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Adverse Health Effects of Fume Events and Air Quality Incidents on Commercial Aircraft

Reports of possible cabin air contamination onboard aircraft on commercial flights have become increasingly common in recent years. Such incidents are often described as fume events.

Most often, fume events describe abnormal odors, smoke, haze or fumes in the cabin which may arise from various internal or external sources in an aircraft.

More specifically, the term “fume event” is used to refer to a potentially toxic environment created by contaminated bleed air used to pressurize and ventilate aircraft cockpit and cabins.

However, bleed air contamination is not the only cause of fume events or medical symptoms among passengers and crew onboard commercial aircraft. Reduced oxygen levels, ozone, de-icing fluids, insecticides, fuel vapor, and fumes from ground service vehicles or other aircraft may also be responsible (1).

Hence, the term “air quality incident” is probably more appropriate than “fume event” or “bleed air contamination.”

Concerns have repeatedly been raised about the possible adverse health effects of exposure to contaminants in cabin air. Although known for decades, air quality incidents continue to represent potential safety hazards for passengers and crew on commercial flights.

Reports of suspected fume events often reach the news media.

In October 2016, British Airways flight BA286 from San Francisco to London was diverted to Vancouver after members of the crew became unwell, the airline said on Tuesday.

Michele Kropf, a spokeswoman for British Airways, said 25 crew members were taken to local hospitals as a precaution, but had now been discharged. There were 22 cabin crew and three pilots on board the plane.

But on Wednesday morning ABC News obtained a recording of the conversation between the pilot and Air Traffic Control.

“Can you say again the emergency for me please?” the controller asked.

The pilot replied: “Toxic fumes. Toxic gas-type fumes.”

BA did not comment on the cause of the problem (2).

Sometimes, crewmembers have reported a visible haze or smoke in the cabin/flight deck, or a smell often described as “dirty socks,” “chemicals,” “vomit,” or “burning oil.”

In 2017 an American Airlines Airbus A319-100, registration N829AW performing flight AA-1927 from Charlotte, NC to Raleigh/Durham,NC (USA), was enroute when a foul odour developed on board causing a number of passengers to suffer from nausea and headache.

The aircraft continued to Raleigh for a safe landing and taxied to the gate, where the passengers disembarked normally. A number of passengers received medical attention at the airport (3).

Not all odors detected within an aircraft cabin arise from oil contamination of the air supply. For example, they can originate from toilets and galley areas.

How often air quality incidents occur is difficult to determine. Furthermore, the nature of contaminants within the cabin air is usually unclear as commercial aircraft do not have air quality monitoring systems on board.

The immediate health effects of exposure to contaminated cabin air have been relatively well documented. However, the causation, diagnosis, and treatment of long-term effects continue to be debated.

What Is Bleed Air?

For decades, aircraft have used engine bleed air for a variety of purposes, spanning everything from engine starting to cabin pressurization and anti-icing.

When air enters the flight engine, it goes through several compressors, increasing the air temperature and pressure before mixing it with fuel and igniting it.

A portion of the compressed air does not enter the combustion chamber but is redirected from the engine to various other parts of the aircraft. This so-called bleed air is very hot, between 200 to 250 degrees C, and very high in pressure, around 40 psi (4).

After leaving the engine and passing through the ­air-conditioning pack, where it is cooled, the bleed air is combined with recirculated cabin air before it enters the cabin.

Temperature controllers in the flight deck and cabin allow adjustment of the target temperature and thermostats provide feedback to the packs to demand an increase or decrease in the output temperature (5).

On most commercial aircraft, engine bleed air is used to provide ­appropriate cabin pressurization and air ­conditioning. In early commercial jet aircraft, passenger cabins were ventilated with 100% outside air. In more recent jet aircraft, approximately 50% of the ventilation air is outside air, and the remaining 50% is filtered recirculated cabin air.

With the introduction of the B787, Boeing has incorporated a new no-bleed systems architecture. Most of the functions formerly powered by bleed air have been replaced by electrically driven compressors.

Bleed Air Contamination

Bleed air is a heterogeneous mixture of constituents that may include gases, vapors, smoke, fumes, and mist, each of which is potentially associated with risk of adverse health effects following exposure (1).

Under certain failure conditions, toxicants such as pyrolyzed engine oils and hydraulic fluids may leak into the cabin air supply systems.

Several factors may contribute; oil seals that otherwise separate the “wet side” of the air compressor from the “dry side” can leak or fail and workers may overfill the oil/hydraulic fluid reservoirs or may spill oil/hydraulic fluid when filling the reservoir (6).

The airborne toxicants form a complex mixture, including 1-5% tricresylphosphates (TCPs) and N-phenyl-L-naphthylamine (PAN). If the air supply system temperature is high enough, engine oil and hydraulic fluid may also generate carbon monoxide (CO).

Tributyl phosphate (TBP), a constituent of hydraulic fluid may also be of health concern.

Tricreslyphosphates (TCPs)

Specific concerns have been raised regarding so-called tricresylphosphates (TCPs) in the cabin air environment and their perceived effects on health.

TCPs are added to most synthetic jet engine oils due to their anti-wear properties.

Although TCP additives are not the only toxic component of jet engine oils, they have repeatedly become a major source of debate.

Small amounts of TCPs have been found in cabin air under normal operating conditions on commercial flights (7).

Interestingly, TCP concentrations do not correlate with visible smoke/fume or odor detection (6).

Ten TCP molecules containing different combinations of the meta, ortho and para isomers, have been described. Jet engine oils contain a mixture of these molecules. These toxic mixtures can cause transitory and permanent damage to the nervous system when swallowed in sufficient quantity (8).

It is believed that the neurotoxicity of TCP is mainly due to its ortho isomers, such as tri-ortho-cresyl phosphate (TOCP). In 1990, the World Health Organisation (WHO) stated that “Because of considerable variation among individuals in sensitivity to TOCP, it is not possible to establish a safe level of exposure” and “TOCP are therefore considered major hazards to human health (9).

Although it is claimed that the para and meta isomers are not known to be toxic to humans(8), a recent article suggests that the widespread belief that only ortho isomers of TCP are dangerous is invalid (10).

A recent study suggests that the combined neurotoxicity measured on a cellular level is similar for the different TCPs. However, the clinical implications of the study are uncertain as the TCP concentrations used are well above current exposure levels in cabin air indicating limited neurotoxic health risk (11).

The reported concentration of TCP used in most aircraft engine oils is less than 3%, of which the ortho isomers constitute less than 0.2% of the total TCP. This results in an overall concentration of ortho isomers of less than 0.006% of the total engine oil (8).

There have been no publicly available sampling data collected during a bleed air contamination event on commercial aircraft. However, wipe sampling data has identified TCPs on aircraft cabin and flight deck walls (6). On the other hand, it has been pointed out that the presence of TCP is widespread and will even be found in wipe samples taken in buildings and other public places (8,12).

A study from 2013 investigated a total of 332 urine samples of pilots and cabin crew members in conventional passenger aircraft, who reported fume/ odor during their last flight. None of the samples contained the ortho isomers of TCP above the limit of detection (LOD). The authors concluded that health complaints reported by aircrews could hardly be addressed to exposure to the ortho isomers of TCP in cabin air (13).

