Vive La Resistance (Training)!

 

The holidays are over. It’s a new year. The decorations are stored away and the New Year’s resolutions are made. What are the top New Year’s resolutions? According to Forbes magazine, the number one New Year’s resolution for 2024 is to improve fitness and exercise more. That is a worthy goal, but what type of exercise should be targeted in 2024? Another top resolution per Forbes is to lose weight. That is also a good goal, but how long will it take to get the holiday weight off?

 

If you are feeling bloated and have gained weight during this holiday season, you are not alone. A study tracked the change in weight for participants in three countries, the US, Germany and Japan. In these three diverse countries, weight started to go up in November and peaked on New Year’s Day. On average, it took until March to lose the weight gained and get back to the pre-holiday weight. How can holiday weight gain be prevented? One strategy is to have smaller meal portions at the family table and eat fewer desserts. Another is to exercise. It has been shown that people who continue exercise training during the holidays can prevent weight gain.

 

It is established that exercise will help with losing weight. It is established that exercising more is the top New Year’s resolution, but what kind of exercising should be done? Aerobic training has well known benefits. The scientific evidence is vast and consistent in showing that cardio exercise (such as running, cycling, swimming or hiking) has many cardiovascular benefits, in addition to increasing longevity. Therefore, aerobic exercise should be a main component of any exercise regimen. What about resistance training? It has been perceived that aerobic exercise is better than resistance training but in fact each is important. It has been estimated that only 28% of US adults perform any form of resistance exercise. Resistance training lowers the risk of dying from any cause by 15% and lowers the risk for cardiovascular disease and death by 17%. Resistance exercise will lower systolic blood pressure by 4 mmHg and diastolic blood pressure by 2 mmHg. It will lower fasting blood sugar by 2 to 5 mg/dl, increase HDL cholesterol (2 to 12 mg/dl), lower total cholesterol (by 8 mg/dl) and reduce triglycerides (7 to 13 mg/dl). Combining resistance and aerobic training gives even greater benefit in terms of weight reduction, diabetes prevention, cholesterol lowering, cardiovascular disease prevention and mortality reduction. 

 

In addition to cardiovascular prevention, resistance training has another very important benefit. As we age, there is progressive decrease in muscle mass and strength. With age, activities such as standing up, sitting down, climbing stairs and maintaining balance are as important as cardiac fitness.  Most of the loss of muscle mass occurs after age 60. Men will lose, on average, 33% of their muscle mass between the ages of 60 and 97. Women will lose 26%. With the loss of muscle mass and strength, significant health problems may ensue as the risk for falls increases by 60% and risk of bone fracture increases by 84%. Resistance training helps to build and maintain muscle strength. Resistance training improves muscle mass (by increasing leg and total body musculature) and muscle strength (by improving handgrip strength, chest and leg press) as well as overall physical performance (by improving sitting to standing, walking speed). 

 

What does a resistance training prescription look like? Resistance training can include free weights, body weight (for example push-ups, squats), machine weights or resistance bands. Resistance training doesn’t necessarily lead to “bulking up” and can be done without great expense (a gym membership or a major set of weights aren’t needed). Ideally 8 to 10 different exercises involving major muscle groups are done (for example, push-up, squat, abdominal crunch, biceps curl). Each exercise is performed for 8 to 12 repetitions. Weight and intensity can be increased gradually over time. Resistance training should be done two or more times per week for maximal muscle strengthening and cardiovascular benefit. 

 

As we get older, we are limited by our heart and/or our orthopedics. Resistance exercise helps with both. So this year resolve to pump up your fitness, build some muscle, lose weight and improve your cardiovascular profile by incorporating resistance training into your exercise routine. 

