Category: Coronary Artery Disease

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The Health Benefits and Risks of Physical Activity, Exercise, and Fitness

Estimated reading time: 20 minutes

“Lack of activity destroys the good condition of every human being, while movement and methodical physical exercise save it and preserve it.”                                                                                                                                                                                                                                                                            — Plato (427–347 BC)

Physical inactivity is a serious health problem worldwide. In contrast, regular exercise is associated with several health benefits. These include lower risks of developing cardiovascular disease, diabetes, chronic lung disease, chronic kidney disease, and some cancers.

In the early 1950s, researchers observed that drivers of London’s double-decker buses were more likely to suffer fatal heart attacks than the conductors. The drivers were sedentary (sitting for more than 90% of their shifts) whereas the conductors were physically active (climbing roughly 500 to 750 steps a day) (1).

Another study published a few years later found that the risk of heart attack was higher among government clerks than physically active postal workers (2).

Consequently, it was concluded that men in physically active jobs have a lower risk of heart disease than men in physically inactive jobs.

In this article, I review the scientific evidence behind the proposed health benefits of physical activity and exercise. I also discuss the role of aerobic and strength training respectively and the health benefits of physical fitness. Finally I address the possible risks of physical exercise and how much activity is needed to gain health benefits.

The term “physical activity” should not be confused with “exercise”, which is a subcategory of physical activity. Here, the term physical activity is used to describe any type of physical movement, including occupational, household, and leisure time activities. Physical exercise, on the other hand, refers to a form of physical activity that is planned, structured, repetitive, and purposeful, aimed at improving and maintain physical fitness (3).

The Scientific Evidence

Most of the evidence for the benefits of physical activity and exercise comes from long-term observational studies.

Observational studies observe the effect of a risk factor (e.g., smoking, high blood pressure, high blood cholesterol or, in this case, the degree of physical exercise), diagnostic test, treatment or other intervention, without trying to influence who is or isn’t exposed to it. Cohort studies and case control studies are two types of observational studies.

Most observational studies show that physical activity and regular exercise are associated with several beneficial health outcomes. In contrast, sedentary behavior is associated with a variety of poor health outcomes.

Unfortunately, this type of evidence is subject to bias. The decision to exercise may simply be one of many choices made in adopting a healthy lifestyle. Hence, the attribution of physical activity and exercise may be confounded by other favorable risk characteristics (4).

For example, individuals who exercise regularly are more likely to adopt a healthy eating pattern and to avoid smoking.

Unfortunately, the evidence of prospective, randomized clinical trials to establish the benefits of physical activity and exercise is limited. Such studies are difficult to perform, largely because individuals initially randomized to physical inactivity may start engaging in exercise and vice versa. The crossover between groups will make the scientific evaluation of the value of exercise almost impossible.

Nevertheless, randomized trials on the benefits of exercise have been performed. However, they have usually involved a small number of patients and the results have been inconclusive.

Most of the evidence for the benefit of physical activity and exercise comes from long-term observational studies. These studies show that physical activity and regular exercise are associated with several health benefits. The evidence from prospective, randomized clinical trials to establish the benefits of physical activity and exercise is limited.

The Role of a Sedentary Lifestyle

One out of five adults around the world is believed to be physically inactive. Physical inactivity is more prevalent among wealthier and urban countries and women and elderly individuals (5).

A sedentary lifestyle can be defined as a type of lifestyle with little or no physical activity. Sedentary behavior includes tasks such as sitting, reading, driving a car, computer use, watching television, office work, and cell phone use.

In 2002, The World Health Organisation (WHO) issued a warning that a sedentary lifestyle could very well be among the ten leading causes of death and disability in the world (6).

Sedentary lifestyle increases all causes of mortality and doubles the risk of cardiovascular diseases, diabetes, and obesity.  It also increases the risks of colon cancer, high blood pressure, osteoporosis, lipid disorders, depression, and anxiety (6).

Approximately 12 percent of deaths in the United States are related to the lack of physical activity.  Furthermore, a sedentary lifestyle may double the risk of coronary heart disease (4).

A large study published in 1993 concluded that physical inactivity was the second leading single external (non-genetic) cause of death in the United States, trailing only tobacco use (7).

Physical inactivity is also associated with an increased risk of worsening of many chronic health conditions. These include cardiovascular disease, heart failure, stroke, certain cancers, osteoporosis, obesity, type 2 diabetes, and hypertension (8).

A recent study found that higher levels of total daily sitting time were associated with an increased risk of cardiovascular disease and diabetes, independent of physical activity.

Numerous observational studies have shown indicators of physical inactivity, such as TV viewing, driving in a car and sitting, are strongly related to the risk for developing adverse blood lipids (9), obesity (10, 11), type 2 diabetes (12, 13, 14), hypertension (15, 16), metabolic syndrome (17), and cardiovascular disease (9, 10, 11, 15).

A recent systematic review found that higher levels of total daily sitting time were associated with an increased risk of cardiovascular disease and diabetes, independent of physical activity (18). The findings support that public health guidelines should focus on reducing total daily sitting time.

A sedentary lifestyle can be defined as a type of lifestyle with little or no physical activity. Sedentary behavior includes sitting, reading, driving a car, computer use, watching television, office work, and cell phone use. The amount of time spent on these indicators of physical inactivity is associated with increased risk of abnormal blood lipids, obesity, type 2 diabetes, and cardiovascular disease.

Strength Training, Muscular Strength and Health Outcomes

Aerobic exercise, also referred to as endurance training or cardiovascular training, includes any activity that improves cardiovascular and pulmonary fitness. Examples of aerobic exercise include walking, running,  swimming, cycling, and rowing.

Strength training is a type of physical exercise that uses resistance to induce muscular contraction.  This type of training builds the strength, anaerobic endurance, and size of skeletal muscles (19).

Strength training can be performed using body weight resistance (eg, push-ups), free weights (eg, barbell squats), or other tools, and resistance bands that place loads on muscles forcing them to work harder. Strength may be displayed dynamically, as in weightlifting or running, or statically, as in activities like gymnastics and yoga (20)

Muscular strength is defined as the ability to produce force against resistance (21).

Observational studies show that both aerobic exercise and strength training are associated with positive health outcomes.

The Prospective Urban-Rural Epidemiology (PURE) study is a large, longitudinal population study done in 17 countries. Participants in the study were assessed for grip strength. The results of this part of the study were published in Lancet in 2015 (22).

Low grip strength was associated with all-cause mortality, cardiovascular mortality, non-cardiovascular mortality, heart attack, and stroke. Low grip strength was a stronger predictor of all-cause and cardiovascular mortality than systolic blood pressure.

A 2017 study tested the association between grip strength, obesity, and mortality. Data from 403.199 participants in the UK Biobank study were used in the analysis. The study showed that obese individuals with greater muscle strength have lower risks of mortality, independent of the degree of obesity (23).

There is overwhelming evidence that muscular strength and strength training are associated with several health benefits and increased life expectancy (24).

Older adults who perform strength training not only improve their physical condition but their survival rate is improved as well (25).

Resistance training counteracts the age-related decline in muscle mass and strength, improves balance and coordination, and reduces the risk of osteoporosis (26).

Strength training may also reduce insulin resistance and improve blood pressure and blood lipids.

Strength training is a type of physical exercise specializing in the use of resistance to induce muscular contraction. This type of training builds the strength, anaerobic endurance, and size of skeletal muscles. Muscular strength is defined as the ability to produce force against a resistance. There is overwhelming evidence that muscular strength and strength training are associated with several health benefits and increased life expectancy.

Physical Fitness and Health Outcomes

Physical fitness is to a large extent determined by physical activity performed over the last weeks or months. It refers to a good physical condition as a result of exercise and proper nutrition.

Physical fitness can be divided into three categories (27):

  1. Aerobic fitness (cardio-respiratory capacity)
  2. Strength and endurance
  3. Flexibility

Aerobic fitness is the ability of the cardiovascular and respiratory systems to supply oxygen to large muscle groups over an extended time. Examples of aerobic activities include running, cycling, and swimming.

Strength is the ability to produce force against resistance. Muscular endurance is the ability to repeat a motion against resistance multiple times.

Flexibility is the ability to stretch muscles and joints.

Several scientific studies show that high physical fitness is associated with improved health outcomes.

Higher levels of physical fitness appear to delay all-cause mortality primarily due to lowered rates of cardiovascular disease and cancer (28,29).

Men who maintain or improve their physical fitness are less likely to die from all causes and cardiovascular disease during follow-up than persistently unfit men (30).

Young individuals with low physical fitness are 3- to 6-fold more likely to develop diabetes, hypertension, and metabolic syndrome than individuals with high fitness (31).

In a cohort of healthy middle-aged adults, fitness was significantly associated with a lower risk of chronic disease outcomes during 26 years of follow-up. These findings suggest that higher midlife fitness may be associated with better health at old age (32).

High levels of physical fitness are associated with improved health outcomes. Higher physical fitness appears to delay all-cause mortality primarily due to lowered rates of cardiovascular disease and cancer. Individuals with low physical fitness are at higher risk of developing diabetes, hypertension, and metabolic syndrome.

The Effects of Physical Activity and Exercise on Health Outcomes

Mortality

Large observational studies indicate that physical activity and regular exercise reduces the risk of mortality for most individuals.

Higher recreational and non-recreational physical activity is associated with a lower risk of mortality in individuals from low-income, middle-income, and high-income countries (33).

Another study found that leisure-time physical activity was inversely associated with all-cause mortality in all age groups. A benefit was found from moderate leisure-time physical activity, with further benefit from sports activity and bicycling as transportation (34).

Daily physical activity is strongly associated with a lower risk of mortality in healthy elderly people. Simply expending energy through any activity may influence survival in older adults (35).

Hence, increasing physical activity is a simple, widely applicable, low-cost global strategy that could reduce the risk of premature deaths in all people.

Cardiovascular Disease

Numerous observational studies show an association between regular exercise and reduced risk of cardiovascular disease.

It has been found that leisure‐time physical activity is effective in the prevention of cardiovascular disease. Such activity is associated with an approximately 20% reduction in cardiovascular events and an increase in life expectancy of approximately 5 years. In this respect, high cardiovascular fitness as a result of vigorous activity levels seems to be more important than total activity time (36).

People who achieve total physical activity levels several times higher than the current recommended minimum level have a significant reduction in the risk of coronary artery disease, ischemic stroke, breast cancer, colon cancer, and diabetes (37).

Clinical trials show that all activities, including aerobic exercise and weight training, lower blood pressure. Daily activity produced greater blood pressure reduction than when performed three times per week. Hence, physical activity has an independent capacity to lower blood pressure (38).

Evidence also suggests that physical activity may reduce the risk of stroke (39).

Aerobic training has beneficial effects on blood lipids such as LDL-cholesterol and HDL-cholesterol, triglycerides,  and non-HDL cholesterol (40).

Furthermore, evidence suggests that increased exercise is associated with reduced inflammation (41).

Cancer

Observational evidence shows that physical exercise is associated with reduced risk of cancer  (42).

Epidemiologic data from 73 studies conducted around the world show a 25% reduction in the risk of breast cancer among the most physically active women compared with those who are least active (43).

A meta-analysis of 19 studies showed that physical activity is associated with reduced risk of cancer of the kidney (44).

Similarly, numerous studies have established the protective role exercise plays in decreasing the risk of many other cancers, including lung, endometrial, colon, and possibly prostate cancer (45, 46, 47, 48).

Diabetes

Regular physical exercise may prevent or delay the development of type 2 diabetes  (49).

Besides, physical exercise improves blood glucose control in type 2 diabetes, reduces cardiovascular risk factors, contributes to weight loss, and improves well-being (50, 51).