The aviation industry claim that engine oil does not contain sufficient quantities of TCPs to cause long-term damage (14).

TurboNycoil 600 oil is developed by a French company named NYCO. It is now used by many military agencies worldwide and its use on commercial engines is growing. Unlike most other oils, it does not contain TCP at any measurable quantity (15).

The Role of Filtration

Bleed air is cooled but not cleaned (ie, filtered) before being mixed with recirculated cabin air (1).

However, recirculated air is cleaned using high-energy particulate air (HEPA) filtration. HEPA filters are designed to capture particles but not gases and vapors, which pass directly through the filter.

Aerosols collected via HEPA filtration include dust, fibers, bacterial cells, fungal spores, and pollen grains As viruses are among the smallest of microorganisms, ranging in size from 0 02 to 0 3 μm in diameter, they are too small to be captured by HEPA filters (1).

How Often Do Air Quality Events Occur?

When it comes to air quality events, there is no standardized incident reporting system in use for either passengers or crew. Hence, the frequency of fume events may be difficult to determine.

According to several data obtained from three US 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 (6).

In 2007, the United Kingdom Committee on Toxicity (COT) undertook an independent scientific review of data submitted by the British Airline Pilots Association (BALPA) relating to concerns of its members about the possible health effects from oil fume contamination on commercial jet aircraft. The COT estimated that cabin air quality events occur on roughly 0.05% of flights (~1 in 2000)(8).

The Allied Pilots Association (APA), which represents American’s pilots, has cited as many as 20,000 fume incidents over the past decade, or about five per day (16).

A study published 2016 found that the contamination events were widely distributed across nearly all common models of aircraft (17).

The Allied Pilots Association (APA) has cited as many as 20,000 fume incidents over the past decade or about five per day.

Adverse Health Effects of Air Quality Events

The lack of a standardized protocol for the medical investigation of crew and passengers following air quality incidents means that consistent data is difficult to obtain.

The most common adverse effects reported following air quality events area acute respiratory symptoms and neurological symptoms. Psychiatric symptoms appear to be fairly common as well.

Among the symptoms reported are upper airway breathing problems (shortness of breath, wheezing, eyes, nose or throat irritation), performance decrement, tremor, memory impairment, headache, vision problems, nausea, fatigue, exhaustion, confusion, disorientation, anxiety, sleep disturbance, depression, chest pain, palpitations, and dizziness (6,10).

Individual susceptibility to damage by TCP exposure appears to be highly variable which may help explain why not all aircrew appear to be equally affected by fume events (10).

Short- and Long-Term Effects of Air Quality Events

There is abundant evidence of the continuous leakage of lubricating oil and hydraulic fluid into aircraft cabin air at all times (18). However, when analyzed in cabin air, the concentration of toxic substances has in most cases been too low to raise any health concerns.

Although the acute health effects of air quality events have been fairly well described, the impact of chronic, continual, low-dose exposure is still a matter of debate. Repeated exposure could explain the apparent differential vulnerability often described between aircrew and passengers.

In most cases of air quality events, symptoms improve and resolve within a few weeks. However, in some instances, such events appear to result in chronic adverse health effects.

Some airline workers may even have recurrent symptoms on return to work due to re-exposure to contaminants in the aircraft environment (6).

Respiratory symptoms appear to be the most common initial symptoms following air quality incidents. Although they often resolve quickly, irritant-Induced asthma may persist for more than 3 months following the exposure episode (6).

Neurological and psychiatric symptoms may in some cases be more persistent. These include headaches, confusion, loss of balance, lightheadedness, muscle weakness, movement disorders, numbness, paraesthesias, cognitive dysfunction, post-traumatic stress disorder (PTSD), emotional lability, depression, sleep and anxiety disorders (6).

Other long-term effects include persistent gastrointestinal problems, increased sensitivity to chemicals, myalgias, arthralgias, palpitations, and unusual fatigue (6).

Aerotoxic Syndrome

Aerotoxic syndrome is a phrase coined by Chris Winder and Jean-Christophe Balouet in 2000, to describe their claims of short- and long-term ill-health effects caused by contaminated cabin air (19).

Although not well defined, the syndrome is supposed to cover most of the symptoms mentioned above associated with severe air quality events or repeated exposure to cabin air contaminants.

British ex-pilot John Hoyte founded the Aertotoxic Association in 2007. Hoyte is also an author of a book called “Aerotoxic Syndrome: Aviation’s Darkest Secret” published in 2014 (20).

The Aerotoxic Association’s primary role is to support aircrew and passengers whose short and long-term health have been affected by toxic oil fume exposure in the confined space of commercial jets and inform the public of the harm associated with poor aircraft cabin air quality and the causative link to aerotoxic syndrome (21).

Bearnairdine Beaumont is an author of a book called “The Air I Breathe – It’s Classified: A True Story and Top Guide to the Aerotoxic Syndrome Phenomena Experienced by Aircrew and Passengers“.  In the book, Beaumont highlights the dangers, toxicity and neurotoxic properties of compounds contained in jet engine oils.

The Aerospace Medical Association has reviewed the available scientific evidence and concluded that there insufficient consistency and objectivity to support the establishment of a clearly defined syndrome. The US National Academy of Sciences performed a similar review and reached the same conclusion, as did the Australian Government CASA Expert Panel on Aircraft Air Quality in 2012.

Thus, the concept of the “Aerotoxic Syndrome” as a well defined entity is not recognized by the aviation medicine community (8).

In a review published 2014 (9), Professor Michael Bagshaw writes that the “reported symptoms are wide-ranging with insufficient consistency to justify the establishment of a medical syndrome. It has been noted that many of the acute symptoms are normal symptoms experienced by most people frequently; some 70% of the population experience one or more of them on any given day.”

In his report, Dr. Bagshaw also claims that “so far as scientific evidence has been able to establish to date, the amounts of organophosphates to which aircraft crew members could be exposed, even over multiple, long-term exposures, are insufficient to produce neurotoxicity.”

Other Factors to Consider During Suspected Air Quality Events

Hyperventilation

In some cases, symptoms attributed to air quality incidents may be caused by hyperventilation.

Hyperventilation, sometimes called over breathing, is breathing in excess of what the body needs.

Hyperventilation may be a normal response to emotional stress. The triggers for hyperventilation may be of physical, mental, emotional or environmental nature.

In the aviation environment, it is recognized that hyperventilation is a common condition.

For pilots and cabin crew, the following in-flight triggers may cause hyperventilation (22):

  • encountering unexpected and/or unfamiliar situations
  • excessive concentration on a flight procedure
  • experiencing a significant emergency
  • having difficulty accomplishing procedures
  • being examined or audited

The symptoms associated with hyperventilation include (22):

  • Paresthesia (“pins and needles” – tickling, tingling, burning, pricking, or numbness) especially in the extremities.
  • Increased heart rate
  • Headache
  • Nausea
  • Blurred vision
  • Impaired judgment
  • Memory impairment
  • Muscle spasms and tics
  • Muscle weakness
  • Drowsiness
  • Unconsciousness

There is an overlap between the wide range of symptoms attributed to contamination of cabin air and those caused by hyperventilation.  Hyperventilation may also be triggered by an air quality incident.