 

 

Jolly Old Visceral Fat

 

It is holiday season and no single figure dominates this time of year like Santa Claus. The figure of Santa Claus is likely based on a combination of ancient legends including St Nicholas (a Greek saint known for his gift giving), Father Christmas (England) and Sinterklaas (a Dutch legend). The name “Santa Claus” was first used in the US press in 1773. The caricature of Santa Claus as a jolly, rotund, white bearded, red suit wearing elf was first defined by Thomas Nast (a famous political cartoonist who lived in Morristown New Jersey) in an illustration for Harper’s Weekly in 1863. How rotund is Santa? According to NORAD (the North American Aerospace Defense Command), who tracks Santa’s course across the world on Christmas Eve, Santa is 5 feet 7 inches tall and weighs about 260 pounds. This would put Santa’s Body Mass Index (BMI) at 40.72 kg/m2 which places him squarely in the obese category. How does Santa’s obesity, his round belly and visceral fat affect his risk for heart disease?  Should we be worried about Santa?

 

It is estimated that 42% of the adults in the United States are obese. Being overweight (BMI 25-29 kg/m2) or obese (BMI >30 kg/m2) increases the risk for cardiovascular disease and cardiovascular death. The BMI was invented in the 1830’s by a Belgian astronomer who was trying to categorize different types of people. The mathematical formula for BMI relies on only two variables, height and weight. Since its inception, the BMI (and similar calculations) have been used by insurance companies to calculate the risk of dying. Since 1972, the BMI has been used to define obesity, even though it is not a perfect measure.  Amongst its flaws, it cannot distinguish between fat and muscle. Consider a 6-foot 9-inch 250-pound man. His BMI is 26.8 kg/m2 putting him in the overweight category. However, if this man is a muscular perennial NBA All Star, then no one would consider him overweight. His higher BMI is due to muscle, not fat. Another flaw is that the BMI cannot distinguish between subcutaneous fat (fat deposited under the skin; think “pinch an inch” or those love handles that have popped up over the years) and visceral fat. Visceral fat is fat deposited in and around the organs in the abdomen and chest. Visceral fat poses many more health risks than subcutaneous fat. Visceral fat interferes with blood sugar regulation and lipid storage, leading to diabetes, elevated triglycerides, high blood pressure and subsequent heart disease. Waist circumference may be a better measure of visceral fat than BMI. Obesity is defined by a waist circumference >40 inches in men and > 35 inches in women.  An elevated waist circumference is associated with heart artery disease and increased risk for cardiac death. Body fat percentage is an even better indicator of obesity than body weight or BMI. Body fat percentage greater than 30% in men and 35% in women is considered obese (the acceptable range is 20-29%).

 

The heart is considered a visceral organ and thus prone to fat accumulation. Normally fat is present in two areas in the heart. Epicardial fat is present between the heart muscle and the pericardium (the sac that encompasses the heart). Epicardial fat provides a layer of fat on the heart muscle and around the heart arteries.  It has beneficial effects both anatomically and functionally. It acts as a buffer and provides mechanical protection for the heart arteries. Epicardial fat also secretes a variety of active substances and since it is in close proximity to the heart arteries these substances help in the regulation of the internal environment of the arteries. These fat depots also store fatty acids and act as an energy supplier for the heart. During times of high demand, the fatty acids are released into the heart muscle. Unfortunately, excess epicardial fat increases inflammation which in turn promotes and worsens blockage in the heart arteries and increases the risk for atrial fibrillation.  Pericardial fat is the second type of fat seen in the heart and is located between the two layers of the pericardium (the pericardium surrounds the heart and the visceral layer is adjacent to the heart muscle while the parietal pericardium faces outside the heart). Like epicardial fat, pericardial fat provides mechanical protection for the heart and helps keep the heart contracting smoothly and friction free (you could say the heart is a well-greased machine!). Also, like epicardial fat, an excess of pericardial fat is detrimental. Excess pericardial fat is associated with congestive heart failure. Both types of fat can be detected and quantified by cardiac CT or MRI scan. CT scan for coronary calcium also provides the opportunity to look for excess epicardial and/or pericardial fat.