Regular exercise also has considerable health benefits for people with type 1 diabetes, including improved cardiovascular fitness, muscle strength, and insulin sensitivity (52).

Obesity

The prevalence of overweight and obesity has increased substantially across the globe during the last few decades. This is a major public health concern because the risk of type 2 diabetes, cardiovascular disease, certain types of cancers, and even mortality is directly proportional to the degree of obesity (53, 54).

Compared with a weight loss diet alone, diet coupled with either aerobic and/or resistance training is associated with a greater reduction in body fat compared with a weight loss diet alone (3).

Furthermore, aerobic exercise and resistance training, even in the absence of caloric restriction, may result in weight loss and a reduction in body fat (55, 56, 57).

However, it has not been firmly established that exercise contributes significantly to weight loss in obese individuals. Nevertheless, physical activity of all types, will likely lead to several health benefits in people with obesity.

Infections

Results from randomized clinical trials and epidemiologic studies suggest that moderate exercise training reduces the risk of upper respiratory tract infections (URTIs). Several epidemiologic studies also suggest that regular physical activity is associated with decreased mortality and incidence rates for influenza and pneumonia (58).

Regular physical activity and frequent exercise may limit or delay the decline in immune function usually associated with aging (59).  Thus, leading an active lifestyle may benefit immune function. This may improve health and reduce the risk of disease in older age.

There is some evidence that intense training is associated with higher levels of infection.  It has been proposed that the relationship between the intensity of exercise and URTIs may be described by a J-curve. Such a relationship suggests that regular moderate-intensity exercise decreases the risk of URTIs compared to sedentary individuals, while a sedentary lifestyle and strenuous intense exercise increase the risk of URTIs (60).

Osteoporosis

During the first three decades of life, bone mass depends to a large degree on levels of physical activity. In women, bone mass begins to decrease around the age of 30 years, often leading to osteoporosis after menopause. Osteoporosis increases the risk of bone fracture and back pain. Thus, it is a major contributor to individual suffering and represents a significant socioeconomic burden (61).

Weight-bearing exercise is associated with increased bone mineral density. Also, exercise is associated with a decreased risk of hip fractures among patients with osteoporosis (3).

Randomized clinical trials strongly support the view that regular exercise programs are effective in preventing or treating osteoporosis (62).

Cognition

The term cognition refers to the ability to think. It describes the mental action or process of acquiring knowledge and processing by thought, experience, and the senses.

Exercise has been associated with improved cognitive function in both young and older adults (63, 64, 65).

Recent study results demonstrate that physical exercise has beneficial effects on cognition and lowers the risk of dementia (66).

Psychological Effects

Regular physical exercise is associated with improved sleep, reduced stress and anxiety as well as a lower risk of depression (67, 68).

A large meta-analysis presents compelling evidence supporting exercise as an evidence-based intervention to improve sleep in healthy individuals. The results indicate that the benefits of exercise for sleep are realized immediately, with exercise having an acute positive impact on many important objective metrics of sleep. Furthermore, the results suggest that regular exercise leads to even greater subjective and objective sleep benefits over time (69).

A population-based study showed that exercisers are on average less anxious and depressed, less neurotic, more extroverted, higher in thrill and adventure seeking than non-exercisers (70).

Regular physical exercise can promote a variety of psychological and physiological conditions that may be beneficial in the primary care of adolescent females with depressive symptoms (71).

The figure shows the mean risk reduction for all-cause mortality and chronic disease in physically active subjects (https://www.bcmj.org/articles/health-benefits-physical-activity-and-cardiorespiratory-fitness#a1)

Regular physical activity and exercise are associated with a lower risk of mortality, cardiovascular disease, cancer, diabetes, osteoporosis, cognitive decline, and upper respiratory tract infections. Furthermore, physical exercise appears to improve sleep, reduce stress and anxiety as well as lower the risk of depression.

The Risks of Exercise

The benefits of physical activity far outweigh the possible associated risks in most individuals.

Musculoskeletal injury is the most common health risk associated with exercise. Various types of strains and tears, inflammation of tendons, and bone fractures may occur as a result of physical activity

More serious but much less common issues include sudden cardiac arrest, and myocardial infarction (heart attack).

Breakdown of skeletal muscle (rhabdomyolysis) may occur following extreme exertion. Massive rhabdomyolysis may lead to kidney failure and several other abnormalities.

Sudden Cardiac Death (SCD) and Acute Myocardial Infarction 

The risk of acute myocardial infarction (heart attack) and sudden cardiac death (SCD) is increased during and shortly after bouts of vigorous physical exertion (72).

The proportion of sudden deaths that occur during physical exertion is higher in younger age groups (73 ,74).

The proportion of sudden deaths that occur during physical exertion in competitive athletes <35 years of age is much higher than in non-athletes in the general population (75,). However, the absolute numbers of sudden cardiac deaths are greater during recreational sports and most of these occur in adults > 35 years of age (76).

Acute heart attacks also occur with higher than expected frequency during or soon after physical exercise. Exercise is also a trigger for acute type A aortic dissection, which has been reported in alpine skiers and weight lifters (72). Aortic dissection occurs when an injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall.

There is an increased relative risk of acute cardiac events with unaccustomed vigorous physical exercise. However, the absolute risk of experiencing SCD or heart attack during physical exertion is very small.

Strenuous physical activity, especially when sudden and unaccustomed, increases the risk of heart attack and SCD. This includes sports such as racket sports, downhill skiing, marathon running, triathlon participation, and high-intensity sports activities (eg, basketball, soccer)(77. 78, 79, 80, 81).

Those at highest risk of exercise-related SCD are individuals with heart failure or a previous history of a heart attack.

Exercise-related SCD in the young is often related to hypertrophic cardiomyopathy or congenital anomalies of the coronary arteries. However, in many cases, no identifiable cause can be found at autopsy and these deaths are often classified as either sudden arrhythmic death or SCD with a structurally normal heart (82).

The benefits of physical activity far outweigh the possible associated risks in most individuals. Musculoskeletal injury is the most common health risk associated with exercise. There is an increased relative risk of acute cardiac events with unaccustomed vigorous physical exercise. However, the absolute risk of experiencing sudden cardiac death or heart attack during physical exertion is very small.

How Much Activity Will Improve Health? Does Too Much Exist?

International guidelines, recommend regular exercise training as a cornerstone for the prevention and treatment of cardiovascular disease. In general, >150 minutes of endurance exercise training per week at moderate to vigorous intensity, ideally spread over 3 to 5 days, is recommended (83).

This recommendation is associated with a 20% to 30% lower risk for premature all-cause mortality and incidence of many chronic diseases, with greater health benefits for higher volumes and greater intensities of activity (84).

Long-term intense exercise training alters cardiac structure and function. The athlete’s heart is characterized by an enlargement of the cardiac chambers, improvement of cardiac function, and slow heartbeat. These adaptations are believed to be benign (72).

Emerging evidence, however, suggests that over time, high-volume, high-intensity exercise training can induce cardiac maladaptations such as
an increased risk for atrial fibrillation, coronary artery calcification, and fibrosis of the heart muscle. Hence, it is currently debated whether intensive exercise can be harmful to the heart (72).

Atrial Fibrillation

Atrial fibrillation is characterized by a chaotic electrical activity of the atria leading to rapid, irregular heart rhythm (85). It is the most common arrhythmia in the general population.

There is evidence that fitter individuals have the lowest risk of atrial fibrillation. However, there is substantial evidence that the risk for atrial fibrillation is higher in athletes than in control subjects (72).

In the US Physician’s Health Study, men who jogged 5 to 7 times per week had a 50% higher risk of atrial fibrillation than men who did not exercise vigorously (86).

Three meta-analyses found that the risk of atrial fibrillation was 2- to 10-fold higher in endurance athletes than in control participants (86, 87, 88).

The mechanisms responsible for the increased risk of atrial fibrillation among athletes are unknown. However, enlargement of the atria following many years of training may play a role. (89).

Coronary Artery Calcification

Exercise training reduces the risk of symptomatic coronary artery disease and clinical cardiovascular events (90, 91). Nevertheless, accelerated atherosclerosis of the coronary arteries has been found among athletes. For example, high coronary calcium scores seem to be more common among marathon runners and male amateur athletes compared with non-athletes (92, 93).

The clinical relevance of accelerated coronary artery atherosclerosis in athletes performing a very high-volume or high-intensity training is unclear. Although elevated coronary calcium scores in athletes might indicate increased cardiovascular risk, definite data to support this hypothesis is lacking (94).

Most active athletes seem to have fewer unstable “mixed” plaques despite their more stable calcified plaques. Mixed plaques are associated with a high risk of cardiac events, whereas calcified plaques are associated with lower risk (95).

Regular exercise training is a cornerstone for the prevention and treatment of cardiovascular disease. Emerging evidence, however, suggests that over time, high-volume, high-intensity exercise training can induce cardiac maladaptations.  These include an increased risk for atrial fibrillation, coronary artery calcification, and fibrosis of the heart muscle.

“If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health”.                                                                                                                                                                                                                                                                             – Hippocrates

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The Health Risks of Being a Flight Attendant

Estimated reading time: 18 minutes

Being a flight attendant is one of the most wanted professions in the world. The association with elegance, confidence, and reliability make it unique – a job to be proud of.

Flight attendants are employed and trained to perform safety functions on aircraft as well as customer service. Hence, being calm, collected, quick thinking, pleasant, and flexible are much-needed characteristics.


Of course, most of the time, the only things you have to do is to put on your uniform, go through the regular security routine, be polite with the passengers and serve food and drinks?

As a bonus, you will probably have a lot of leisure time and flexibility? And you get to see new places and learn about distinctive cultures all the time?

You might even make new friends all over the world.

But let’s be more pragmatic? For every two minutes of glamour, there are eight hours of hard work. And, I’m sorry to say, you might even be gambling with your health.

However, before we dig into the medical issues, let’s explore some history.

Early History

It is almost one hundred years since being a cabin or flight attendant became known as an occupation.

In March 1912, Heinrich Kubis became the first flight attendant in history when he served passengers on the German airline DELAG (1).

Kubis, famous for serving Zeppelin passengers, was in Hindenburg’s dining room when the ship burst into flame at Lakehurst, New Jersey on May 6 1937. He encouraged passengers and crew to jump from the windows and then jumped to safety himself (2).

When passenger air travel began in the early 1920s, flight attendants were called couriers.  They were often the sons of businessmen who had financed the airlines (1).

In 1922, the British company “Daimler Airways” hired “cabin boys,” whose job was to assist passengers by handing out leather steamer rugs, hot water bottles, and cotton earplugs. They reassured passengers during the flight and helped them during landing and when disembarking the aircraft (3).

On 15 May 1930 Ellen Church, a registered nurse, was the first appointed American senior flight attendant. She operated a flight with eleven passengers on board an aircraft flying from San Francisco to Cheyenne.

Church’s duties included winding the clock in the cockpit, killing the flies after take-off, and preventing passengers from throwing cigarette stumps out of the windows. She was also supposed to clean passengers’ shoes, if necessary (3).

In 1930 “Boeing Air Transport” hired eight women flight attendants, historically known as the “Original Eight.” By the late 1930s, United airlines hired stewardess or “female helpers.” Initially, these were registered nurses (1).

In the 1940s, “restrained elegance” in the sky became popular.

Back in those days, the airplanes, mostly DC-3, were noisy and uncomfortable compared with today. The idea was that air travelers would feel safer in the hands of the stewardess, whose main job often was to attend those who became airsick.

According to sources, stewardesses were often treated poorly by male passengers, groping, pinching, and padding their butts (1).

Initially, the airlines required the stewardess to take an oath that she would not marry nor have children.