However, it would be nonsensical to suggest that hyperventilation may explain all cases of suspected air quality events.

The Nocebo Effect

The nocebo effect describes an illness, often with physical symptoms and signs, which is triggered through psychological processes in response to a perceived harmful exposure. The phenomenon is analogous to a placebo effect in which symptoms improve in response to a perceived beneficial exposure (22).

Hence, awareness of irritation or an odor on board may trigger a psychologically mediated nocebo effect. Such a response may also be triggered by observing other flight personnel or passengers feeling unwell or experiencing symptoms possibly attributed to air quality issues.

The Bottom Line

Reports of possible cabin air contamination onboard aircraft on commercial flights have become increasingly common in recent years. Such incidents are often described as fume events or air quality incidents.

It is estimated that upto five such events occur every day in the United States.

Contamination of bleed air used to pressurize and ventilate aircraft cockpit and cabins may be responsible for air quality incidents. Under certain failure conditions, toxicants such as pyrolyzed engine oils and hydraulic fluids may leak into the cabin air supply systems.

Sometimes, crewmembers have reported a visible haze or smoke in the cabin/flight deck, or a smell often described as “dirty socks,” “chemicals,” “vomit,” or “burning oil.”

Specific concerns have been raised regarding so-called tricresylphosphates (TCPs) in the cabin air environment and their perceived effects on health. TCPs are added to most synthetic jet engine oils due to their anti-wear properties.

Although the acute health effects of air quality events have been fairly well described, the impact of chronic, continual, low-dose exposure is still a matter of debate.

In some cases, symptoms attributed to air quality incidents may be caused by hyperventilation or a nocebo effect.

In most cases, symptoms improve and resolve within a few weeks. However, in some instances, air quality events appear to result in chronic adverse health effects. Some airline workers may even have recurrent symptoms on return to work due to re-exposure to contaminants in the aircraft environment.

Respiratory symptoms appear to be the most common initial symptoms following air quality incidents.

Neurological and psychiatric symptoms may in some cases be more persistent. These include headaches, confusion, loss of balance, lightheadedness, muscle weakness, movement disorders, numbness, paraesthesias, cognitive dysfunction, post-traumatic stress disorder (PTSD), emotional lability, depression, sleep and anxiety disorders.

The phrase “aerotoxic syndrome” is often used to describe the short- and long-term ill-health effects caused by contaminated cabin air.

Although known for decades, air quality incidents continue to represent potential safety hazards for passengers and crew on commercial flights.

In 2015, a Norwegian thesis by Tonje Trulssen Hildre and June Krutå Jensen concluded that “further research is necessary to clarify whether the reported negative health effects can be explained by fume events. The air-quality in aircraft needs to be measured by the use of incident samplers. These should be placed in all aircraft to continuously measure the concentrations of contaminants entering the cabin and cockpit during a fume event. If the general population acquire better knowledge about fume events, the aircraft industry may be willing to implement mitigating measures to prevent such events, given that they are proven to cause the reported health impacts (15).”

Dr. Susan Michaelis, a leading global aviation health and safety consultant and PhD researcher in the field of aircraft contaminated air, believes that the use bleed air system to supply the regulatory required air quality standards is not being met or being enforced as required (23).

In 2011, Dr. Michaelis wrote: There is a large volume of clear and convincing evidence that there is a link between cabin air contamination by leaking synthetic turbine oils and subsequent adverse health and compromised flight safety. To ignore this evidence with assertions that there is none or no link is highly reprehensible. The failure of the industry to react appropriately to this volume of evidence is indicative of “manufacturing uncertainty” to delay regulation (24).




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12 Steps to Diagnose High Blood Pressure – Understanding Hypertension

Estimated reading time: 10 minutes

High blood pressure (BP), also called hypertension, increases the risk of heart disease, stroke, and kidney disease. It is one of the most important causes of premature death worldwide.

In 2025, an estimated 1.56 billion adults will be living with hypertension (1). According to the World Health Organization (WHO), hypertension kills nearly 8 million people every year.

Overall, approximately 20% of the world’s adults are estimated to have hypertension. In 1991, the National High Blood Pressure Education Program (NHBPEP) estimated that 43.3 million adults had hypertension in the United States (2). The prevalence dramatically increases in patients older than 60 years.

It is crucial for health professionals and patients to understand how BP is measured, how hypertension is diagnosed and what are the most common pitfalls to avoid when deciding if hypertension is present or not.

1. The Definition of Blood Pressure

Each time the heart muscle contracts it pumps blood into the arteries to supply the tissues and organs of the body with oxygen-rich blood. BP is the measure of pressure in the arteries. This may be compared to the pressure of water in a garden hose, except that the arterial wall is a living tissue.

BP is recorded as two numbers, e.g., 125/80 millimeters of mercury (mm Hg). The first number is the systolic pressure, that is when the heart muscle contracts and blood is pumped into the arteries. The lower figure, the diastolic pressure, is the pressure when the heart is relaxing and filling up with blood, between strokes.

2. The Definition of Normal Blood Pressure and Hypertension

The following is the most widely used classification of BP and hypertension (3):

  • Normal: Systolic BP lower than 120 mm Hg, diastolic BP lower than 80 mm Hg
  • Prehypertension: Systolic BP 120-139 mm Hg, diastolic BP 80-89 mm Hg
  • Stage 1 hypertension: Systolic BP 140-159 mm Hg, diastolic BP 90-99 mm Hg
  • Stage 2: Systolic BP 160 mm Hg or greater, diastolic BP 100 mm Hg or greater

In 2017, the American College of Cardiology/American Heart Association (ACC/AHA) updated their guidelines for the prevention, detection, evaluation, and management of high blood pressure in adults by eliminating the classification of prehypertension and dividing it into two levels (4).

  • Normal: Less than 120/80 mm Hg;
  • Elevated: Systolic between 120-129 and diastolic less than 80;
  • Stage 1: Systolic between 130-139 or diastolic between 80-89;
  • Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
  • Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage.

However, many experts have refused to give support to the 2017 ACC/AHA guidelines (5). Their main objections relate to the new hypertension classification and blood pressure target of 130 mm Hg systolic, with specific concerns about the elderly.

The American College of Physicians (ACP) and the American Academy of Family Physicians (AAFP) have issued their own guidelines for older adults (age 60 years and older) recommending a target systolic pressure less than 150 mm Hg, or less than 140 mm Hg in selected persons at high cardiovascular risk, which they conclude “provides an optimal balance of benefits and harms (6).”

3. Understanding How Blood Pressure Changes With Age

A progressive rise in BP is seen with increasing age.

However, age-related hypertension appears to be predominantly systolic rather than diastolic. The systolic BP rises into the eighth or ninth decade, whereas the diastolic BP remains constant or declines after age 40 years. Hence, pulse pressure, the difference between the systolic and diastolic blood pressure, increases with age

The prevalence of hypertension grows significantly with increasing age in all sex and race groups. It has been estimated that the incidence of hypertension increases by approximately 5% for each 10-year interval of age.