 

After Santa has given out all of his gifts on Christmas Eve (and eaten a billion cookies in the process), how should we treat Santa’s obesity and visceral fat? Obesity management involves 5 interventions: behavioral changes, nutrition, physical activity, medications and surgery. Lifestyle modifications can produce 5% to 10% weight loss. Newer medications have been quite effective in reducing weight. Semaglutide (Ozempic) can reduce weight by 10-15% while tirzepatide (Mounjaro) can result in 15-20% weight loss. On average, surgical procedures reduce weight by 20-30%, but even greater reductions can occur. Do these weight loss strategies reduce cardiac outcomes and cardiac fat? Surgery reduces the risk for dying from any cause by 37%, heart failure by 54% and heart attack by 37%. Semaglutide has recently been shown to improve cardiac outcomes by 20%, especially in the those with established cardiac disease or diabetes. Lastly weight loss by lifestyle modification or surgery reduces epicardial fat thickness by 9% to 32%.

 

So, this year instead of leaving Santa milk and cookies on Christmas Eve, perhaps a plate of vegetables and a prescription for Ozempic would be better for his health.

 

 

The Trouble With Triglycerides

In the classic Star Trek episode, “The Trouble with Tribbles”, the crew find themselves on an alien planet. A trader gives a tribble to one of the officers, who brings it on board the Enterprise. The tribbles are purring balls of fluff that ease human anxieties. They are instantly loved by the crew. Unfortunately, the tribbles reproduce rapidly, taking over all of the space on the ship and eating all of the food on board. Because the tribbles are killing their hosts, they have to be removed.

 

Triglycerides transport the fat that we eat to the cells in the body to use for energy. Unlike tribbles, triglycerides are not cute and fuzzy, although high levels of triglycerides make the blood look milky and cloudy. Also, like tribbles, as triglycerides accumulate (the blood level goes up) it can kill its host (the risk for heart disease goes up). Elevated levels of triglycerides are either primary (genetic, running in families) or secondary to other medical conditions or lifestyle choices. Secondary causes include type 2 diabetes, thyroid disease, or fatty liver disease. Lifestyle factors include obesity, being sedentary, smoking, alcohol use, or a diet high in saturated fats or processed sugars. Hypertriglyceridemia is defined as blood levels above 150 mg/dl. World-wide more than 25% of people have high triglycerides. High triglyceride levels have been strongly and significantly associated with elevated cardiovascular risk, independent of LDL (“bad cholesterol”) levels. People can have normal or low LDL values, but if their triglycerides are high, they are still at risk for a heart attack. In addition, a very high level of triglycerides is a risk factor for pancreatitis (a potentially life-threatening inflammation of the pancreas). The trouble with triglycerides is how to treat them or whether to treat them at all.

 

The first step in treating elevated triglycerides is lifestyle modification. This starts with reducing excess weight, alcohol intake and dietary carbohydrates. Additional measures include exercise, smoking cessation and diabetes control. Together, these interventions can lower triglycerides by 60%. Medications for high triglycerides include statins, fibrates and omega-3 fatty acids. Certain statins (for example, atorvastatin) lower triglycerides as well as LDL cholesterol and should always be the initial agent chosen. Atorvastatin (Lipitor) reduces triglycerides by about 25%. Fibrates (such as fenofibrate) have the highest potency in reducing triglycerides. However, despite lowering triglycerides by 30-50%, fenofibrates have not been shown to reduce the risk of cardiac events. There are three omega-3 fatty acid formulations in clinical use. These are: eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and icosapent ethyl (IPE, a highly purified form of EPA).  EPA is found in plants and fish. Medications with high dose EPA reduce triglycerides by 14-33%. One study showed that EPA reduced cardiac events by 19%. Another study looked at IPE in patients with heart disease or diabetes on a statin. High dose IPE reduced cardiac events by 25%. However, triglycerides were only modestly reduced in the study and it was felt that other factors improved the outcomes (possibly anti-inflammation or anti-oxidant effects of IPE). On the other hand, a large review of multiple trials did not show a reduction in cardiac events with omega-3 fatty acid therapy. In addition, a study of EPA and DHA did not show a reduction in outcomes. The reason for this discrepancy is currently being hotly debated in the cardiology community. 