The first in-flight hostesses during the 1930s and 1940s wore military-inspired skirt suits in bland hues with white gloves and matching hats (4).

In the 1940s, the functionality of uniforms improved as “restrained elegance” in the sky became the norm.

At that time, flying was often a unique experience. Passengers wore their most elegant outfits. Hence, airline cabins were full of tailored suits and of course, cigarette smoke.

Post World War II

In 1945, flight attendants founded the present-day Association of Flight Attendants union, formerly known as the Airline Stewardess Association, or “ALSA.”

In the 1960s high fashion came to the skies. Restrained elegance was replaced by miniskirts and hot pants.

In the 1950s, more and more airlines added age clauses to contracts for flight attendants and the profession grew into a symbol of sophistication and glamour.

In 1956, flight attendants were grounded at age 32. However, male flight attendants were allowed to fly until they reached their sixties (6).

In the 1960s, high fashion came to the skies. Restrained elegance was replaced by miniskirts and hot pants and stewardesses became a marketing tool for the airline companies.

The words of Braniff hostess Muffet Webb who in the year 1956 won the first Miss Skyway contest (a beauty pageant for flight attendants) certainly reflect the undertone when she said;  “Does your wife know you’re flying with us?” 

Back in those days, being an air stewardess became an extremely popular job. In 1967, TWA accepted fewer than three percent of its applicants—a lower acceptance rate than Harvard (6).

Modern Day

With the Airline Deregulation Act in 1978, U.S. federal law deregulated the airline industry, removing federal government control over areas such as fares, routes, and market entry of new airlines (7).

The age structure of flight attendants has changed dramatically since 1980. While flight attendants were younger than the overall U.S. workforce in 1980, they are now older.

Hence, a free market was introduced in the commercial airline industry, leading to an increase in the number of flights, lower fares, increasing number of passengers, and consolidation of carriers.

Consequently, flying became less of a luxury. The word “stewardess” fell out of favor and was replaced by the more gender-neutral “flight attendant.”

The age structure of flight attendants has changed dramatically since 1980. While flight attendants were younger than the overall U.S. workforce in 1980, they are now older (8).

Today, there are over 100,000 flight attendants in the U.S. (9).

According to the Population Research Bureau, half of all flight attendants are age 45 and older, and nearly 22 percent of them are 55 and older.

Although flight attendants continue to be predominantly female, males have increased their presence in the U.S. between 1980 (19.3 males per 100 females) and 2007 (26.4 males per 100 females) (8).

There has also been a dramatic shift in the earnings of flight attendants in the U.S. since 1980. After adjusting for inflation, the median hourly wages dropped by 26 percent between 1980 and 2007. In contrast, the median hourly wages of all U.S. workers rose by 13 percent during this period (8).

Asian countries still tend to use flight attendants as one of their unique selling points. Flight attendants have to be physically attractive and fit and fall within a stringent requirement of age, height, and weight.

Although flight attendants continue to be predominantly female, males have increased their presence in the U.S. between 1980 (19.3 males per 100 females) and 2007 (26.4 males per 100 females)

The Health Risks of Being a Flight Attendant

Despite the unique occupational environment, the health consequences of flight attendant work have not been intensively studied.

Flight attendants are continuously exposed to a range of job-related exposures such as poor cabin air quality, cosmic ionizing radiation, elevated ozone levels, pesticides from cabin disinfection, high levels of occupational noise, circadian rhythm disruption, heavy physical job demands, and verbal and sexual harassment (10).

The flight attendant is the only person on an aircraft who is engaged in intense physical activity at reduced oxygen levels (11). Hence their health hazards may differ significantly from those of pilots and passengers

The most recent and reliable information about the health risks of being a flight attendant comes from the Harvard Flight Attendant Health Study (FAHS) (12, 13).

The study began in 2007 and has since then recruited over 12,000 people in 2 waves (14).

The Cabin Environment

The cruising altitude of commercial aircraft is usually maintained between 30.000 to 45.000 feet (9.100 to 13.700 m). Because the low atmospheric pressure at such heights is not compatible with survival, aircraft cabins are pressurized during flight to the equivalent of 5.000 to 8.000 feet (1.500 – 2.400 m) above sea level (15).

Hence, the partial pressure of oxygen in cabin air at cruising altitude is 25-30% lower than at sea level.

A part of the cabin air (40-50%) is recirculated and cleaned with special filters, while the remainder is derived from the outside air (bleed air). The humidity onboard ranges from 6-18% depending on the compartment. Optimal humidity varies between 40-70%. Hence, cabin air is arid (16).

The air conditioning and ventilation system on commercial aircraft maintain low counts of microorganisms in the cabin. However, there are reports of individuals contracting several infectious diseases through airborne transmission (17, 18).

Higher than standard rates of viral gastroenteritis, colds, and flu-like symptoms are reported in-flight attendants than other occupations (19).

While high-efficiency particulate air (HEPA) filters effectively limit the risk of disease transmission, person-to-person transmission in the aircraft cabin may occasionally cause clusters of infections such as SARS, tuberculosis, coryza, influenza, measles, and meningitis. Furthermore, flight attendants may be exposed to infectious disease hazards during a layover.

For decades, flight attendants were exposed to secondhand tobacco smoke. Some of the health conditions caused by secondhand smoke in adults include coronary heart disease, stroke, and lung cancer (20).

Cabin Air Quality

There has been a significant reduction in cabin environment toxicological risks since the elimination of smoking onboard commercial aircraft (21).

Today, general concerns about air quality often focus on air dryness. Prolonged exposure to dry air is reported to cause symptoms of local irritation such nasal stuffiness, sore eyes, nose, throat, and chest wheeziness, or symptoms such as headache, fatigue, and difficulty in concentration.

In a Swedish study of flight attendants published in 2005, the most common complaint about cabin air quality was dry air (53%). Airline crew had more nasal, throat, and hand skin symptoms, than office workers did (22).

However, despite some recent improvements, there are still serious concerns about air quality incidents affecting flight attendants (23).

Flight attendants may be exposed to cabin air contamination by toxic substances from engine bleed air, ozone (in jet airliners not fitted with catalytic converters), or sources within the passenger cabin.

Many cases of severe symptoms from cabin air contamination have been reported.

Although the immediate health effects of exposure to contaminated cabin air have been relatively well documented, the causation, diagnosis, and treatment of long-term effects is still debated. However, why only some cabin occupants are particularly affected, and not others is unclear (24).

According to several data obtained from three U.S. airlines, frequency estimates of bleed air contamination events range from 0.09 to 3.88 incidents per 1,000 flight cycles. Using the lowest estimate of 0.09 events per 1,000 flight cycles, there may be an average of two to three contaminated bleed-air events every day (25).

The term “aerotoxic syndrome” is a phrase used by some experts to describe the short- and long-term health effects caused by contaminated cabin air (26). However, the concept of aerotoxic syndrome as a well-defined entity is still not recognized by the aviation medicine community (27).

Cosmic Ionizing Radiation

Cosmic ionizing radiation is a form of radiation that comes from outer space. A minimal amount of this radiation reaches the earth.

At flight altitudes, passengers and crew members are exposed to higher levels of ionizing radiation.

Cosmic radiation exposures on aircraft include galactic cosmic radiation, which is always present and solar particle events, sometimes called “solar flares (28).”

Evidence suggests that cosmic ionizing radiation causes cancer in humans (29). Ionizing radiation is also known to cause reproductive problems.

The National Council on Radiation Protection and Measurements reported that aircrew has the largest average annual effective dose (3.07 mSv) of all U.S. radiation-exposed worker (30).

The European Cockpit Association (ECA) recommends air carriers to inform potential new employees about radiation exposure before recruitment. All employees should be aware that that high altitude flying exposes them to significantly higher ionizing radiation levels with associated health implications (31).

Reducing exposure times by flying fewer hours may help to reduce yearly limits of flight hours in the interest of flight safety.

Similarly, flight crew members may influence their lifelong radiation exposures by making use of their options regarding the selection of aircraft type(s) flown, the types of operation (short haul/ long haul), and their retirement age. Airline operators are encouraged to provide crews with the possibility of such career choices.

At flight altitudes, crewmembers and passengers are exposed to higher levels of cocmic ionizing radiation

Cancer

In 2018, the FAHS reported that flight attendants have higher rates of several types of cancer than the general population (13).

In 2014 and 2015 the FAHS studied 5,300 flight attendants through surveys that were disseminated online, via mail and in person at airports. The surveys asked respondents about flight schedules and cancer diagnoses. The researchers then compared the responses to the health status of 2,729 non-flight attendant adults with similar socioeconomic backgrounds, using data from the National Health and Nutrition Examination Survey (NHANES).

The study revealed higher rates of uterine, cervical, breast, gastrointestinal, thyroid, and melanoma cancers among flight attendants. The gastrointestinal cancers included cancer of the colon, stomach, esophagus, liver, and the pancreas.

The disparity was most pronounced with breast, melanoma, and non-melanoma cancers. Flight attendants had more than double the risk of developing melanoma, and more than quadruple the risk of developing non-melanoma skin cancers. They also had a 51 percent higher risk of developing breast cancer than the general population.

Job tenure was associated with the risk of cancer among both females and males.

It is not clear why flight attendants appear to be at increased risk of several types of cancer. However, factors such as occupational exposure to ionizing radiation, circadian rhythm disruption with resulting sleep disorders, and previous exposure to secondhand smoke may all play a role.

Cabin crew members are also regularly exposed to more UV radiation than the general population

Furthermore, ongoing exposure to several chemical agents from engine leakages, pesticides, and flame retardants may be present. These contain compounds that may increase the risk of some cancers (32).

Obesity, Smoking, High  Blood Pressure, and Disease of the Heart and Lungs

Data from the initial wave of the FAHS found about a 3-fold increase in the age-adjusted prevalence of chronic bronchitis among flight attendants despite considerably lower levels of smoking.

In addition, the prevalence of heart disease in female flight attendants was 3.5 times greater than the general population while their prevalence of high blood pressure (hypertension) and being overweight was significantly lower (12). Thus, chronic bronchitis and coronary artery disease were both more common among flight attendants compared to the general population

The more recent second wave of the FAHS found that flight attendants still had lower rates of overweight, obesity, and current smoking compared to the general publication (13). However, they also had a lower rate of heart and lung disease, which contrasts with the results from the first wave of the study.

Chronic bronchitis and coronary artery disease are both severe conditions that might impair the ability of flight attendants to perform their duties. Hence, flight attendants diagnosed with these conditions in 2007 (the first wave of the FAHS) may not have continued to work until the second wave of the study in 2015. This could partly explain the differences in the rates of heart and lung disease between the two waves of the study.

The “healthy worker effect” is a phenomenon explaining why workers usually exhibit lower overall death rates than the general population because the severely ill and chronically disabled are ordinarily excluded from employment (33).

Furthermore, smoking-related bronchitis and heart disease among flight crew presumably become less frequents as more time elapses since smoking bans were instituted on commercial flights.

Fatigue, Sleep, and Mental Health

Studies have indicated that fatigue is a significant problem among flight attendants (34).

The FAHS found an increased prevalence of adverse sleep and mental health outcomes such as anxiety, depression, and alcohol abuse among flight attendants (13).

Fatigue and depression are symptoms that often coexist (35,36). Int the second wave of the FAHS, these conditions were much more common among flight attendants than in the general population.

Risk factors for mental health problems among flight crew may include extended and irregular working hours, sexual harassment, and lack of employer protections for occupational hazards (37).

Another study has reported elevated rates of suicide among cabin crew (38).

Sleep disorders, including circadian rhythm disruption, have been associated with adverse mental outcomes, including suicidal ideation, suicide attempts, and suicide deaths (39).