4. The Circadian Pattern of Blood Pressure

Blood pressure is typically lower at night, during sleep and then starts to rise a few hours before we wake up. It reaches a peak in the morning shortly after awakening. Then in the late afternoon and evening, BP starts dropping again.

Blood pressure is typically lower at night, during sleep and then starts to rise a few hours before we wake up. It reaches a peak in the morning shortly after awakening.

The onset of many acute cardiovascular and cerebrovascular events shows a daily pattern, with the highest incidence of morbidity and mortality in the early morning hours. Strong, although circumstantial, evidence suggests that the early morning surge in blood pressure may contribute to the onset of acute cardiovascular episodes (7).

5. Understanding How Blood Pressure Is Measured

Correct measurement of BP is essential in the diagnosis of hypertension. BP machines have to be properly calibrated, and appropriate cuff sizes have to be selected.

The patient should be in a seated position with the back supported and legs uncrossed. The diastolic pressure may be higher by 6 mm Hg if the back is unsupported and the systolic pressure may be raised by 2-8 mm Hg if the legs are crossed (8).

The patient should not talk during the procedure as it can raise the measured value by as much as 8-15 mm Hg (9)

Checking blood pressure at home (JAMA. 2017;318(3):310. doi:10.1001/jama.2017.6670)

Here is what you can do to ensure a correct reading (10):

  • Don’t drink a caffeinated beverage or smoke during the 30 minutes before the test.
  • Sit quietly for five minutes before the test begins.
  • During the measurement, sit in a chair with your feet on the floor and your arm supported so your elbow is at about heart level.
  • The inflatable part of the cuff should completely cover at least 80% of your upper arm, and the cuff should be placed on the bare skin, not over a shirt.
  • Don’t talk during the measurement.
  • Have your blood pressure measured twice, with a brief break in between. If the readings are different by 5 points or more, have it done a third time.

6. Different Measurement Strategies For Detecting Hypertension

There are three different measurement strategies to detect hypertension:

  • Ambulatory BP-monitoring (ABPM)
  • Home BP monitoring
  • Office-based measurements

Although screening for hypertension is often performed at the doctor’s office, many individuals with high BP measurements at the office will not have hypertension upon further testing (11). This is commonly due to white coat hypertension.

ABPM monitoring is the preferred method for detecting hypertension. If ABPM is not feasible, home BP monitoring may be used.

7. White Coat Hypertension

It is essential to understand that BP is not a fixed number. BP varies throughout the day in response to what we are doing and what is happening around us.

Some people with normal BP find that it spikes when they visit the doctor. This condition is called white coat hypertension or the white coat effect (also called isolated clinic or office hypertension).

The white coat effects will often happen because we are nervous about having our BP tested by a doctor or nurse.  Most of us tend to feel tenser in medical settings than we do in surroundings that are familiar to us, although we do not always notice it.

Sometimes the white coat effect may be powerful, making it impossible to establish a correct resting blood pressure in the doctor’s office. Hence, it is imperative not to rely on office-based BP measurements when diagnosing hypertension.

People with white coat hypertension may sometimes be at increased risk for cardiovascular events and can go on to develop hypertension. Hence, close follow-up is recommended (12).

The white coat effect may persist for years. It may be avoided by using ABPM or home-based BP-monitoring.

8. Ambulatory Blood Pressure Monitoring (ABPM)

ABPM is performed by using a small digital BP machine, usually attached to a belt around the body and connected to a cuff around the upper arm. The device takes BP measurements regularly over a 24-48 hour period, usually every 15-20 minutes during daytime and every 30 to 6 minutes during nighttime.

The BP measurements are recorded on the device, and the average day (diurnal) and night (nocturnal) BPs are determined from the data by a computer.

ABPM has been considered to be the reference standard for the diagnosis of hypertension and is a better predictor of cardiovascular disease risk as compared with conventional office-based measurements (13).

Ambulatory blood pressure monitoring (ABPM) is performed by using a small digital BP machine, usually attached to a belt around the body and connected to a cuff around the upper arm

9. Reference Values for Ambulatory Blood Pressure Monitoring (ABPM)

When ABPM is used, hypertension is defined as a 24-hour average BP greater to er equal to 125/75 mm Hg (13).

A 24 hour mean BP during ABPM of 115/75 is considered normal and mean BP higher than 125/75 is considered too high.

When looking at individual measurements, normal ambulatory blood pressure should not be above 135/85 mm Hg during the day and not above 120/70 mm Hg at night. Levels above 140/90 mm Hg during the day and 125/75mm Hg at night should be considered as abnormal (13).

10. Dipping and Non-Dipping

The average nighttime BP is approximately 15 percent lower than daytime values. People who undergo this normal physiological change are described as dippers.

Failure of the blood pressure to fall by at least 10 percent during sleep is called non-dipping.

The underlying mechanisms of non-dipping are unknown, but melatonin may play a role (14).

Non-dipping may be associated with increased cardiovascular risk (15).

11. Home Blood Pressure Measurements

Relatively inexpensive semiautomatic devices may be used for home BP measurements. These measurements correlate more closely with the results of 24-hour ABPM than with BP taken in the clinician’s office (16).

The optimal schedule for home blood pressure measurements is unclear. Evidence suggests that 12-14 measurements should be obtained to assess blood pressure correctly. These should include both morning and evening measurements during one week (17).

While seated, the patient should take two measurements (separated by one to two minutes) in the morning and the evening for at least three, and preferably seven consecutive days. Measurements from the first day should be discarded; the home blood pressure is defined as the average of all remaining measures.

It is important to acknowledge that home BP measurements may vary widely depending on factors such as stress caffeine intake, smoking, exercise, and natural circadian variation.

12. Office-Based Blood Pressure Measurements

Despite their limitations, office-based BP measurements continue to be the primary technique used worldwide for the detection and management of hypertension.

Clinicians and patients should be aware of the possibility of white coat hypertension.

Multiple measurements on different days may be necessary. The patient should sit quietly for five minutes before the BP is measured. Patient position, cuff size, and cuff placement are all important.

The Bottom-Line

It is crucial for health professionals and patients to understand how BP is measured, how hypertension is diagnosed and what are the most common pitfalls to avoid when deciding if hypertension is present or not.

Office-based BP measurements are of limited value because of the frequency of white coat hypertension.

Ambulatory blood pressure measurements (ABPM) are considered to be the reference standard for the diagnosis of hypertension and provide a better predictor of cardiovascular disease risk as compared with conventional office-based measurements.

It is important to acknowledge that reference values for ABPM measurements are different from those used for office-based measurements.

If ABPM is not feasible, home BP monitoring may be used. Educating patients about when and how to perform such measurements is of crucial importance.



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Melatonin – 15 Questions and Answers About Melatonin and Sleep

Estimated reading time: 11 minutes

Melatonin is a hormone that regulates sleep, wakefulness, and circadian rhythms in humans.