  

It is well established that higher triglyceride levels are associated with higher cardiac events. However, while there is strong evidence for lowering LDL (the current principle is lower is better) to reduce cardiac risk, the data regarding triglyceride treatment is less conclusive. So, what should we do about high triglycerides? Should we ignore them and not treat them since there is no therapy that unequivocally reduces outcomes? Should we treat them with our current agents and hope that future research proves these therapeutics useful? Should we beam up to the Enterprise and find a new planet? Right now, there is no definite answer, but a few recommendations can be made. The first and strongest recommendation is to start atorvastatin (Lipitor) in patients with established heart artery disease or high risk for heart artery disease (for example diabetics) and elevated LDL and triglyceride levels. A second recommendation can be made for the high-risk patient (as defined above) who has triglyceride levels above 150 mg/dl and whose LDL is at goal with a statin. This type of patient should be started on high dose IPE. Lastly, patients with triglyceride levels over 300 mg/dl should start fenofibrate to reduce the risk for pancreatitis. What about the lack of data? Never fear, the science officers are combing the galaxy, doing the research, trying to find an answer to the triglyceride question. Stay tuned.

 

My Watch Says I Am in Atrial Fibrillation. What Should I do?

 

Recently there has been an explosion in consumer wearable smart devices. It is estimated that 1.1 billion devices were in use worldwide in 2022. These devices can detect and monitor a variety of health-related parameters including heart rate and arrhythmias (abnormal heart rhythms). Devices include smartwatches worn on the wrist, fitness bands with chest strap, and a stand-alone handheld single lead electrocardiogram (EKG) monitor. Smart devices can monitor heart rate and determine if there is an arrhythmia using two methods. The first method is photoplethysmography (PPG). The second way is to obtain an actual EKG strip, either a single lead or multiple leads, using electrotrodes as would be done with an EKG in a doctor’s office. PPG works by sending light pulses to the skin. The intensity and pulsatility of light reflected from the blood vessels can determine heart rate and algorithms can provide an estimate of whether there is an arrhythmia. Smartwatches such as Apple Watch (series 4 or later) and Samsung Galaxy Watch 3 utilize both PPG and EKG. PPG is used for routine monitoring, but the user can be prompted to obtain a single lead EKG by holding the crown of the watch for 30 seconds. The KardiaMobile device is connected to a phone but is a stand-alone monitor. It has two pads and the user places a finger on each pad to record a single lead EKG. Smartwatches using PPG can accurately detect heart rate, but accuracy drops off with activity.  One study showed a 30% reduction in accuracy during exercise. For a more accurate determination of heart rate with exercise, a chest strap using PPG can be used.  Patients often see their doctor for advice about arrhythmias that are detected on their smart devices. How accurate are the readings? What should one do if the device says there is atrial fibrillation (Afib)?

 

Before diving into wearable devices and Afib, a few words about Afib itself. Afib is a very common arrhythmia. In this condition, the upper chambers of the heart (the atria) fibrillate, beat chaotically, not in a regular coordinated manner. When the atria fibrillate, blood doesn’t flow into the lower heart chambers (the ventricles) efficiently and blood can stagnate in the atria. If blood is not flowing it can form clots. These clots break off and can cause a stroke. To treat this and prevent a second stroke in someone who already has had a stroke, blood thinners are prescribed. How important is the Afib/stroke connection? In a patient with a stroke, or a “mini-stroke” (TIA), a cause for the stroke cannot be found in 30%. This is called cryptogenic stroke, a stroke of unknown origin. It turns out that Afib is a major cause of cryptogenic stroke. If a patient is hospitalized with a stroke and a cause cannot be found, they often are prescribed a monitor to wear for one month to see if they have Afib. If Afib is found, they are prescribed a blood thinner. The use of blood thinners in Afib is quite effective, but comes at a cost. These medications can cause bleeding. In a patient with Afib, who should be placed on a blood thinner? The answer is not easy and there is lots we know, and still lots we don’t know. Some Afib patients are straightforward and should be on blood thinners. These include patients who are known to be in Afib for 48 hours of more. Also, patients with Afib and a history of stroke or mini-stroke should be on one of these agents. Patients with Afib who haven’t had a stroke but who are at high risk for a stroke (older patients, women, diabetics, heart failure patients, hypertensives, and patients with vascular disease) should be on a blood thinner. If a patient is not in one of these categories, how much Afib is needed before committing them to a blood thinner: an hour of Afib? several hours of Afib? a day of Afib? Unfortunately, we don’t yet know that answer, but a recent study did shed some light. The study looked at pacemaker patients without prior history of Afib. A pacemaker can be interrogated and can tell precisely how long a patient has an arrhythmia such as Afib. The study looked at pacemaker patients who had short duration episodes of Afib; the average time in Afib was about three hours. Patients who were given a blood thinner did not have fewer strokes than patients who were not on a blood thinner. In fact giving the blood thinner caused harm, more patients had bleeding. So, putting patients on a blood thinner for short duration episodes of Afib does not prevent strokes and may be causing harm.  We still do not know the burden of Afib necessary to start treating to prevent a stroke. 