An Italian mortality study on commercial flight crew found an increased risk for death by suicide among female flight attendants. This was also seen in male cockpit crew members but to a lesser extent. However, a lower than expected suicide risk was seen for male flight attendants (40).

It has been shown that job stressors such as mental and psychological demands, an imbalance between job demands and outside obligations, low supervisor support, and job dissatisfaction seem to predict psychological distress (41).

Experts have suggested that interventions aimed at reducing conflicts between work and private life, and at increasing social support for flight attendants may enhance their wellbeing and job satisfaction.

Studies have indicated that fatigue is a major problem among flight attendants

Infertility, Miscarriage, Preterm Birth, and Fetal Abnormalities

Reproductive problems, including adverse pregnancy outcomes, among female flight attendants have been reported since the 1960s (42).

Indeed, the second wave of the FAHS observed an association between job tenure as a flight attendant during a woman’s reproductive years and infertility, miscarriage, preterm birth, and fetal abnormalities (13).

Another study found an association between rates of miscarriages and circadian rhythm disruption, cosmic ionizing radiation exposure, and high physical job demands among flight attendants (43).

It is hugely worrying that cabin crew have the largest annual ionizing radiation dose of all U.S workers (30). Of course, this may be particularly problematic for pregnant flight attendants.

What is even more daunting is that these radiation exposures are not regulated among flight crew.

Musculoskeletal Symptoms

Flight attendants are at risk for musculoskeletal disorders.

Work-related strains and sprains of muscles, tendons, and supporting tissues can be caused by lifting, bending, carrying, reaching, working in confined spaces, and using repetitive motions.

Turbulence or sudden airplane movements are a frequent cause of injury among flight attendants.

Lower‐back musculoskeletal disorders are among the musculoskeletal problems most commonly reported by flight attendants.

Musculoskeletal symptoms may be associated with work-related psychological factors among flight crew, including mental job demands, harassment, and job insecurity (43).

Workplace Harassment and Abuse

Workplace harassment and abuse, especially against women, occur with high frequency worldwide (44).

Estimates suggest that as many as 50% of U.S. women experience sexual harassment during their working lives (45). However, only a minority report it.

A survey of cabin crew working for Australian airlines recently found that 65 percent experienced sexual harassment (46).

The research found that 70 per cent of cabin crew who experienced harassment said they chose not to report the incident because they did not think it would be dealt with appropriately or they were concerned reporting it would make the situation worse.

Incidents ranged from serious sexual assault, groping, passengers exposing themselves, sexualised and degrading remarks, and workers being abused because of their sexual orientation.

A 2018 survey by the U.S. Association of Flight Attendants (AFA) shows that than one-in-three flight attendants have experienced verbal sexual harassment from passengers, and nearly one-in-five have experienced physical sexual harassment from passengers, in the last year alone (47).

Only 7% of the flight attendants who experienced the abuse did report it to their employer.

Despite the high prevalence of abuse and the emergence of the #MeToo movement, 68 percent of flight attendants said they saw no efforts by airlines to address workplace sexual harassment over the last year (47).

Flight attendants may be particularly susceptible to harassment due to employment in a profession that is primarily female and has been previously sexualized by the airline industry. Furthermore, they are expected to suppress and regulate their emotional responses according to employer and passenger expectations (48).

Repeated exposure to sexual harassment, bullying, violence, and threats are related to physical and psychological wellbeing among flight attendants (37).

Another study observed strong associations between all types of abuse and depression, sleep disturbances, fatigue, workplace injuries, and musculoskeletal conditions among cabin crew (49).

The AFA has called on the entire airline industry to step up to combat harassment and recognize the impact it has on safety.

With flight attendants reporting that they often deal with harassment by avoiding further interaction with abusive passengers, airlines must also ensure that staffing levels on flights are sufficient to allow this strategy to work (47).

The Tailpiece

For the past fifteen years, I have, as an Aviation Medical Examiner, interviewed and examined thousands of flight attendants.

They have been females and males, young and older, experienced and inexperienced, confident and disheartened, healthy and sick, happy and unhappy, calm and agitated, smiling and crying. What most of them have in common is that they love their job and they are proud of their profession.

This article is dedicated to all those ambitious and devoted people.

I applaud your professionalism.

However, I can’t stop agonizing over your unpredictable occupational environment.




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21 Important Questions and Answers About Heart Failure

Estimated reading time: 27 minutes

Heart failure is a common medical condition and remains an increasing global problem.

In many ways, heart failure is synonymous with end-stage heart disease. Of course, prognosis varies depending on the severity of the disorder. However, in advanced heart failure survival is dismal.

All diseases of the heart may ultimately lead to heart failure.

A simple way of defining heart failure is to say that it is a condition that arises when the heart muscle is not able to accomplish its primary role which is to continuously receive and pump blood through the body’s arteries and veins. The inability of the heart to do so may affect every organ in the body and lead to diverse symptoms that negatively affect quality of life.

Recent reports indicate that heart failure affects 6.5 million people in the US. aged 20 years or older (1).

Due to improved survival of patients with heart disease, heart failure will likely continue to increase in prominence.

Furthermore, it is well established that the risk of heart failure increases with advancing age. With the growing number of elderly people, the burden of the disorder will continue to pose challenges for future healthcare.

The American Heart Association (AHA) predicts a 46% increase in prevalence from the year 2012 to the year 2030, resulting in 8 million or more Americans aged 18 years or older with heart failure (1).

It is estimated that heart failure accounts for 1-2% of all healthcare expenditure (2). The bulk of these costs are driven by frequent, prolonged, and repeat hospitalizations (3).

1. What Is Heart Failure?

In medical literature, heart failure is generally not considered to be a disease. Instead, it is a syndrome or a constellation of symptoms, usually resulting from an underlying pathology of the heart.

Controversy has always surrounded the use of the phrase heart failure, partly because advances in physiology have rendered earlier definitions inadequate. Furthermore, the clinical scientist may sometimes use the term differently than the clinical physician (4).

Many attempts have been made to come up with a comprehensive set of criteria that describe heart failure.

In 1950, Dr. Paul Wood defined heart failure as a state in which the heart fails to maintain an adequate circulation for the needs of the body despite a satisfactory filling pressure (5).

In 1980, Dr. Eugene Braunwald defined the condition as a pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues (5).

In 1985, Dr. Phillip Poole Wilson, defined heart failure as a clinical syndrome caused by an abnormality of the heart and recognized by a characteristic pattern of hemodynamic, renal, neural and hormonal responses (5).

According to the current definition by the American Heart Association and the American College of Cardiology, heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood (6).

The European Society of Cardiology (ESC) recently defined heart failure as a clinical syndrome characterized by typical symptoms (e.g., breathlessness, ankle swelling, and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral edema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress (7).

Heart failure is a complex clinical syndrome that results from a structural or functional impairment of the pumping capacity and/or filling of the left ventricle of the heart. It is characterized by shortness of breath, ankle swelling, and fatigue.

2. How Common Is Heart Failure?

During the 1980s, the Framingham study reported that the prevalence of heart failure increased dramatically with increasing age, with an approximate doubling in the prevalence with each decade of aging (8)

The age-adjusted annual incidence was 0.14% in women and 0.23% in men. Survival in the women was generally better than in the men, leading to the same point prevalence.

Since then it is well established that the risk of heart failure increases with advancing age, with an incidence of 0.3 per 1,000 in those <55 years old up to 18 per 1,000 for those ≥85 years (9).

Heart failure is present in 2 percent of persons age 40 to 59 and 5 percent of persons age 60 to 69.

African-Americans are 1.5 times more likely to develop the condition than Caucasians.

During the 1990s, there was a rising trend in the incidence and prevalence of heart failure leading many experts predicted that it would become an epidemic during the first decades of the new millennium. However, the incidence of heart failure-related deaths in the U.S. seemed to decrease between 2000 – 2012.

Recent data shows that heart failure deaths rose again between 2012-2014, particularly among men and non-Hispanic black populations (10).

The risk of heart failure increases with advancing age. Heart failure is present in 2 percent of persons age 40 to 59 and 5 percent of persons age 60 to 69.

3. What Are the Most Common Causes of Heart Failure?

As heart failure in itself is not considered to be a disease, it is imperative to establish the underlying disorder that causes heart failure to occur.

In the 1970s, high blood pressure (hypertension) and coronary artery disease were the primary causes of heart failure in the United States and Europe. Disorders of the heart valves were also considered as common causes.

More recently, hypertension and valve disorders are less often considered to be the underlying cause of heart failure, probably due to improvements in the detection and treatments of these disorders (11).

At the same time, coronary artery disease, obesity, and diabetes mellitus have become increasingly responsible for heart failure.

In fact, multiple risk factors may co-exist and interact with each other in an individual patient. Studies show that the burden of risk factors in patients with established heart failure has increased over time (12). Hence, several disorders, such as diabetes, obesity, hypertension, and coronary artery disease, are often present in the same patient.

Smoking is a strong risk factor for heart failure (13).

Several diseases of the heart muscle itself, so-called cardiomyopathies, are relatively common causes of heart failure, particularly among younger people.

Myocarditis, an inflammation of the heart muscle commonly caused by a virus infection are also known underlying causes.

Congenital heart defects may lead to heart failure later in life.

Obstructive sleep apnea (OSA), overconsumption of alcohol, and abnormal heart rhythms, such as atrial fibrillation, may sometimes cause heart failure.may sometimes lead to heart failure.

Lately, exposure to cardiotoxic drugs (e.g., anthracyclines used for the treatment of cancer) have become a relatively common underlying cause of the condition.

It is imperative to establish the underlying cause of heart failure in every patient. Coronary artery disease, high blood pressure, cardiomyopathy, myocarditis, heart valve disorders, obesity, diabetes, heart arrhythmia, and congenital heart defects are the most common causes.

Coronary artery disease is a common underlying cause of heart failure

4. What Is Systolic Heart Failure?

Heart failure is characterized by a dysfunction of the heart muscle, usually the left ventricle.

The left ventricle is responsible for pumping oxygenated blood to all the tissues and organs of the body. By contrast, the right ventricle solely pumps blood through the lungs.

Conditions leading to damage of the heart muscle and reduced pump capacity of the left ventricle commonly lead to heart failure. A typical example is a patient with a history of coronary heart disease and previous heart attack (myocardial infarction).

Systolic heart failure, also called heart failure with reduced ejection fraction, describes a condition caused by the inability of the heart muscle to contract normally. Hence, blood flow to vital organs is limited, leading to many of the symptoms of heart failure.

Systolic heart failure, also called heart failure with reduced ejection fraction, describes heart failure caused by the inability of the heart muscle to contract normally.

5. What Is Ejection Fraction (EF)?

An ejection fraction (EF) is an essential measurement of how well the heart muscle is pumping. Despite some limitations, EF is used to help classify heart failure and guide treatment.

EF is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction. An ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out with each heartbeat (14).

In a healthy heart, the EF is 50 percent or more.

  • An ejection fraction of 55 percent or higher is considered normal.
  • An ejection fraction of 50 percent or lower is considered reduced.
  • An ejection fraction between 50 and 55 percent is usually considered “borderline (15).”

The following methods may be used to calculate EF:

  • Echocardiogram – the most widely used test
  • MUGA scan
  • CT scan
  • Cardiac catheterization
  • Nuclear stress test

Ejection fraction (EF) is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction.

6. What Is Heart Failure with a Normal Ejection Fraction (HFNEF)?

In many patients with heart failure, the pumping capacity of the heart muscle is preserved. This has variously been labeled as diastolic heart failure, heart failure with preserved left ventricular function or heart failure with a normal ejection fraction (HFNEF)(16).

Various cutoffs for ejection fraction have been used to define HFNEF, usually ranging from 40 to 50% (17).