Circadian rhythm describes the sleep/wake cycle, a biological clock that runs in our brain and cycles between sleepiness and alertness. It explains why we may feel energized or sleepy at around the same time each day.

We all know that sleep is crucial for our health and wellbeing. But, sadly, millions of people suffer from sleep disorders. It is believed that about one-third of Americans suffer from some sleep problems.

The most common issues are waking up in the morning feeling drowsy or tired, followed by waking up in the middle of the night, difficulty going back to sleep after waking up and difficulty falling asleep initially (1).

Insomnia is defined as difficulty falling asleep or staying asleep, even when we have the chance to do so. People with insomnia are usually unhappy with their sleep and often experience fatigue, low energy, difficulty concentrating, mood disturbances, and decreased performance in work or at school (2).

Insomnia can be acute (short-term) or chronic (ongoing)(3). Acute insomnia is often caused by situations such as stress at work, family issues or a traumatic event. This type of insomnia may last for days or weeks. Chronic insomnia lasts for a month or longer.

There are several ways to deal with insomnia. Treating a possible underlying cause is usually the first step. This may include avoiding caffeine, tobacco and other stimulants. Alcohol and certain medicines may also disrupt sleep.

Cognitive behavioral therapy may be helpful (4). Such treatment targets thoughts and actions that may disrupt sleep and encourages good sleep habits.

Several medicines are available to treat insomnia, including over-the-counter (non-prescription) and prescription medications. Such sleep aids may cause side effects such as daytime sedation and dizziness, and some are associated with risk of tolerance, dependence, and addiction.

Melatonin is often recommended to treat insomnia. It is available as a food supplement in health food stores. No substantive risks from melatonin use have been reported. However, several questions remain about its efficacy which may depend on drug dose and formulation, as well as the timing, frequency, and duration of administration (5).

1. What Is Melatonin?

Melatonin (N-acetyl-5-methoxy tryptamine) is a hormone produced by the pineal gland in animals and humans.

The pineal gland is a small gland located deep in the center of the brain

Three centuries ago, the French philosopher René Descartes described the pineal gland as “the seat of the soul.” However, it was not until the late 1950s that melatonin was identified (6)

Melatonin is synthesized from the essential amino acid tryptophan.

2. What Foods Contain Tryptophan?

Essential amino acids cannot be made by the body. As a result, they must come from food.

The highest levels of tryptophan are often found in complete proteins like red meat, fish, poultry, milk, and eggs. While most plant sources do not contain as much tryptophan as meat or dairy products, there are many plant-based options available including chickpeas, cashews, cauliflower, kidney beans, and quinoa (7).

Serotonin is a brain neurotransmitter, and an essential biochemical messenger and regulator. The metabolism of tryptophan into serotonin requires nutrients such as vitamin B6, niacin, and glutathione.

3. What Is the Relationship Between Tryptophan, Serotonin, and Melatonin?

The biosynthesis of melatonin is initiated by the uptake of the uptake of tryptophan into the pineal gland.

The cells of the pineal gland convert tryptophan to another amino acid, 5-hydroxytryptophan, through the action of the enzyme tryptophan hydroxylase and then to 5-hydroxytryptamine (serotonin) by the enzyme aromatic amino acid decarboxylase (8).

Serotonin concentrations are higher in the pineal than in any other organ or in any brain region. There is a striking diurnal rhythm with serotonin remaining at a maximum level during the daylight hours and falling by more than 80% soon after the onset of darkness as the serotonin is converted to melatonin, 5-hydroxytryptophol and other methoxyindoles (8).

In short:

  • Tryptophan is an essential amino acid
  • Tryptophan is a precursor for the formation of serotonin and melatonin
  • The pineal gland converts tryptophan to serotonin which is then converted to melatonin
  • Serotonin levels are maximal during daylight hours
  • Serotonin levels drop after the onset of darkness as the pineal gland converts most of the serotonin to melatonin
Serotonin levels are maximal during daylight hours Serotonin levels drop after the onset of darkness as the pineal gland converts most of the serotonin to melatonin

4. When Does the Pineal Gland Secrete Melatonin?

Melatonin secretion manifests a circadian rhythm. Secretion is low during daylight, ascending after the onset of darkness, peaking in the middle of the night between 11 PM and 3 AM, and then falling sharply before the time of light onset (9).

Interestingly, high nocturnal concentrations of melatonin are characteristic of both diurnally active species (like humans), in which high levels promote sleep, and nocturnally active ones (like rats), in which melatonin has no apparent relationship to sleep (10).

The melatonin produced by the pineal gland diffuses into the cerebrospinal fluid and the bloodstream. Melatonin is highly lipid soluble and diffuses freely across cell membranes. It travels in blood primarily bound to the protein albumin.

5. Is There a Seasonal Variation in Melatonin Concentration?

Melatonin secretion by the pineal gland appears to have a seasonal rhythm. Hence, melatonin levels are higher in the fall and winter and lower in the spring and summer (6).

People with seasonal affective disorder (SAD) typically feel sad or down during the winter months. In some cases, this may develop into a subtype of clinical depression that lasts throughout the late fall and winter months.

Excessive duration of melatonin secretion has been implicated in SAD, but researchers are far from settled on this theory.

Some studies have shown that people with SAD may have increased duration of melatonin secretion in the early morning hours. This would explain why people with SAD have difficulty waking up and don’t feel alert in the morning. Nevertheless, low-dose melatonin taken at night may sometimes be useful in improving mood in patients with SAD (11).

6. Does Age Affect Melatonin Levels?

There is a marked age variation in melatonin secretion by the pineal gland.

Melatonin Secretion starts during the third or four months of life, coincident with sleeping at nighttime becoming more common. It then increases rapidly to peak at ages two and three years, then declines slightly to a plateau that lasts throughout early adulthood (10).

Melatonin secretion declines with advancing age. At the age of 70, nocturnal concentrations are only a quarter or less of what they are in young adults (12).

One rationale for administering supplemental melatonin to older adults with sleep disorders is to compensate for the age-related decline in melatonin secretion.

7. What Are Melatonin Sleep Aid Supplements?

In the United States, melatonin is defined by the US Food and Drug Administration as a dietary supplement. Hence it can be purchased at any dose without a prescription.

In the European Union, melatonin is defined as a prescription drug and is not available over-the-counter. Based on the currently available evidence, 1 mg of melatonin is recommended close to bedtime to reduce sleep onset latency.

Melatonin supplements are available as pills, liquids, and chewable. You may find them in natural or synthetic forms.

Despite claims to the contrary, all of the melatonin sold in the United States is of synthetic origin (10).

As the sale of melatonin is not regulated in the US, very high doses can be sold and may contain additives with potential side effects.

Unlike with many other sleep medications, you are unlikely to become dependent on melatonin, have a diminished response after repeated use (habituation) or experience a hangover effect (13).

8. Is It Scientifically Proven that Melatonin Can Help You Sleep?

Yes, indeed it is. Several studies have shown that melatonin may positively affect several measures of sleep.

A systematic analysis of several placebo-controlled studies showed that melatonin treatment significantly reduced sleep onset latency, increased sleep efficiency, and increased total sleep duration (14).