 

How accurate are smartwatches and KardiaMobile devices in detecting Afib? More and more studies are being performed to check the validity of these devices. One study found that Apple Watch and Samsung Galaxy Watch were 80% accurate in picking out Afib, while KardiaMobile was 74% accurate. One issue with the devices was the high number of inconclusive tracings: Apple 18%, Galaxy 17%, KardiaMobile 26%. Another study of KardiaMobile also showed 74% accuracy and 16% of tracings could not be classified. The bottom line is that these devices are readily available, not very expensive (KardiaMobile is less than $100), reasonably accurate and the technology will only continue to improve.     

 

So, what should you do if your smartwatch tells you that you are in Afib? First, realize that these devices should only be used as a screening tool. See your doctor, bring your phone or tracings for your doctor to review. Afib should be confirmed with medical grade devices such as a Holter monitor (worn for one to three days) or an event monitor (worn for two to four weeks) or an implantable recorder (used for months to years). Next discuss with your doctor whether you should be on a blood thinner, remembering that short duration episodes of Afib likely don’t need to be treated. However, if you have had a stroke, or mini-stroke (TIA) especially if cryptogenic, then starting a blood thinner may be appropriate. Even if the detection of Afib by your smart device doesn’t lead to a blood thinner, it can make a difference in your treatment plan. Medications may be changed to try to avoid Afib. In addition, triggers for Afib can be discussed and corrected (treating high blood pressure or sleep apnea, decreasing or eliminating alcohol, starting an exercise program or weight loss). Listen to your body and watch your watch.

 

Deconditioning and the Flabby Heart

 

You know the feeling. Every weekend warrior knows the feeling. You spend time building up your exercise capacity by biking, running, swimming, hiking, or going to the gym. Then for some reason (illness, injury, other obligations) you have to stop exercising for weeks or months. When you return to your activity, you are more short of breath, you don’t have the same exercise capacity, and you feel “out of shape”. What happens to the heart during deconditioning (the medical term for “out of shape”)?  Does deconditioning occur with elite athletes or astronauts? Does it happen on weekdays to weekend warriors?

 

The heart is a muscle. With training athletes can build up their arm and leg muscles.  The same process builds up the heart muscle as well. The cardiac effects of long-term exercise include increases in the size of the heart, the thickness of the heart’s muscle and the cardiac mass.  (The heart enlarges to accommodate the increased blood flow during exercise. The walls of the main pumping chamber, the left ventricle, thicken and become more muscular to pump the excess blood.  Cardiac mass is the weight of the heart and represents the long-term effective of blood pressure on the heart). A larger, thick walled heart is called an athlete’s heart. Unfortunately, a thick muscular athlete’s heart resembles a form of cardiac pathology, hypertrophic cardiomyopathy (a congenital abnormality where the heart muscle is very thick and there is a risk for arrhythmia).  Congenital hypertrophic cardiomyopathy is the most common reason for sudden cardiac arrest in the athlete. Athletes are screened to see if they have hypertrophic cardiomyopathy and, if present, vigorous exercise is prohibited. Unfortunately, it is difficult to differentiate between pathologic hypertrophic cardiomyopathy and an athlete’s heart. One way to tell the difference is to have the athlete stop exercising for a period of time, a method called detraining. If the heart muscle reverts to normal thickness during detraining, then it is an athlete’s heart.  Studies on Olympic athletes have shown that after about 12 weeks of detraining left ventricular thickness rapidly decreases (thickness goes down by 15-33%).  In addition, cardiac mass decreases quickly as well, within 4 to 8 weeks. For full regression of left ventricular thickening, detraining should last 6 months.