Interestingly, approximately 30–50% of patients with heart failure have a normal or near-normal contraction of the left ventricle function (18). Hence, a large fraction of patients with heart failure do not have systolic heart failure.

HFNEF is a major public health problem in the western world, currently representing approximately half of all the patients with heart failure (19).  It is especially common in elderly people with comorbid conditions such as hypertension, diabetes, obesity, and coronary artery disease.

Heart failure with a normal ejection fraction (HFNEF) describes heart failure where the pumping capacity of the heart muscle is preserved. HFNEF is a major public health problem in the western world, currently representing approximately half of all the patients with heart failure.

7. What Is Diastolic Heart Failure?

In diastolic heart failure, the left ventricle loses its ability to relax normally, usually due to increased stiffness of the heart muscle. Hence, the left ventricular chamber may not fill adequately with blood during the resting period between each heartbeat (diastole).

When the left ventricle becomes stiff, diastolic pressure also called filling pressure, increases. The increased pressure is transported back to the lungs, leading to elevated pressure within the pulmonary circulation. This may cause shortness of breath and even cause congestion of the lungs which, if severe, may lead to pulmonary edema.

Sometimes heart failure with normal ejection fraction (HFNEF) is regarded as diastolic heart failure. However, this is an oversimplification.

Of course, many patients with HFNEF have diastolic dysfunction, but usually, other factors come into the picture. Hence, diastolic dysfunction may not be the sole cause of symptoms in these patients.

Primary diastolic dysfunction is typically seen in patients with hypertension. It is commonly associated with thickening (hypertrophy) of the left ventricle, has a particularly high prevalence in the elderly population and is more common in women than men.

Diastolic heart failure is commonly associated with thickening (hypertrophy) of the left ventricle, has a particularly high prevalence in the elderly population and is more common in women than men.

Although diastolic heart failure is regarded as common in clinical practice, its existence has been questioned for several reasons (20).

Firstly, many of these patients may not indeed have heart failure. Instead, their symptoms may be caused by other conditions such as obesity or pulmonary disease that can mimic heart failure (21).

Some patients with HFNEF may even have subtle abnormalities of systolic function although the ventricular ejection fraction is normal (22).

The diagnosis and treatment of diastolic heart failure has lagged behind that of systolic heart failure mainly to the heterogeneity of HFNEF.

However, diastolic heart failure seldom occurs in isolation. Most patients with diastolic heart failure don’t have an entirely preserved systolic function. Thus, the term HFNEF is preferred.

In diastolic heart failure, the left ventricle loses its ability to relax normally, usually due to increased stiffness of the heart muscle. However, diastolic heart failure seldom occurs in isolation.  Many other disorders, such as obesity, diabetes, and lung disease, are often present as well and systolic function is not always preserved. Hence, the term heart failure with normal ejection fraction (HFNEF) is generally preferred.

8. What Are The Symptoms of Heart Failure?

Breathlessness (dyspnea), fatigue, and exercise intolerance are key symptoms of heart failure. Initially, breathlessness is mainly present on exertion, but in the later stages, it may be present at rest.

Orthopnea (dyspnea when lying down, usually in the supine position) is typical.

Furthermore, nocturnal episodes of dyspnea (paroxysmal nocturnal dyspnea) may be present. Then, the patient typically experiences sudden attacks of shortness of breath, which awakens him/her from sleep.

Fatigue and weakness are common features.

Patients with heart failure commonly have a reduced ability to excrete sodium and water through the kidneys leading to what is often called refractory volume overload.

Volume overload may present as elevated jugular venous pressure

Volume overload can manifest as pulmonary congestion (collection of fluid in the lungs), peripheral edema (swollen legs and ankles), and elevated jugular venous pressure.

Furthermore, swelling of the abdomen may occur if fluid accumulates in the abdominal cavity.

Some patients may experience a persistent cough or wheeze with white or pink blood-tinged phlegm (23)

Unintentional weight loss, sometimes leading to cachexia, is a common complication of advanced heart failure (24).

Signs of inadequate perfusion with low blood pressure (hypotension) cold extremities and mental status changes are also signs of advanced disease. At this stage, renal function often becomes impaired as well.

The most common symptoms of heart failure are breathlessness (dyspnea), fatigue, exercise intolerance, and refractory volume overload leading to edema. Other symptoms include cough, lack of appetite, nausea, and swelling of the abdomen.

9. What Is Asymptomatic Left Ventricular Systolic Dysfunction (ALVSD)?

Many patients with reduced ejection fraction do not have symptoms of heart failure. Because of the absence of symptoms, they are not considered to have heart failure. This condition is called asymptomatic left ventricular systolic dysfunction (ALVSD).

ALVSD is at least as common as heart failure with reduced ejection fraction. Patients with ALVSD are at risk of progression to symptomatic heart failure (25).

Studies have used a variety of thresholds for ejection fraction, ranging from 30 to 54 percent, to identify left ventricular systolic dysfunction (26).

The causes of ALVSD include coronary heart disease, cardiomyopathy, myocarditis, valve disease, hypertension, and exposure to cardiotoxic drugs (e.g., , anthracyclines).

The rationale for early detection of ALVSD is that appropriate pharmacologic therapy can significantly improve outcomes in patients with ALVSD if ejection fraction is ≤35 to 40 percent (27).

Asymptomatic left ventricular systolic dysfunction (ALVSD) is considered present when ejection fraction (EF) is reduced, but no symptoms of heart failure are present.

10. What Are the Stages of Heart Failure?

Heart failure is a chronic long-term condition that tends to gets worse with time.

The American College of Cardiology/American Heart Association has defined four stages (28). The stages cover a broad spectrum ranging from asymptomatic people risk factors for heart disease to refractory end-stage heart failure.

Stage A: Patients at risk for heart failure who have not yet developed structural heart changes (i.e., those with diabetes or coronary artery disease without prior heart attack)
Stage B: Patients with structural heart disease (i.e., reduced ejection fraction, left ventricular hypertrophy, chamber enlargement) who have not yet developed symptoms of heart failure
Stage C: Patients who have developed clinical heart failure
Stage D: Patients with refractory heart failure requiring advanced intervention.

Stage A is considered pre-heart failure. Patients with stage A have no structural damage to the heart.

Stage A includes patients with known coronary artery disease, individuals with conventional risk factors such as hypertension, diabetes, and metabolic syndrome. It also includes people with a history of alcohol abuse, family history of cardiomyopathy, history of taking drugs that may damage the heart muscle, such as some cancer drugs.

Stage B includes patients with asymptomatic left ventricular function. These patients have signs of structural damage to the heart but have not yet developed symptoms of heart failure.

Stage C and D include patients with symptomatic heart failure with stage D representing end-stage disease.

The four stages of heart failure (A, B, C, and D) cover a broad spectrum ranging from asymptomatic risk factors to refractory end-stage heart failure.

11. What Is the New York Heart Association (NYHA) Functional Classification of Heart Failure?

The New York Heart Association (NYHA) functional class is a subjective estimate of a patient’s functional ability based on symptoms (29)

Class Patient Symptoms
I No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).
II Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath).
III Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnea.
IV Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases.

The New York Heart Association (NYHA) functional class is a subjective estimate of a patient’s functional ability based on the severity of symptoms. Patients in Class I have no limitation of physical activity. Patients in Class IV are unable to carry on any physical activity without discomfort.

12. What Is the Difference Between Acute and Chronic Heart Failure?

Acute heart failure, sometimes called acute decompensated heart failure, is defined as a gradual or rapid change in signs and symptoms, resulting in a need for urgent therapy (30).

The symptoms are primarily the result of severe pulmonary congestion resulting in sudden shortness of breath.

Acute heart failure encompasses at least three distinct clinical entities (31):

  1. Worsening chronic heart failure associated with reduced or preserved ejection fraction (70 percent of all admissions)
  2. New-onset heart failure that may, for example, occur following a large myocardial infarction or a sudden increase in blood pressure superimposed in a stiff, noncompliant left ventricle (25 percent of all admissions).
  3. Advanced heart failure associated with severe left ventricular systolic dysfunction and a continually worsening low-output state (5 percent of all admissions).

Acute heart failure is an emergency and needs in-hospital treatment.

Chronic heart failure, also called congestive heart failure, on the other hand, is a long-term condition that can usually be kept stable with adequate treatment. Symptoms typically include shortness of breath, problems exercising, fatigue, and swelling of the feet, ankles, and abdomen.

Acute heart failure is defined as a gradual or rapid change in heart failure signs and symptoms, resulting in a need for urgent therapy. The symptoms primarily occur from pulmonary congestion leading to sudden shortness of breath. Chronic heart failure is a long-term condition that can usually be kept stable with adequate treatment.

13. What Is Right-Sided Heart Failure?

The right ventricle of the heart pumps the blood out of the heart, through the pulmonary artery and into the lungs where it is replenished with oxygen.

In most cases, heart failure is caused by dysfunction of the left ventricle. Right-sided or right ventricular heart failure usually occurs as a result of left-sided failure.

When the left ventricle becomes dysfunctional, increased fluid pressure is transferred back through the lungs and ultimately to the right ventricle.

Increased fluid pressure in the lungs is called pulmonary hypertension. Although pulmonary hypertension can occur in isolation, it most commonly results from a dysfunction of the left ventricle.

The right ventricle has a limited capacity to deal with increased resistance caused by a pressure increase in the pulmonary circulation. Consequently, when the right ventricle starts to fail, blood backs up in the body’s veins, causing congestion and swelling of the legs and ankles. Furthermore, the liver may become congested, and fluid may accumulate in the abdominal cavity (ascites).

Right-sided heart failure is caused by dysfunction of the right ventricle. Right ventricular heart failure usually occurs as a result of left-sided failure. Symptoms include congestion and swelling of the legs and ankles and swelling of the abdomen.

Right-sided heart failure is caused by dysfunction of the right ventricle. Right ventricular heart failure usually occurs as a result of left-sided failure. Symptoms include congestion and swelling of the legs and ankles and swelling of the abdomen.

14. How Is Heart Failure Diagnosed?

The approach to the patient with suspected heart failure includes the history and physical examination and diagnostic tests to help establish the diagnosis, assess severity, and determine the underlying cause (32).

It is essential to take a blood sample to assess hemoglobin, kidney function (serum creatinine), sodium and potassium, blood sugar, and liver enzymes.

A measurement of brain natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) can help to confirm the diagnosis and severity of heart failure.

An electrocardiogram (ECG) will help to determine the rhythm of the heart. It may also provide information about previous damage to the heart muscle caused by a heart attack (myocardial infarction).

An ultrasound examination, also called echocardiogram, provides essential information about the structure of the heart, the heart valves, the pumping capacity of the heart muscle, the presence of pulmonary hypertension, and the the stiffness of the left ventricle (diastolic function). It is commonly used to calculate the ejection fraction (EF).

A chest X-ray may be used to determine if the heart is enlarged and whether there are signs of congestion of the lungs.

A stress test may be performed to assess how the heart responds to exertion.

A more specific stress test may be used to determine VO2 max, also known as maximal oxygen uptake. It is the measurement of the maximum amount of oxygen a person can utilize during intense exercise and is commonly used to measure cardiovascular fitness.

Computerized tomography (CT) and magnetic resonance imaging (MRI) provide essential information about the anatomy and function of the heart muscle and heart valves. These imaging techniques may help determine the underlying cause of heart failure.

Coronary angiography is often performed to study the coronary arteries and whether coronary artery disease is present or not.

The approach to the patient with suspected heart failure includes the history and physical examination, and diagnostic tests to help establish the diagnosis, assess severity, and determine the underlying cause.