9. What Doses of Melatonin Should be Used to Promote Sleep?

A dose of 0.1 – 0.3 mg of melatonin before sleep is adequate. This dose will raise the nocturnal plasma concentration of melatonin into the normal range observed in young adults (15).

Although melatonin is generally considered relatively nontoxic, it is worth keeping in mind that some marketed doses, such as 10 mg, can raise plasma concentrations 60 times their normal values (16).

Very high levels of melatonin may be associated with side effects such as daytime sleepiness, tiredness, and hypothermia.

Experts have also suggested that when the melatonin receptors in the brain are exposed to too much of the hormone, they may become unresponsive (17). This would mean that the drug stops doing what it is supposed to do.

10. When Is the Best Time to Take Melatonin?

If you have trouble falling asleep you should take melatonin at night. Taking melatonin 30-60 minutes before you go to sleep is a good option.

People who are night owls and usually go to bed late may want to take melatonin 2-3 hours before the desired bedtime, at least if they want to go to sleep earlier than usual.

11. What Is the “Phase Shift Theory” About?

The circadian rhythm of melatonin production typically reflects our biological clock, sometimes called the circadian pacemaker.

According to the “Phase Shift Theory”, some people may be “phase-advanced,” meaning their bodies release melatonin too early in the evening, while others may be “phase-delayed,” meaning they continue to release melatonin for too long into the day.

A substantial number of studies have shown that the onset of melatonin secretion under dim light conditions (the dim light melatonin onset or DLMO) is the single most accurate marker for assessing the circadian pacemaker (18).

The DLMO has been used to assess whether an individual is entrained (synchronized) to the 24-h light-dark cycle or is free-running, or whether an entrained individual is abnormally phase-advanced or phase-delayed (19).

Phase-advanced individuals have DLMOs that occur abnormally early in the evening, usually between 6 and 8 p.m. Phase-delayed individuals have DLMOs that occur after 10 p.m.

Winter depressives tend to have slightly delayed DLMOs. They also have difficulty waking up in the morning, a clinical finding that is associated with phase-delayed circadian rhythms (20). These people are similar to individuals who have delayed sleep phase syndrome (DSPS). Characteristic of DSPS is difficulty falling asleep before 1 a.m.

People who tire easily in the evening and cannot extend their sleep past 3-5 a.m. often have advanced sleep phase syndrome (ASPS).

12. Can Melatonin Be Used to Phase Shift the Human Circadian Clock?

Air travelers have transient DSPS after flying eastward and transient ASPS after flying westward.

Hence, when traveling eastward, it will be more difficult to fall asleep in the evening and harder to get up in the morning. When going westward, staying awake in the evening will be more difficult and we’ll be likely to wake up early in the morning.

Night workers have ASPS during their work weeks and DSPS on their off-work days.

Melatonin, even when administered at a physiological dose (0-3- 0.5 mg) can shift our circadian phase (21). This could promote the adaptation to air travel and night work.

13. Can Melatonin Be Used To Prevent and Treat Jet Lag?

Melatonin has been widely studied as a jet lag remedy. Melatonin may aid sleep during times when you wouldn’t normally be resting which may be helpful against jet lag.

According to an analysis of Cochrane data, melatonin is remarkably effective in preventing or reducing jet lag, and occasional short-term use appears to be safe (22). It should be recommended to adult travelers flying across five or more time zones, particularly in an easterly direction, and especially if they have experienced jet lag on previous journeys. Travelers crossing 2-4 time zones can also use it if need be.

According to this data, daily doses of melatonin between 0.5 and 5 mg are similarly effective, except that people fall asleep faster and sleep better after 5 mg than 0.5 mg. Doses above 5 mg appear to be no more effective.

The timing of the melatonin dose is important: if it is taken at the wrong time, early in the day, it is liable to cause sleepiness and delay adaptation to local time. The incidence of other side effects is low.

14. Can Melatonin Improve Daytime Sleep In Night-Shift Workers?

There is substantial evidence that the prevalence of sleep disorders is a significant occupational health problem among night shift workers.

Melatonin may be an effective treatment for shift workers with difficulty falling asleep.

One study found that melatonin may improve daytime sleep in night-shift workers (23).

Another study found that 5 mg of melatonin taken 30 minutes before nighttime sleep reduced sleep onset latency among nurses following recovery from night work (24). 

15. What Are the Side Effects of Melatonin?

Even though melatonin is an unregulated drug in many countries and is commonly used in excessive doses, adverse effects seem to be relatively uncommon.

Drowsiness, headache, fragmented sleep, dizziness, and nausea are among the side effects that have been described.

It is not known whether melatonin will harm an unborn baby or a nursing infant. Hence, it should be avoided during pregnancy and breastfeeding.

Furthermore, there have been no long-term safety studies of the use of melatonin in children and adolescents.

Also, melatonin supplements can interact with various medications, including anticoagulants and antiplatelet drugs, anticonvulsants, contraceptive drugs, diabetes medications and drugs that suppress the immune system.




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10 Important Symptoms of Depression

Estimated reading time: 16 minutes

Major depression affects more than 16 million American adults each year (1). It can occur to anyone, at any age. And, importantly, depression is not a personal weakness but a severe medical illness.

Of course, we all have times when our mood is low. Gloom, heartache, melancholy, woe, desolation. These are all parts of life’s journey and fortunately most often normal temporary reactions to daily events. But, at what stage should such feelings be defined as clinical depression?


The British writer and poet, Giles Andreae who himself has battled depression once said: “Thinking you’ve had depression makes about as much sense as thinking you’ve been run over by a bus. Trust me – you know when you’ve got depression (2)” 

Although this is not entirely true, it emphasizes the difference between clinical depression and occasional episodes of low mood. However, unfortunately, too many people don’t acknowledge their depression or think it isn’t serious or even believe that it is a personal weakness.

Only about a third (35.3%) of those suffering from severe depression seek treatment from a mental health professional (3). Hence, it is estimated that as many as two-thirds of people with depression do not realize that they have a treatable illness and do not seek treatment.

According to The American Psychiatric Association, “depression (major depressive disorder) is a common and serious medical illness that negatively affects how you feel, the way you think and how you act. Fortunately, it is also treatable. Depression causes feelings of sadness and/or a loss of interest in activities once enjoyed. It can lead to a variety of emotional and physical problems and can decrease a person’s ability to function at work and home” (4).

Hence, we might conclude that depression reflects long and persistent periods of low mood without reason? But, that’s a misinterpretation. The truth is that there is a reason. That reason is the disease we call depression.

The British actor and writer Stephen Fry has talked openly about his depression. He says: “Why should I be depressed? I’ve got enough money. I’ve got a job. People like me. There is no reason to be depressed. That’s as stupid as saying there is no reason to have asthma or there is no reason to have the measles. You know you’ve got it. It’s there. It’s not about reason.”

Depression is often considered to be a mood disorder. Fry says: “To me, mood is like the weather. Weather is real. It is absolutely real: when it rains, it rains – you get wet, there is no question about it. It is also true about weather that you can’t control it; you can’t say if I wish hard enough it won’t rain. It is equally true that if the weather is bad one day, it will get better and what I had to learn was to treat my moods like the weather.”