 

The healthy heart needs exercise, but it also needs gravity. Both of those items are in short supply to astronauts on a long-term space mission. The lack of gravity has the same effect as prolonged bed rest on the heart, worsening the deconditioning that takes place in space.  Studies performed on astronauts who spend months in space show that space flight causes significant cardiac atrophy. After only a few weeks in space, there is a reduction in the heart’s muscle mass. It is estimated that cardiac muscle mass decreases about 1% per week in flight. This deconditioning has obvious consequences for prolonged space missions. A recent study followed astronauts on the International Space Station. The astronauts were in flight for many months and spent 2 hours each day doing endurance and resistance training. Cardiac work load was 12% lower in space than on Earth due to zero gravity and the confines of the station. Despite the lower work load, the astronauts’ heart muscle mass stayed intact. It seems that exercise can preserve the heart’s structure and function offsetting space flight deconditioning. 

 

Most people don’t have to worry about their heart becoming too thick from exercise or losing cardiac muscle mass on a space flight. However, deconditioning occurs in the average person, with changes similar to the detrained athlete or the astronaut in space. Deconditioning is defined as the adaptation of the body to a less strenuous environment and the decreased ability to function with physical exertion. The body resets to a lower level of functioning so that when it is asked to increase physical activity, it is unable to meet the demand. Deconditioning occurs when people stop exercising; the most extreme example is bed rest.  Many studies of patients during bed rest show that skeletal muscle strength is lost rapidly (10-20% in a week, 50% in 3 to 5 weeks). Skeletal muscle mass also decreases 3% within a week of bed rest. In addition, bone density decreases as well. From the cardiovascular standpoint, blood volume goes down and heart rate goes up with bed rest. This means that the body cannot compensate when going from a supine to a standing position; blood pressure drops on standing and patients can pass out. Lastly, bed rest causes cardiac atrophy. With 2 weeks of bed rest, there is a reduction in cardiac muscle mass of 5%, similar to what happens with astronauts in space and the detrained athlete.

 

Can the “weekend warrior”, someone who only exercises one or two days per week, become deconditioned during the work week? Likely this is not the case as loss of cardiac structure and function occurs after weeks to months of inactivity. In fact, a recent study showed that as long as weekend warriors exercised for 150 minutes per week or more, they had similar reductions in their risk for heart attack, stroke, atrial fibrillation and heart failure as people who exercise daily. 

 

You worked hard to build up your exercise capacity. Don’t stop now and let your heart become flabby and deconditioned. Keep active and keep exercising a minimum of 150 minutes per week, even if it is only two days a week.

 

 

 

The Café Coffee Culture and Cardiac Disease

 

Imagine yourself walking down a street in a French town. You spot a picturesque café in the square, perhaps one that had been painted by Van Gogh. People are in the café, relaxed, sipping their coffees. It looks so inviting. You want to join them and order a nice café Americano, but you wonder how good is coffee for the heart? 