15. What Is the Role of  Brain Natriuretic Peptide (BNP) and N-Terminal-Pro-B-Type Natriuretic Peptide

B-type natriuretic peptide (BNP) and N-terminal pro-b-type natriuretic peptide (NT-proBNP) are peptides (small proteins) produced by heart muscle cells (33).

BNP was initially named brain natriuretic peptide because it was first found in brain tissue. However, BNP is actually produced primarily by cells in the left ventricle of the heart.

Small amounts of a precursor protein, pro-BNP, are continuously produced by the heart muscle. Pro-BNP is then split by to release the active hormone BNP and an inactive fragment, NT-proBNP, into the blood.

BNP has many biologic functions. It increases the excretion of sodium and water through the kidneys (diuretic effect). It also reduces the secretion of aldosterone from the adrenal glands, and it relaxes vascular smooth muscles in arteries and veins (vasodilatation).

The concentrations of BNP and NT-proBNP produced can increase markedly in patients with left ventricular dysfunction and heart failure.

Measurements of plasma BNP are helpful in the evaluation of patients with dyspnea.  They are commonly used for the evaluation of suspected heart failure when the diagnosis is uncertain (34). Hence, the main clinical utility of either BNP or NT-proBNP is that a normal level will help to rule out heart failure.

In general, the following cut off values may be employed for patients with acute dyspnea (35):

BNP NT-proBNP
< 100 pg/mL – heart failure unlikely < 300 pg/mL – heart failure unlikely
>400 pg/mL – heart failure likely Age < 50 years, NT-proBNP >450 pg/mL – heart failure likely
100-400 pg/mL – use clinical judgment Age 50-75 years, NT-proBNP >900 pg/mL – heart failure likely
  Age >75 years, NT-proBNP >1800 pg/mL – heart failure likely

Plasma BNP also provides prognostic information in patients with chronic heart failure and those with asymptomatic or minimally symptomatic LV dysfunction (36)

Measurements of BNP and NT-pro BNP may be used to monitor patients with heart failure, especially those with moderate to severe symptoms. A rise in plasma BNP above the patient’s own baseline value should trigger closer assessment for a possible worsening of the condition.

The main clinical utility of either BNP or NT-proBNP is that a normal level will help to rule out heart failure. Measurements of BNP and NT-pro BNP may also be used to monitor patients with established heart failure.

16. What Is the Prognosis of Patients with Heart Failure?

Unfortunately, the prognosis for patients with advanced heart failure has remained alarmingly poor over the last thirty years. However, long-term mortality rates have improved over time (37).

On the other hand, left ventricular dysfunction and heart failure cover a broad spectrum ranging from minimal symptoms to advanced disease. Hence it is vital to acknowledge that prognosis varies according to the stage of the condition.

The two leading causes of death in patients with heart failure are sudden death and progressive pump failure. Evidence suggests that approximately 30 to 50 percent of all cardiac deaths in patients with heart failure are sudden deaths (38).

There are some data to suggest that heart failure-related mortality is comparable to that of cancer (39). For example, in the original and subsequent Framingham cohort, the probability of someone with a diagnosis of heart failure dying within five years was 62% and 75% in men and 38% and 42% in women, respectively (40). In comparison, five-year survival for all cancers among men and women in the US during the same period was approximately 50%.

The need for hospitalization is an important marker for poor prognosis (41).

The mortality rate in treated patients with heart failure increases with age.

Most studies suggest that the prognosis is better in women than men (42).

A study from the Mayo Clinic showed that for the periods 1979 to 1984 compared with 1996 to 2000, the one-year mortality fell from 30 to 21 percent in men and from 20 to 17 percent in women in patients hospitalized for heart failure. The five-year mortality fell from 65 to 50 percent in men and from 51 to 46 percent in women (43).

Advanced heart failure has a dismal prognosis. The mortality rate increases with age but prognosis is better in women than men. Hospitalization for heart failure is a marker for poor prognosis.

17. How Is Heart Failure Treated?

The treatment of heart failure depends on the underlying cause and the severity of symptoms.

In patients with stage A and B the, main goal is the prevent the occurrence of clinical heart failure.

Patients at risk of heart failure but no structural damage to the heart (stage A) should quit smoking and exercise regularly. High blood pressure and lipid disorders should be treated. Alcohol should be used in moderation or not at all. Underlying conditions, such as diabetes and coronary heart disease, should be addressed.

Patients with heart disease without signs of heart failure (stage B) should be treated according to the underlying condition. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are recommended for patients with left ventricular dysfunction (44).

Acetylsalicylic acid (baby aspirin) and statins are recommended for patients with established coronary artery disease.

Beta-blockers are usually recommended for patients who have suffered a heart attack (myocardial infarction).

Patients with symptomatic heart failure (stage D and E) usually need diuretic drugs to relieve congestive symptoms and restricting dietary sodium intake is generally recommended. Furosemide is the most commonly used loop diuretic for the treatment.

In patients with stage E and D, treatment with ACE inhibitors, ARB’s or angiotensin receptor-neprilysin inhibitors (ARNI) is recommended. A beta-blocker should be added if tolerated.  Aldosterone antagonists (antimineralocorticoid) should be added on top of this treatment. All these drugs may improve prognosis and reduce the need for hospitalizations, particularly in patients with reduced ejection fraction (EF)(45).

African American patients may benefit from the addition of a hydralazine/nitrate combination (46).

Patients with advanced symptoms should be evaluated for cardiac resynchronization therapy (CRT) and the use of an implantable cardioverter-defibrillator (ICD).

The treatment of heart failure depends on the underlying cause and the severity of symptoms. Prevention is the main target in patients with stage A and B heart failure. Patients with stage D and E should be given multidrug therapy to limit the progression of the disorder and improve prognosis.

18. What Is the Role of Cardiac Resynchronization (Therapy CRT)?

A CRT device has 2 or 3 leads (wires) that are positioned in the right atrium, right ventricle, and the left ventricle (via the coronary sinus vein). https://www.fairview.org/patient-education/90148

Cardiac resynchronization therapy (CRT), also called biventricular pacing, may benefit heart failure patients with moderate to severe symptoms and whose left and right heart chambers do not beat in unison.

The CRT pacing device is an electronic, battery-powered device that is surgically implanted under the skin.

The device has 2 or 3 leads (wires) that are positioned in the right atrium, right ventricle, and the left ventricle (via the coronary sinus vein) (47). The leads are implanted through a vein.

CRT is not valid for everyone and is not recommended for those with mild symptoms or diastolic heart failure.

Furthermore, CRT is only useful when the left and right heart chambers do not beat synchronously. Whether this is the cased can usually be found out on a regular twelve lead electrocardiogram (ECG).

Most patients who receive a CRT device have a left bundle branch block (LBBB) on the ECG.

There are two types of CRT devices. Depending on your heart failure condition, a Cardiac Resynchronization Therapy Pacemaker (CRT-P) or a Cardiac Resynchronization Therapy Defibrillator (CRT-D).

Cardiac resynchronization therapy (CRT), also called biventricular pacing may benefit heart failure patients with moderate to severe symptoms and whose left and right heart chambers do not beat in unison.

19. What Is the Role of Implantable Cardioverter-Defibrillators (ICD)?

Studies suggest that approximately 30 to 50 percent of all cardiac deaths in patients with heart failure are sudden deaths (35). These deaths are usually caused by lethal arrhythmia, most often sustained ventricular tachycardia or ventricular fibrillation.

An implantable cardioverter-defibrillator (ICD) is a battery-powered device placed under the skin. The device keeps track of the heart rhythm. Wires connect the ICD to the heart through a vein. If an abnormal, fast heart rhythm is detected, the device will deliver an electric shock to restore a normal heartbeat.

ICDs are useful in preventing sudden death in patients with known, sustained ventricular tachycardia or fibrillation or high risk of such arrhythmias.

Selecting patients for ICD treatment is complicated because the devices do not benefit all patients with heart failure.

The usefulness of ICD depends on the severity of left ventricular systolic dysfunction, the underlying cause of heart failure, and the severity of symptoms (48).

An implantable cardioverter-defibrillator (ICD) is a battery-powered device placed under the skin that keeps track of the heart rhythm. If an abnormal, fast heart rhythm is detected, the device will deliver an electric shock to restore a normal heartbeat.

20. What Is a Ventricular Assist Device (VAD)?

A left ventricular assist device (LVAD) is an implantable pump that helps pump blood from left ventricle to the aorta.

A ventricular assist device (VAD) is an implantable pump that helps pump blood from the ventricles.

A VAD is most frequently used to assist the left ventricle. Hence, the term left ventricular assist device (LVAD).

The devices are only used in patients with advanced, end-stage heart failure.

A VAD can be used both temporarily, for example, while waiting for heart transplantation (bridge to transplantation), or as permanent support.

Interestingly, VAD’s may be quite useful in relieving symptoms (49). Patients may even be able to exercise and return to work.

However, the use of VAD’s is sophisticated, and there is a risk of complications, including infections, neurological events, pump thrombosis blood clotting), and bleeding.

A ventricular assist device (VAD) is an implantable pump that helps pump blood from the ventricles. VAD’s are only used in patients with advanced, end-stage heart failure.

21. What Is the Role of Heart Transplantation?

Heart transplantation is the procedure by which the failing heart is replaced with another heart from a suitable donor.  

It is generally reserved for patients with end-stage heart failure who are estimated to have less than one year to live without a transplant and who are not candidates for or have not been helped by conventional medical therapy (50).

Candidates for heart transplantation usually have New York Heart Association (NYHA) class III (moderate) symptoms or class IV (severe) symptoms and en ejection fraction lower than 25 percent.

Immunosuppressive drug therapy is started soon after surgery to prevent rejection of the new organ.

A thorough workup is necessary to decide if a patient is a candidate for heart transplantation.

The upper age limit is generally considered to be 65 years. However, older patients may also be treated under specific circumstances.

Patients with active systemic infection, severe underlying disease (e.g., cancer, collagen-vascular disease), ongoing history of substance abuse (e.g., alcohol, drugs, or tobacco), psychosocial instability or inability to cope with follow-up care are not candidates for heart transplantation.

Heart transplantation is the procedure by which the failing heart is replaced with another heart from a suitable donor. It is generally reserved for patients with end-stage heart failure who are estimated to have less than one year to live without the transplant and who are not candidates for or have not been helped by conventional medical therapy.




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Why and How To Lower Triglycerides in People at Risk of Heart Disease

Estimated reading time: 11 minutes

Triglycerides are important organic compounds. Most of the fat we consume in our diet is triglyceride and so is most of the fat we store in our body.

Fatty acids contained in triglycerides are an essential source of energy for human cells.

Triglyceride concentration can be measured in blood and may provide valuable information about metabolism and general health. High levels may reflect underlying metabolic disorders and evidence shows that high blood triglycerides are associated with increased risk of heart disease (1,2,3).

However, association only means that there is a correlation between two or more variables. In this case, the higher the blood triglycerides, the higher the risk of developing heart disease.

Hence, discovering an association between variables does not prove a causative relationship. Here, a correlation between triglyceride levels and the risk of heart disease does not prove that triglycerides cause heart disease. Nor does it prove that lowering them will prevent disease.

Interestingly, when it comes to assessing the risk of cardiovascular disease, triglycerides have always played second fiddle to cholesterol.

As a result, dietary advice for people with heart disease usually aims at lowering blood cholesterol, particularly LDL-cholesterol. Targeting LDL- cholesterol has become common practice.

Therefore, replacing saturated fat with polyunsaturated and monounsaturated fats, and increasing the intake of food products rich in fiber and complex carbohydrates such as whole grains, is usually recommended.

