placements at age 63 (2010).

#6) Do you have diabetes?
Diabetes is most commonly diagnosed by two fasting blood sugars of 126 or greater. However, a normal fasting blood sugar is less than 100. Diabetes is considered a “cardiovascular event equivalent”, meaning that the risk of having a heart attack is similar to the risk of a person that already had a heart attack. If one knows one’s cholesterol, blood pressure, and blood sugar numbers, a very informative calculator has been created by the American Heart Association to allow individuals to obtain their 10 year risk of heart disease. I advise you to play around with the numbers on this calculator. Notice if a 45-year-old man has a healthy body mass index of 23 and has good cholesterol numbers and a good blood pressure, the risk of heart disease may only be 1-2%, but if that individual has diabetes, the risk jumps to > 20%.

#7) Do you have cancer? Or are you at increased risk of cancer?
For nearly all cancers, life expectancy is increased if one catches it an earlier stage. However, I view cancer as a process and the best treatment, if possible, is to avoid its creation in our bodies if at all possible. Knowing the risk factors for various cancers, as well as informed knowledge about appropriate screening tests, can be beneficial. MD Andersen has some nice online calculators to determine survivability of breast, colorectal, esophageal and pancreatic cancers.

#8) Are you sedentary?
The Sedentary Behavior Research Network (did you even know there was such an organization?) defines sedentary behavior as “any waking activity characterized by an energy expenditure ≤ 1.5 metabolic equivalents and a sitting or reclining posture” Without a commitment to activity, it is possible for many of us to exist as sedentary individuals throughout our work and home life. With normal activity, an individual usually walks around 4000-6000 steps a day. It requires a commitment to obtain 10,000 steps a day, which is the amount recommended by many public health agencies. However, more studies are also coming to light stating that the intensity of exercise may also play a role as well. For instance, running may equal 250 to 300 steps a minute.

#9) Are you depressed or stressed?
Depression is commonly based on questions associated with sadness, lack of initiative, excessive feelings of guilt, decreased energy, decreased concentration, change of appetite, and feelings of suicidality. If symptoms are overwhelming, one should seek professional help immediately, but often many of us can harbor simmering feelings of depression. Further, it is not only depression or stress, but the way we react to these feelings (such as overeating, smoking or excessive rumination and sedentary behavior) which can lead to future disease states.

Now, write a short descriptive statement of yourself. Such as, “I am a 44-year-old male non-smoker with a BMI in the obese range. I am sedentary. I do not know if I have high blood pressure and I am not aware of my cholesterol. My mother, who smoked, had a heart attack at 61 and is still living and my father is 75 in fair health on no major medications (but he does not see a physician regularly). Maybe I’m a little depressed.”

Or

“I am a 50-year-old female smoker with a BMI in the normal range. My cholesterol is slightly elevated by my last physical exam and my blood pressure would place me in the prehypertensive range. My father died at the age of 76 (he smoked and had emphysema) and my mother is alive at the age of 80 and is in good health (she stopped smoking at the age of 60). I don’t consider myself depressed. Based on a Framingham Risk Factor calculation, my risk for cardiovascular disease in the next 10 years is 6%.”

A basic root cause of medical illness in both examples is different. While obesity is probably the greatest concern for the 44-year-old male in the former example, in the latter example her smoking is the most likely cause of her ill health.

Now, after identifying the individual behavior, it is best to go a step further. Why is the 44-year-old male overweight? Does he eat at night? Is it stress eating? Does he exercise enough? Why doesn’t he know his cholesterol and blood pressure? Does he live in a state of fog of his overall health? If a root cause of the primary ill health can be identified, action can be taken at both the psychological and physical level to effect change. Asking the deeper questions about why we participate in an unhealthy activity may unlock a psychological answer to help implement the physical changes which are required.

Regardless, once the undesirable activity is targeted, it can help to take some time to research or develop a SYSTEM for behavioral change for yourself. The key point here is to invest in a SYSTEM for change -- using something consistently -- a video, a coach, a book, a youtube, whatever works and whatever makes you accountable to effect this change. I view both health and disease not as static events but as processes. We want to move from disease progression to health progression. Lastly, aspects which can help develop effective systems are often stronger if we have knowledge about the benefits of change. That is why the next few postings will go into detail regarding the earlier questions.