1. Depressive Mood

Persistent sad, anxious or “empty” mood is an essential feature of major depression.

However, frequently those who have suffered from depression describe their depressive mood in a more specific manner. It is not just about feeling sad all the time. It is somewhat different and usually much worse.

In fact, people with depression not always feel sad. They may be able to speak with their friends and have a laugh. On the outside, it may look like there’s nothing wrong. But inside, there is something missing. There is an emptiness, so hard to describe and so hard to understand unless you have experienced it yourself.

Let me quote Stephen Fry again: “There comes a time when the blankness of the future is just so extreme, it’s like such a black wall of nothingness. Not of bad things like a cave full of monsters and so, you’re afraid of entering it. It’s just nothingness, the void, emptiness and it is just horrible.”

Fry even goes further and says: “It’s like contemplating a future-less future and so you just want to step out of it. The monstrosity of being alive overwhelms you.”

Some patients with depression express intense sadness and emotional distress whereas others have a sense of emotional numbness (“blahs”). Hence, the magnitude and nature of the depressive mood may vary between patients.

2. Anxiety

Depression is often associated with anxiety. Both are facilitated by stress, either recent or dating back to childhood (5). Up to 70 percent of patients with depression experience anxiety (6).

Anxiety may be described as a feeling of worry, nervousness, or unease about something with an uncertain outcome.

Today, many experts believe that depression and anxiety are not two disorders that coexist but two faces of one disorder (7).

Often, anxiety precedes depression, sometimes by several years. Typically the onset of anxiety is in late childhood or early adolescence. Depression usually begins a few years later with typical onset in the mid-20s (8). But, of course, depression may occur at any age.

One person suffering from depression and anxiety wrote (9): I’ve always lacked self-confidence, even before my anxiety disorder was identified. I try to mingle with the best of them, but at the same time on the inside, I’m an intolerable nervous wreck and always wish I was at home watching repeats of “Friends” with a slab of fudge cake, even when I’m socializing with my nearest and dearest. Sadly, I don’t think this will ever change. So when I’m at that point where I’m trying just to leave the house, let alone do anything adventurous, my fragile mind always says “But, why? Why bother? You’re going to fail at this anyway?”

In fact, isolation may become quite severe. Simple tasks such as going to the supermarket may become a major hurdle.

3. Loss of Interest or Pleasure in Activities Once Enjoyed (Anhedonia)

The word Anhedonia describes the inability to experience pleasure from activities usually found enjoyable, e.g., exercise, hobbies, and social interactions. In Greek, anhedonia directly translates to “without pleasure.”

Most patients with depression have anhedonia. It is a crucial feature of major depression. Events and activities we used to enjoy become less interesting or fun. We may even lose interest in our friends. Libido and interest in sex often decrease as well.

Some experts suggest that anhedonia comes not from a reduced capacity to experience pleasure, but instead from an inability to sustain good feelings over time. In other words, maybe pleasure is experienced fully, but only briefly, not long enough to sustain interest or involvement in life’s good things (10).

In anhedonia, the simple and satisfying sensation of joy seems to be lacking.

Following his experience with depression, Giles Andrea wrote: “And if depression has taught me one thing, it is this: what a rare and beautiful treasure is the simple human gift of joy. For me now, joy – our capacity to delight in one another and the world – is the reason why we are here. It is as simple as that. And I feel compelled to spread the word (2).”

Anhedonia may promote social withdrawal and negative feeling towards yourself and others. Emotional abilities may be reduced, and there may be a tendency to show fake emotions. We may struggle to adjust to social situations and our interest in intimacy may diminish.

Sometimes, anhedonia is divided into social anhedonia (a general disinterest in social contact), and physical anhedonia (an inability to feel pleasure from things likes eating, touching or sex)(11).

4. Fatigue or Loss of Energy

Contrary to many other medical symptoms, fatigue is an entirely normal phenomenon in particular situations. We all become tired, but it usually gets better by rest or sleep. However, chronic fatigue as a medical symptom is typically persistent and not relieved by rest (12).

Chronic fatigue is prevalent among patients with depression. It is often described as feeling tired all the time, exhausted or listless. Some people with depression experience total lack of energy sometimes called ‘anergia’.

Fatigue and depression seem to have a circular relationship. For some, fatigue will come first; for others, depression will come first, but for most, it will probably be unclear (13). The fatigue may lower self-esteem and make the depression worse, leading to more fatigue.

If the fatigue that comes with depression becomes overpowering, basic tasks such as getting out of bed and walking may be exhausting.

The symptoms of fatigue can affect physical, cognitive, and emotional function, impair school and work performance, disturb social and family relationships, and increase healthcare utilization (14).

5. Feelings of Worthlessness or Excessive Guilt

A study of patients with major depression published 2015 showed that self-blaming emotions occurred in more than 80% of patients with self-disgust/contempt being more frequent than guilt, followed by shame (15).

The majority (85% of patients) reported feelings of inadequacy and self-blaming emotions as the most bothering symptoms compared with 10% being more distressed by negative emotions towards others.

Patients with depression often tend to misinterpret events or minor setbacks as evidence of personal failings (16).

A patient with depression has described her feelings in the following manner (17):

“I should be a spy; I am so good at leading a double life. I can put on a smile, muster up a good conversation (after ignoring a few calls and messages), but the reality is, all those “normal,” happy interactions exhaust me, and for that, I feel guilty.

I feel guilty that I want to scream at my boyfriend who is just trying to be understanding. I feel guilty that I cause those closest to me to worry. My parents, my partner, my family, and friends, all of them try to support me, to ensure I don’t get too low. How do I tell them it isn’t them and no matter what they do often I just feel low? I feel guilty that their efforts to help sometimes just make it worse.

I feel guilty for canceling plans last-minute. I mean to go, I want to go, but often I just don’t have the strength. I am brilliant at making excuses, but the shame I feel for letting people down is ever-present.

I even feel guilty for feeling guilty. Maybe some other people understand this warped way of thinking. I would tell anyone else with depression to not be so hard on themselves, to acknowledge their efforts. But to me, I just feel guilty.”

6. Sleep Disturbance (Insomnia and Hypersomnia)

Several types of sleep disorders may occur in patients with depression. The term insomnia is used often used to describe the symptoms associated with these sleep disorders.

Insomnia may be a difficulty falling asleep, waking up frequently during the night with difficulty returning to sleep, waking up too early in the morning, or merely an unrefreshing sleep. It is not defined by the number of hours slept but reflects the satisfaction with sleep. Insomnia is often associated with tiredness, lack of energy, difficulty concentrating, and irritability.

Depression may be associated with difficulty getting to sleep (initial insomnia). Waking in the middle of the night (middle insomnia) or earlier than usual (terminal insomnia) with difficulty turning to sleep is common. Prolonged nighttime sleep or daytime sleeping (hypersomnia) may occur as well.