 

Before we drip into the medical data, some fun facts about coffee. Coffee grows on a bush and the beans are actually the pit of a berry, which makes coffee a fruit. Coffee has been consumed for about 500 years. In the US, about 85% of adults drink coffee daily, averaging 1.5 standard cups per day. Brazil is the largest exporter of coffee in the world and Finland is the worldwide leader in coffee consumption.Now let’s pour over the physiological effects of coffee. Coffee is not just caffeine; the beans have over 100 active substances which have a variety of metabolic effects. Drinking coffee causes the heart rate and blood pressure to increase. Effective sleep may be suppressed. Caffeine increases catecholamines (adrenaline). Coffee stimulates the electrical system of the heart. For these reasons, many cardiologists recommend decreasing or stopping caffeine use. Is that recommendation justified?

 

Does coffee cause heart arrhythmias?

Doctors have always felt that coffee may increase the number of premature atrial contractions (PACS) and premature ventricular contractions (PVCs).  Increased PACS may result in atrial fibrillation (Afib) while increased PVCS may cause ventricular arrhythmias. A recent study in healthy volunteers showed that coffee did not increase the number of daily PACs, but may increase PVCs. The accumulated medical literature has shown that coffee drinkers have a lower risk for Afib than those who do not drink coffee. Drinking one cup per day lowers the risk for Afib by 20%. The reason for this may be that long-term coffee drinkers develop a tolerance to the electrical stimulating effects of caffeine. However, there is a lot of individual variation in terms of response to coffee. Approximately 25% of patients report coffee as a trigger for Afib. Clearly those patients should avoid it. Similarly, the literature does not show an increase in ventricular arrhythmias with coffee consumption, despite a possible increase in PVCs. This holds true even for patients with history of significant ventricular arrhythmias. It appears that drinking coffee is safe for most patients in terms of their potential for arrhythmia.

 

Is it the caffeine?

Coffee is the most commonly used stimulant in the world. Coffee activates the central nervous system, boosts alertness and has a variety of psychoactive effects. Are these effects due solely to caffeine? In an interesting study people were given coffee or plain caffeine in water and then underwent MRI scans of the brain. The coffee drinkers had a heightened state of preparedness, were more responsive and had higher executive brain functioning than the plain caffeine group. It appears there is more to coffee than just caffeine. 

 

Does coffee raise blood pressure?

The effect of coffee on blood pressure is still not decided. Drinking a cup of coffee will transiently increase blood pressure for about 30 minutes.  Coffee stimulates catecholamines and stimulates receptors in the blood vessels to constrict, causing an increase in blood pressure. However, this is counterbalanced by an increase in nitric oxide, which dilates blood vessels. Over time, the acute effect of a blood pressure bump with each cup is blunted in regular coffee drinkers. In fact, regular consumption of coffee is associated with lower overall blood pressure readings compared to nondrinkers. It appears that coffee doesn’t cause hypertension.

 

What are the other metabolic effects of coffee?

Coffee has both good and bad effects. Regular coffee drinking lowers body fat and reduces the risk for obesity.  In addition, coffee lowers the risk for type 2 diabetes. On the other hand, coffee may increase cholesterol levels. The effect depends on the type of coffee, the degree of roasting and the type of brewing. Boiled, unfiltered coffee (such as Turkish or Greek coffee, made by boiling water with coffee grounds in a pot) raises cholesterol more than filtered coffee. Other nonfiltered coffees, such as espresso, are significantly associated with raised serum cholesterol levels. Filtered coffee can raise cholesterol but not as significantly as unfiltered coffee. There is no increase in cholesterol with instant coffee. It appears that drinking filtered coffee is the safer than alternatives. 

 

Does coffee reduce the risk for cardiac events?

In the literature, coffee drinkers have consistently had a lower risk for heart problems and death. A study from Europe in 2017 showed that drinking 2 to 4 cups of coffee per day reduced the risk of dying by 15%, reduced the risk of cardiac death by 17% and reduced the risk of dying from cancer by 4%. A more recent study confirms and expands these findings. The study followed 500,000 people for 10 years. In people without known heart disease, drinking 2 to 3 cups of coffee per day lowered the risk for heart artery disease, heart failure, stroke and dying from any cause. People withheart disease also showed improved survival and no increased risk for arrhythmias. The relationship held regardless of instant versus ground coffee, or decaf versus caffeinated coffee. The reason for these favorable benefits may be coffee’s metabolic effects (lower risk for obesity and diabetes), as well as coffee’s anti-inflammatory and anti-oxidant properties. In addition, coffee drinkers consistently do more physical activity than nondrinkers.  It seems that 2 to 3 cups of coffee per day is the sweet spot, a level of consumption where coffee is not only safe, it may be cardioprotective.