Interestingly, it may be tricky to address triglycerides at the same time as LDL cholesterol. The reason is that a diet that lowers LDL cholesterol may raise triglycerides and vice versa. For example, low-fat diets may lower LDL cholesterol but are less effective in lowering triglycerides compared to low-carbohydrate diets (4).

Another reason why main stream medicine has tended to ignore triglycerides is that the pharmaceutical industry has shown limited interest in developing drugs that influence triglycerides. However, this may have changed recently with the publication of the highly important REDUCE-IT trial (5).

Triglyceride-Rich Lipoproteins

High blood levels of triglycerides are most often associated with high levels of the two most important triglyceride-rich lipoproteins; chylomicrons and very low density lipoproten (VLDL).

The main role of these lipoproteins is to transport triglycerides and other types of lipids, such as cholesterol, in the circulation.

Triglycerides are composed of three molecules of fatty acids attached to a glycerol molecule.

Chylomicrons are formed in the intestine after a meal. They contain triglycerides and small amounts of cholesterol.

Chylomicrons are subsequently broken down by an enzyme called lipoprotein lipase into free fatty acids that are utilized for energy production by the heart and skeletal muscles or stored in fat (adipose) tissue.

The chylomicron remnants are then removed from the circulation by liver cells.

VLDL is produced by liver cells. It transports both triglycerides and cholesterol. Once in the circulation, VLDL is broken down by lipoprotein lipase in capillary beds, releasing triglycerides for energy utilization by cells or storage in adipose tissue.

The composition of VLDL changes when triglycerides have been released. VLDL then becomes becomes intermediate-density lipoprotein (IDL). Later, when the amount of cholesterol increases, IDL becomes low-density lipoprotein (LDL).

Triglyceride-Rich Lipoproteins Are Associated With Inflammation and Atherosclerosis

Triglyceride rich lipoproteins are associated with inflammation and increased atherosclerosis (6).

High levels of chylomicrons increase the risk of acute pancreatitis, an inflammation of the pancreas. Chylomicron and VLDL remnants increase inflammation of the endothelium (the innermost layer of the artery).

Chylomicron remnants and VLDL remnants have been shown to rapidly penetrate the arterial wall and promote atherosclerosis (7).

Recent data suggests that VLDL cholesterol or remnant cholesterol is a stronger promoter of atherosclerosis than LDL cholesterol (8).

Definition of Normal and High Levels of Triglycerides

Blood levels of triglycerides are stratified according to population data and their associated risk of coronary artery disease.

In the USA, triglycerides are measured in mg/dL but in Australia, Canada, and most European countries they are measured in mmol/L.

To convert from mg/dL to mmol/L, divide by 88.5

Here is how triglyceride levels are looked at in terms of cardiovascular risk:

Normal: <150 mg/dL (1.7 mmol/L)

Borderline high: 150 to 199 mg/dL (1.7 to 2.2 mmol/L)

High: 200 to 499 mg/dL (2.3 to 5.6 mmol/L)

Very high: ≥500 mg/dL (≥5.7 mmol/L)

The term hypertriglyceridemia is used to describe high blood levels of triglycerides.

Hypertriglyceridemia is a relatively common disorder. In the United States, 33 percent of adults have triglyceride levels above 150 mg/dl (1.7 mmol/L) and 18 percent have levels above 200 mg/dl (2.3 mmol/L)(9).

Fasting and Non-Fasting Levels of Triglycerides

Following a fatty meal, blood levels of triglycerides will rise. Hence, raised blood triglycerides following a meal (postprandial hypertriglyceridemia) are caused by chylomicrons produced in the intestine.

Chylomicrons disappear from the circulation soon after the triglycerides have been delivered to the tissues.

Moderate fasting hypertriglyceridemia is usually due to increased VLDL production by the liver. This is often a result of excessive carbohydrate intake.

Triglycerides may also become elevated with obesity, physical inactivity, smoking, diseases such as diabetes and renal failure, drugs such as estrogen, tamoxifen and corticosteroids, and genetic disorders (familial hypertriglyceridemia, familial combined hyperlipidemia, and familial dysbetalipoproteinemia).

There are several types of familial hypertriglyceridemia. These disorders are associated with increased risk of coronary artery disease (10) which appears independent of cholesterol levels (11).

Serum triglyceride values above 1000 mg/dL (11 mmol/L) are rare (less than 1/5000 individuals). The serum in these patients is opalescent due to an increase in VLDL or milky due to elevated chylomicrons.

Triglycerides and Cardiovascular Disease

Despite evidence that chylomicron and VLDL remnants promote atherosclerosis, the importance of lowering triglycerides has so far not been considered a priority for patients with coronary heart disease.

However, several conditions associated with high triglycerides, such as insulin resistance, a preponderance of small LDL particles, and low HDL- cholesterol, may play an important role in the development of atherosclerosis.

Reduced activity of lipoprotein lipase, which is common in insulin resistance, may slow the clearance of triglyceride-rich lipoproteins from the circulation.

VLDL remnants may enter the vessel wall or be converted to small LDL particles. Small LDL particles tend to circulate for a longer duration where they become susceptible to oxidation, glycation, and glyco-oxidation leading to increased risk of atherosclerosis.

Small dense LDL particles appear more strongly associated with the risk of cardiovascular events than larger particles (12,13). 

In the so-called SCRIP trial, high triglyceride levels were associated small, dense particles in 90 percent of subjects whereas lower triglyceride levels were associated with larger buoyant particles in 90 percent of subjects (14).

Recent genetic studies have addressed the relationship between triglyceride-rich lipoproteins and the risk of cardiovascular events. The results of one of these studies imply that the elevated cholesterol content of triglyceride-rich lipoprotein particles may cause coronary heart disease (15).

Another study found that a genetic mutation associated with low blood levels of triglycerides was associated with less risk of cardiovascular disease (16).

These studies strongly support the hypothesis that high blood levels of triglycerides may increase the risk of cardiovascular disease and that low levels may be protective.

The REDUCE-IT Trial – A Landmark Cardiovascular Study

The results of the REDUCE-IT trial were recently published in the New England Journal of Medicine and The Journal of the American College of Cardiology) (5,17).

The study randomized 8,179 statin-treated patients with triglycerides ≥135 and <500 mg/dL and LDL-cholesterol >40 and ≤100 mg/dL , and a history of atherosclerosis (71% patients) or diabetes (29% patients) to icosapent ethyl 4g/day or placebo.

Icosapent ethyl is a highly purified and stable EPA ethyl ester that has been shown to lower triglyceride levels.

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are the two most common long chain n-3 polyunsaturated fatty acids (PUFAs) in fish oil. Both are omega-3 fatty acids.

The primary cardiovascular outcome of cardiovascular death, nonfatal myocardial infarction, stroke, coronary revascularization, or unstable angina, for icosapent ethyl vs. placebo, was 17.2% vs. 22.0%. The absolute risk reduction of 4.8% is highly significant.

Triglyceride levels were lowered at one year by 39.0 mg/dl vs. 4.5 mg/dl on on icosapent ethyl vs. placebo. LDL cholesterol was lowered by 2 mg/dl vs. 7 mg/dl.

The rate of cardiovascular death was 9.6% vs 12.4 % on icosapent ethyl vs. placebo which is statistically significant. All-cause mortality was 6.7% vs. 7.6%, which is not statistically significant.

The risk of atrial fibrillation/flutter was 5.3% vs 3.9% and the risk of serious adverse bleeding was 2.7% vs. 2.1% on icosapent ethyl vs. placebo

Why Is the REDUCE-IT Trial so Important?

The large number of important ischemic events averted with icosapent ethyl, including a significant reduction in fatal and nonfatal stroke (28%), cardiac arrest (48%), sudden death (31%), and cardiovascular death (20%), is indicative of a very favorable risk- benefit profile

Although several mechanisms may explain the efficacy of the drug it has to be assumed that the lowering of blood triglycerides is the most important.

The study results are in stark contrast to cardiovascular outcome studies with other agents that lower triglyceride levels and with low-dose omega-3 fatty acid mixtures, where cardiovascular outcome benefit has not been consistently observed in statin-treated patients (17).

The distinction of the cardiovascular benefits observed in REDUCE-IT from the lack of cardiovascular benefits observed in statin-treated populations with add-on omega-3 fatty acid mixtures may likely be due to the high EPA levels.

EPA has unique lipid and lipoprotein, anti-inflammatory, anti-platelet, anti-thrombotic, and cellular modifying effects.

REDUCE-IT is the first trial to show that lowering triglycerides without affecting LDL-cholesterol significantly improves clinical outcome in high risk patients.

With the rapidly increasing prevalence of central obesity and metabolic syndrome , targeting triglycerides me even become more important in the near future.

Whether targeting triglycerides by dietary measures will improve cardiac outcome remains to be proven.

However, it would be naive to believe that dietary measures that tend to lower triglycerides are less important than those intended to lower LDL-cholesterol.

The Management of High Triglycerides

Non-Pharmacological Therapy

Lifestyle modification is the first-line therapy for people with elevated triglycerides.

Many individuals with high triglycerides have insulin resistance and metabolic syndrome. In these cases, hypertriglyceridemia is often associated with visceral obesity low levels of HDL cholesterol, high blood pressure and type 2 diabetes.

In mild to moderate hypertriglyceridemia, losing weight and reducing carbohydrate intake (especially high glycemic index foods and high fructose foods) can lower VLDL and triglycerides.

For these patients, weight loss, regular physical exercise, and avoidance of added sugars (18) are all important. Other risk factors such as smoking and high blood pressure should also be addressed (19).

Fatty acids used by the liver to produce VLDL are derived mainly from two sources.

Firstly, during conditions such as obesity, diabetes, and insulin resistance, there is increased fatty acid flux from adipose tissue to the liver. Secondly, there is an increased de novo synthesis of fatty acids in the liver mainly from carbohydrates.

For this reason, in mild to moderate hypertriglyceridemia, losing weight and reducing carbohydrate intake (especially high glycemic index foods and high fructose foods) can lower VLDL and triglycerides.

Dietary fat is not a significant source of liver triglyceride (20), and high fat diets usually don’t raise fasting triglycerides.

The situation may be different in more severe hypertriglyceridemia (above 500 to 1000 mg/dL (5.6 to 11.3 mmol/L)), where the clearance of chylomicrons becomes very slow. Under these circumstances, it is crucial to reduce dietary fat intake to lower triglycerides.

It is necessary for patients with severe hypertriglyceridemia to avoid alcohol abuse as it can cause substantial increases in triglyceride levels and cause acute pancreatitis.

Pharmacological Therapy

Several drugs are used for the management of hypertriglyceridemia.

Although statins are not very effective for lowering triglycerides per se, they are often used to reduce the risk of cardiovascular events in patients with hypertriglyceridemia.

One of the most commonly used drug to lower triglycerides is gemfibrozil (21).

Gemfibrozil belongs to a group of drugs called fibrates which lower triglycerides by increasing the synthesis of lipoprotein lipase which increases the clearance of triglycerides. 

Fibrate therapy with either fenofibrate or gemfibrozil can reduce triglyceride levels by 20 to 50 percent. In severe hypertriglyceridemia, gemfibrozil may lower triglycerides as much as 70 percent (22).

In the Helsinki Heart Study, a clinical benefit of gemfibrozil therapy was found in the group with a triglyceride level >201 mg/dL (2.3 mmol/L) and an LDL-C/HDL-C ratio >5.0 (23).

The VA-HIT trial assessed the efficacy of gemfibrozil in patients with low HDL cholesterol, relatively low LDL cholesterol, and mild to moderate hypertriglyceridemia (24). Gemfibrozil raised HDL cholesterol by 6 percent, lowered triglycerides by 31 percent, but had no significant effect on LDL cholesterol. At five years, there was an absolute risk reduction of 4.4 percent with gemfibrozil.