About three-quarters of depressed patients have insomnia symptoms, and hypersomnia is present in about 40% of depressed young adults and 10% of older patients, with a preponderance of females (18).

Disturbed sleep is a very distressing symptom which has a significant impact on quality of life in depressed patients (19).

Many patients with depression wake up prematurely in the early morning hours, unable to get back to sleep. This early-morning awakening is often associated with dysphoria and depressive thoughts, and sometimes there is an agitated, even a panicky feeling. This may often get better during the day and the evenings are often more comfortable.

7. Neurocognitive Dysfunction (Difficulty Concentrating, Remembering or Making Decisions)

Neurocognitive dysfunction is common in patients with depression (20).

Memory loss and an inability to focus or concentrate may be pronounced. Working memory, fluency, and planning and problem-solving abilities may be impaired.

People with depression often feel like they can’t focus. Comprehending what you are reading may become difficult and affect the ability to store information. This may negatively impact enjoyment when reading for pleasure.

The ability to receive information or directions may be impaired. We may appear easily distracted. This may affect performance at school and work. Sometimes these symptoms may be misinterpreted as lack of interest or consideration.

In most cases, neurocognitive dysfunction in depression is readily distinguished from that caused by dementia.

8. Change in Appetite and Body Weight

Reduced appetite and weight loss are common in patients with depression. However,  increased appetite and weight gain may also occur.

Changes in eating habits are often related to other symptoms of depression, such as lack of energy and interest or pleasure from activities.

While a loss of appetite is common in depression, the sadness or worthlessness experienced by many patients may be associated with overeating (emotional eating). Emotional eating is eating in response to emotional rather than physical hunger.

9. Psychomotor Disturbances (Restlessness, Irritability, Retardation)

Psychomotor disturbances that are common in depression include both agitation and retardation (16).

Psychomotor agitation is a series of unintentional, nonproductive or purposeless motions. In patients with depression, this may present as hand-wringing, pacing, and fidgeting.

Psychomotor retardation is a slowing down of thought and physical movements and may include slowing of body movements, thinking, and speech.

10.  Thoughts of Suicide or Death

Depressed patients often experience recurrent thoughts of death. Suicidal ideation often occurs and there is a risk of suicidal attempt in some patients with depression (21).

Sometimes, suicidal ideation is passive. Patients often consider life not worth living and that their closest family and friends would be better off if the patient were dead.

In contrast, active suicidal ideation is marked by thoughts of wanting to die or commit suicide (16). There may be suicide plans and preparatory acts (e.g., selecting time and location, choice of method, or writing a suicide note). Such behavior indicates the patient is severely ill.

Suicidal ideation is usually preceded by hopelessness and negative expectations for the future. The patient may regard suicide as the only option to escape a never-ending and intense emotional and often physical pain

Alarmingly, many patients with suicidal ideation have not been recognized as having depression. In a large Canadian study, 48% of patients who had suicidal ideation and 24% of those who had made a suicide attempt reported not receiving care or even perceiving the need for care (22). The investigators concluded that future research should be directed toward finding better ways to identify these individuals and address barriers to their care and other factors that may interfere with their receiving help.

The annual suicide rate in the United States is approximately 13 per 100,000 individuals. Suicide is the tenth leading of cause of death. In 2014, the total number of suicide deaths in the United States was 42,773 (23). This equals 117 suicide deaths every day.

It is recognized that certain occupations and professions may be more susceptible to depression and suicide. Occupations that require frequent or difficult interactions with the public or clients, and have high levels of stress and low levels of physical activity seem to be at highest risk (24).

The medical profession has the highest risk of death by suicide of any profession or occupation. Other high control and highly regulated professions such as law enforcement, military, and the legal profession may be more likely to experience depression and suicidal behavior, and less likely to seek intervention because of the associated stigma and possible licensure implications (25).

Recent research suggests that suicide is three times more likely in individuals who have experienced a concussion, so occupations that might result in head injuries may be predisposed to suicide, with or without concomitant depression (26, 27).

A few patients with depression have described their thoughts concerning suicide on the website The Mighty (27). Here are a few examples:

“It feels like you’re all alone and no matter what’s said to you, you feel like it’s not true or doesn’t matter. It feels like you just need to end it all because you’re so tired of fighting every single day.”

“I didn’t realize what I was feeling until I came out of it. It felt like I wasn’t breathing, I was drowning, and someone was holding my head under water. I was lost, alone and there was no other way out. No one understood me and no one ever would. When I finally broke free of the deep suicidal thoughts, I was able to see them for what they were, not before or during. I felt choked by the emotions and blinded by them.”

“A constant ache in my heart, my lungs, my wrists, my legs, my mind and the pit of my stomach. The ache that tells me nothing is sacred; everything is pointless. That nothing ever has or ever will matter. Why must I continue breathing? Why must I keep getting out of bed every day when I am so incredibly tired? Feeling utterly worthless, to the point that you wonder if your own children would be better off without you around.”

 “The thought of death formed as a monster in my head. It is after me; I cannot run away from it. I don’t want to die, but I don’t want to live, either. The pain is too much strong, so I desperately think I cannot take another day. But deep down inside of me, I always have a tough wish to see another day — as a human instinct, I guess. I grabbed this very little feeling to go on. I hope everyone else will [too].”

“And if depression has taught me one thing, it is this: what a rare and beautiful treasure is the simple human gift of joy. For me now, joy – our capacity to delight in one another and the world – is the reason why we are here. It is as simple as that. And I feel compelled to spread the word.” Giles Andrea

Diagnosing Depression

Symptoms of depression may include the following:

  • Persistently sad, anxious, or empty moods
  • Loss of pleasure in usual activities (anhedonia)
  • Feelings of helplessness, guilt, or worthlessness
  • Crying, hopelessness, or persistent pessimism
  • Fatigue or decreased energy
  • Loss of memory, concentration, or decision-making capability
  • Poor abstract reasoning
  • Restlessness, irritability
  • Sleep disturbances
  • Change in appetite or weight
  • Physical symptoms that defy diagnosis and do not respond to treatment – (very commonly pain and gastrointestinal complaints)
  • Thoughts of suicide, death, or suicide attempts
  • Poor self-image or self-esteem

To establish a diagnosis of major depression, a patient must express one of the first two items above and at least five of the other symptoms listed. Such disturbances must be present nearly daily for at least two weeks (25).

The Bottom-Line

Dear reader. If you have read this article, it may be for general information purposes or because you fear or believe that you may be suffering from symptoms associated with depression. If the latter is true, I want to remind you that depression is not a personal weakness but a serious medical disorder.

Because depression is a disease, it can not be “willed” or “wished away”. Unfortunately, that is a common misperception by the public and some medical professionals.

Patients with depression often feel terrible. The combination of physical and emotional symptoms may be overwhelming. The tiredness, darkness, and emptiness may seem unbearable. However, depression is a treatable disease. Almost all people who have suffered from depression will tell you that things will get better. And that is true.

And, remember; Never be ashamed of your depression. You wouldn’t be if you had a brain tumor, heart attack or leukemia.

Oh, and finally; Don’t try to deal with your depression by yourself. Seek professional help.




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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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