 

It can be concluded that coffee is not associated with high blood pressure, significantly elevated blood cholesterol (if the coffee is filtered) or dangerous arrhythmia. It is associated with a lower risk for obesity, type 2 diabetes, heart artery disease, stroke and death.  So find yourself a nice little café. Order one or two cups of (filtered) coffee. Then sit and watch the world go by, guilt free.

 

 

 

Personality Traits And Cardiovascular Disease

 

One of the classic scenarios in psychological evaluations is to show a person a glass that is 50% filled with water.  Is the glass half full or half empty?  How the person answers that question can determine a lot about their psychological state and may show their risk for future heart disease. 

 

For years the face of heart disease was a man who was highly ambitious, competitive, aggressive, impatient, goal- directed and willing to take risks. The type A personality was originally described in the 1950's by two cardiologists. They went on to show that the type A person had higher levels of cholesterol and a higher risk for heart disease. In addition, they found that the opposite of the type A, a relaxed, easy going, laid-back person, a type B personality, had a lower risk for heart disease. These stereotypes have persisted to this day.  More recent data found no significant link between type A personality and heart disease. However, two components of the type A personality, anger and hostility, are strongly associated with cardiac disease.  Studies have shown that anger and hostility significantly increase the risk for cardiac events in healthy people as well as those with established heart disease.  Anger causes excess catecholamine (adrenaline) release, an increase in heart rate and elevated blood pressure which can lead to angina and a heart attack. An outburst of anger is a well-established trigger for an acute heart attack. Chronic anger and hostility lead to the initiation and progression of blockages in the heart arteries, especially in young men. A new personality type was identified in 2000 and named type D (or “distressed”) personality. The type D personality has two components. The person exhibits negative emotions (anxiety, worry, neurotic) and social inhibition (can’t express emotions, thoughts or behaviors in a social situation). It is often associated with anger, hostility and social isolation as well. The type D personality is associated with cardiac disease including angina, heart attack and an increased risk for cardiac death

 

Neuroticism is another personality trait tied to adverse cardiac disease. Neurotic individuals have emotional instability, difficulty handing stressful situations and “fly off the handle” when under pressure. On the other hand, those with low neuroticism scores are more emotionally stable, calmer, even-tempered and less reactive to stress. Individuals with high neuroticism scores have more anxiety, moodiness, fear, anger, frustration, pessimism, and loneliness than those with lower scores.  They often turn to maladaptive behaviors (substance abuse, alcohol). In addition, people with high neuroticism scores were more likely to develop atrial fibrillation and to be diagnosed at an earlier age then those with lower scores. 

 

On the other hand, certain personality traits are cardioprotective. These include optimism, conscientiousness, openness to new experiences and curiosity.  Optimism is defined as the expectation of good things in the future (while its opposite, pessimism, is expecting something bad to happen down the road).  Individuals with high optimism scores have lower risk for angina, heart attack, stroke, cardiac death and all cause death. Why is this? Optimists and people with psychological well-being have favorable physiologic parameters including lower blood pressure, better cholesterol levels and less sympathetic activation (lower adrenaline levels).  They smoke less, exercise more, eat better and have less tendency for obesity. In addition, optimists are more likely to seek help in difficult social situations. They have larger and stronger social networks for support. They act on medical advice more readily. Lastly, optimists can weather the harmful effects of stress due to their inner and outer support systems. Meanwhile, pessimism has been shown to increase the risk for cardiovascular mortality.

 

So, when confronted with the question about that glass of water, don’t get angry. Don’t become hostile. Don’t get depressed if you can’t come up with an answer. Look for the positives, try to maintain an optimistic viewpoint and say that it is half full. Your heart will thank you.