In the ACCORD Lipid trial, fenofibrate improved outcomes in type 2 diabetes in a subset of patients with elevated triglyceride levels and low HDL cholesterol (25).

Nicotinic acid at doses of 1500 to 2000 mg daily can reduce triglyceride levels by 15 to 25 percent (26). However, studies supporting a clinical efficacy of nicotinic acid are lacking. There is data suggesting worsening of glycemic control when nicotinic acid is administered to patients with type 2 diabetes (27).

The AIM-HIGH trial studied the addition of nicotinic acid to statin therapy in patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of less than 70 mg/dL (1.81 mmol/L)(28). 

There was no incremental clinical benefit from the addition of nicotinic acid during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels.

Intake of fish oil (29) can lower blood triglycerides by as much as 50 percent (30). Relatively high doses of omega-3 fatty acids (EPA + DHA) are needed to achieve this effect (up to 3-4 g/day).

Lovasa (Omecor) and icosapent ethyl (Vascepa) are commercial preparations of omega-3 fatty acids that can lower blood triglycerides by as much as 45 percent (31,32).

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Exploring the “Lore of Nutrition”

Estimated reading time: 10 minutes

For the last few days, my Kindle has been my closest companion.

“What are you reading”? my wife asked. “I’m reading Lore of Nutrition.”

“Ooh, I was sure it was a thriller or one of your crime stories.”

In fact, she was right. Although Lore of Nutrition is a book about nutrition, it reads like a novel. The omertà, the courtroom drama, the hero and the villain (lots of them). Lore of Nutrition has it all.

And, if you’re a cardiologist, the book may read like a Stephen King horror story. However, this time, the horror is real. You’ll just have to hope for a happy ending.

Of course, Lore of Nutrition is not the first book to challenge accepted medical and scientific dogma. But, it rises above most of them due to its reliance on scientific evidence, its honesty, and bravery. Apart from being a book about nutrition, it is a fascinating story about a man fighting for his credibility and beliefs and his right speak out to the public.

Lore of Nutrition

Lore Of Nutrition is co-authored by two South Africans; sports scientist Professor Tim Noakes and journalist Marika Sboros.

In the preface, Professor Noakes summarizes his background as a doctor and scientist. And what a distinguished career it is. Of course, one might wonder why he has to recapitulate it in such detail. However, when reading on, one learns why he is forced to underscore his credibility.

Tim Noakes has all the characteristics of an opinion maker. His charisma and ability to speak out and explain will make most of us want to listen.

Noakes describes his “Damascene moment”: “It happened after I came face to face with compellingly robust evidence that contradicted everything I believed was true about optimum nutrition to treat and prevent serious diseases, such as obesity, diabetes, and heart disease.”

Noakes challenges two deeply held dogmas: “the role of carbohydrate in nutrition and the diet-heart hypothesis that saturated fat causes heart disease”.

Unfortunately, Noakes learned that the results of his choice to admit his errors and try to correct them would be brutal for himself and his family, “beyond anything that he possibly could have imagined.”

Lore of Nutrition has three main parts.

The first part is about the low-carb revolution in South Africa and Noakes’s first experience with a low-carb, high fat (LCHF) diet. It covers, among other things, the 2015 Low-Carb Summit in Cape Town, the so-called UCT Professor’s letter, The Naudé Review (1), and “The Banting for Babies Tweet” which sparked the now famous Noakes Trial.

The second part covers the trial that was spread over three years, the hearing, the closing arguments and the verdict.

The third part summarizes essential scientific evidence supporting the LCHF dietary plan.

Noakes now claims the evidence for the LCHF dietary model is the “best evidence-based model of modern human nutrition. Conversely, the low-fat, high-carb (LFHC) “prudent”, “balanced” diet promoted by most health authorities, and religiously taught at all South African medical schools is at best not evidence-based, at worst completely wrong and extremely harmful because it has caused the obesity and type-2 diabetes epidemic.”

Why Does Tim Noakes Have so Many Powerful Enemies?

For an outsider, it is hard to understand why Tim Noakes has so many powerful enemies in his home country and why they believe it’s so important to demolish him. Why do the medical and dietic professional societies in South Africa (HPSCA and ASDA) go to such great lengths to shut him down? After all it’s just a scientific debate, isn’t it?

Of course, Noakes has expressed opinions that conflict with those taught at the universities. He believes that “the function of universities is to advance knowledge, not to insulate professorial opinions from external scrutiny and thus institutionalize what he calls the power of the anointed.” He writes: “I believe the very reason why universities exist is because we do not (yet) know everything. If we did, we would have no reason to invest so much in costly institutions.”

Noakes also claims the low-fat diet that has been highly promoted for decades is the most likely cause of the epidemic of obesity and type-2 diabetes. He writes: “It is difficult for those who have advocated this fallacy for the past 40 years to suddenly find the courage to acknowledge and apologize for their gross error.”

Or is it Noakes’s methods and how he reaches out to the public that is the problem? Is using social media inappropriate for medical professionals and scientists?

When covering the 2015 Low-Carb summit, Marika Sboros mentions that one of the attendees at the meeting was Jacques Rousseau, a lecturer at the UCT Faculty of Commerce, and an active critic of LCHF and Tim Noakes. Rousseau writes a personal blog called Synapses (2).

Being curious to find out more about a Noakes critic, I took a look at Rousseau’s blog. It is about politics, science, religion, and rationality.

Of course, I was not able to read everything Rousseau has written, but his blog appears to be of high quality, regardless of whether one agrees with him or not.

There are 32 articles on his blog in the series “Noakes”. I wonder if that should that be defined as an obsession?

Interestingly, I found a podcast interview with Rousseau where he says about Noakes: “My criticism has always been about the tone and the approach taken in making the arguments but not about the science and the arguments themselves (3).” So could it be that it is not about what Noakes believes is right or wrong but about how he goes about it?

In Lore of Nutrition, Noakes mentions that the regular headaches he had suffered from disappeared after adopting an LCHF eating plan. He writes: “This is understandable if an allergy to wheat gliadin is a common cause of recurrent headaches, as cardiologist Dr. William Davis proposed in his bestselling book Wheat Belly. Or if a majority of common headaches are caused by gluten sensitivity, as neurologist Dr. David Perlmutter suggested in another New York Times bestseller, Grain Brain.

Being a Noakes admirer, I thought: Please don’t say this. Speculating may be fine, but citing such controversial literature is not very scientific and best avoided in my opinion. I wonder if that’s what Rousseau’s all about.

In a blog post addressing Lore of Nutrition, Rousseau writes: “In short, there’s no vendetta, and if there is a conspiracy, I don’t know of it. Some people (like me) just think Prof. Noakes expresses contingent and as-yet-unproven claims too boldly, in a way that runs ahead of available evidence, whether or not they end up being proven true.”

In another instance, Rousseau writes: “There’s certainly a possibility that he (Noakes) and others are right. As I’ve tried to emphasize, it’s the tone and content of the argument for the conclusion – not the conclusion itself – that I’m addressing (4).”

Tima Noakes, Gary Taubes, and Axel F. Sigurdsson (Reykjavik 2016)

How Will the Cardiologists Respond?

Cardiologists get a fair share of beating in Lore of Nutrition. The critic is specifically aimed at those who do percutaneous coronary interventions (i.e., coronary angioplasty and stenting). I guess it’s fair to mention that I’ve been doing these procedures for more than 20 years myself.

Noakes writes: “Cardiology is responsible for initiating and performing more unnecessary, non-evidence based and costly medical interventions than perhaps any other medical discipline.”

In fact, he may be right. On the other hand, I would like to claim that cardiology is probably the most evidence-based of all medical disciplines.

Noakes goes on by saying that coronary artery bypass surgery “is unnecessary for the vast majority of patients with stable coronary artery disease.” He also says that “in patients with chronic stable coronary artery disease, in the absence of recent myocardial infarction (heart attack) percutaneous coronary intervention does not offer any benefit in terms of death, myocardial infarction, or the need for subsequent revascularization compared with conservative medical treatment.”

Of course, one might be surprised that I don’t disagree with these claims, but I wish Noakes would have mentioned that coronary angioplasty and stenting is an effective treatment strategy for acute coronary syndrome, particularly ST-elevation myocardial infarction (STEMI).

Acute coronary syndrome is a disorder caused by a ruptured atherosclerotic plaque which Noakes elegantly explains in Lore of Nutrition and is the most common reason for a sudden obstruction of blood flow to the heart. There is probably no medical intervention as effective as immediate angioplasty with stenting to open up a recently obstructed coronary artery.

Noakes’s take on statins is fast and furious: “It is of little value to take a drug that might marginally reduce one’s risk of suffering a heart attack or stroke if it increases the risk of dying from something else, without any extension in life expectancy.” Here he is citing the fact that no study has shown benefits of statin treatment in terms of mortality in patients without established cardiovascular disease (primary prevention).

Noakes writes: “Perhaps cardiologists should take heed of the old dictum that “those who live in glass houses should not throw stones”. If you make your money prescribing drugs or performing invasive procedures that have little or no proven benefit and which may cause harm, you need to be very wary of accusing others of doing harm. When it comes to the dietary advice that I promote you should be especially cautious, as there is no published scientific evidence that it causes harm.”

Luckily, not all cardiologists are stone throwers.

The Role of Insulin Resistance

According to recently published evidence, at least 50% of the adult population in the U.S. have insulin resistance, manifested as diabetes or prediabetes (5). Noakes believes this number may be at least 60%. He writes: “Insulin resistance is now certainly the most prevalent medical condition in the world, yet it is not taught or discussed in medical schools.

In the last part of Lore of Nutrition, Noakes writes: “By now it should be clear that all the evidence incriminates carbohydrates and insulin resistance as the key drivers of our current epidemics of ill health.”

Interestingly, he believes that insulin resistance is a relatively benign condition. However, a high carbohydrate diet turns it into a killer. Hence, if you’re insulin resistant, you cannot eat carbohydrates (6).

The Noakes Trial

On 3 February 2014, Twitter user Pippa Leenstra tweeted the following to Tim Noakes and Sally-Ann Creed, his co-author on The Real Meal Revolution: 

is LCHF ok for breastfeeding mums? Worried about all the dairy + cauliflower = wind for babies??

Two days later, Noakes tweeted his response to Pippa Leenstra and Sal Creed (7).

Baby doesn’t eat the dairy and cauliflower. Just very healthy high fat breast milk. Key is to ween [sic] baby onto LCHF.

Time Noakes’s tweet is basically what initiated the HPCSA’s charge against him and the subsequent trial. He was accused of acting in a manner not in accordance with the norms and standards of his profession and for providing unconventional advice on breastfeeding babies on social networks.

Marika Sboros was the only journalist to cover all the hearing sessions of the Noakes trial. She elegantly summarizes the hearing, the closing arguments, and the verdict in Lore of Nutrition.

The Bottom-Line

Lore of Nutrition is a fascinating book. It contains a story that must be told and a message that has to be read.

However, don’t let the name fool you. It’s about so much more than nutrition. It’s about science, public health, cardiovascular disease, fatty liver disease, diabetes, the food industry, the diet-heart hypothesis, the pharmaceutical industry, obesity, social media, politics, corruption and academic bullying.

Noakes’s knowledge, passion, and courage allow him to write in a ruthless manner that is shockingly revealing. Of course, this may be too much and too bold for some of his peers.

Clearly, Noakes can’t be right about everything, but he certainly deserves to be listened to.

Marika Sboros’ contribution adds to the diversity of the book. Her coverage of the Noakes trial strengthens the storyline and makes the book unique.

It is quite clear that Lore of Nutrition will not help Tim Noakes make peace with his enemies. However, he might make some new friends.




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