The mystery of Bruce Lee’s death finally solved

[Nov 22, 2022: JD Shavit, The Brighter Side of News]

Bruce Lee was the most influential martial artist of all time. He inspired millions of people and brought attention to martial arts in the Western world.

He was born Lee Jun-fan on 27 November 1940, in San Francisco, California, while his opera singer father was touring the United States. He returned with his parents to Hong Kong as an infant and worked as a child actor. At age 13, he began learning martial arts.

At age 18, he returned to the United States where he studied drama and philosophy and opened a martial arts school. At age 26, he first appeared as a martial arts fighter on American television.

Lee created his own combat method that he called Jeet Kune Do or the Way of the Intercepting Fist, which combined different training methods such as kung fu, fencing, boxing and philosophy. He also popularized philosophical quotes, such as the one starting ‘Be water, my friend…’. He returned to Hong Kong at the age of 29, where he became a writer, director, lead actor and fight scene choreographer.

Lee died at the age of 32 in Hong Kong on 20 July 1973, under mysterious circumstances. Up to now, the cause of Bruce Lee's death was unknown, although numerous hypotheses have been put forward, from assassination by triad gangsters to the more recent suggestion in 2018 that he died from heatstroke. The necropsy showed cerebral oedema. A prior episode was diagnosed as cerebral oedema 2 months earlier.

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Some facts about Bruce Lee's death are public. On the day of his death, he and the producer of his films, Raymond Chow, drove to the house of Betty Ting Pei, who was thought to be the mistress of Lee. Lee spent some hours alone with Ting Pei and used marijuana before driving to the house, and while there Lee actively acted out some scenes of an upcoming movie.

He experienced headache and dizziness around 7:30 pm, after drinking water. Ting Pei gave him an ‘Equagesic’ pill (a combination of meprobamate and aspirin which he had taken before) and Lee went to the bedroom to rest. Raymond Chow left at that time. At 9:30 pm, Ting Pei found Lee unconscious. She called Chow who went to the house and tried to wake Lee up without success. They called a doctor, who spent another 10 min unsuccessfully doing cardiopulmonary resuscitation. Lee was sent to the nearest hospital, where he was pronounced dead.

At autopsy, there were no signs of external injuries and no tongue bite. Severe cerebral oedema had resulted in brain weight of 1575 g compared with the normal 1400 g. Traces of marijuana were found in the stomach. Bruce Lee's death was officially ruled to be the result of cerebral oedema caused by hypersensitivity to Equagesic.

Among the multiple plausible and implausible causes of death, three merit identification.

Cerebral oedema caused by hypersensitivity to Equagesic. Hypersensitivity to the components of Equagesic (aspirin and meprobamate) was identified as the official cause of death. However, Lee had taken this drug before and on the day of his death, he took it AFTER he felt unwell, already having symptoms that may be explained by cerebral oedema (i.e. headache) and cerebral oedema would not be expected to be the only necropsy finding if indeed hypersensitivity to Equagesic was the cause of death.

Epilepsy. A seizure was considered a potential cause of the 10 May 1973 episode described above, although as it was a sole episode, a diagnosis of epilepsy was not made. On 29 and 30 May 1973, Lee underwent a full neurologic evaluation: ‘a complete physical, a brain flow study, and an electroencephalogram’, reviewed by neurologist David Reisbord, who did not find abnormalities in his brain functions.

Heatstroke. This latest hypothesis about the cause of death was proposed by Matthew Polly in his 2018 book Bruce Lee, A Life.

Heatstroke refers to when body core temperature increases above 40°C, associated with hot dry skin and central nervous system abnormalities. Typically, heatstroke results from strenuous exercise (exertional) or from an inability to regulate body temperature (non-exertional), in patients with risk factors such as older age, obesity, heart disease, dementia and others. Initially, heat exposure leading to hyperthermia facilitates the leakage of endotoxin from intestinal mucosa and interleukins from muscles to the systemic circulation, thereby causing a systemic inflammatory response syndrome, disruption of the blood–brain barrier and cerebral oedema. Typically, the disorder has three phases resulting in death after 24–96 hrs, hence sudden death is unusual.

Researchers believed that any hypothesis about the cause of death should account for the necropsy finding of cerebral oedema without further evidence of central nervous system injury and for the acute time-course of the final illness.

The four main pathophysiological mechanisms of cerebral oedema are as follows. (i) Vasogenic; commonly seen in conditions with disruption of the blood–brain barrier, e.g. peritumor oedema. (ii) Cellular or cytotoxic; the consequence of brain injury, such as trauma or stroke. (iii) Interstitial oedema resulting from the outflow of cerebrospinal fluid from the intraventricular space to interstitial areas, e.g. hydrocephalus or meningitis. (iv) Osmotic oedema; in which the cells of the brain pull water from the plasma, due to a disequilibrium in osmolarity, e.g. during hyponatraemia.

Thus, they believe that hyponatraemia stands out as a serious possibility that may account for cerebral oedema and the time-course of the illness, as it is well accepted that acute hyponatraemia itself can be lethal if not treated promptly. Could hyponatraemia-induced cerebral oedema have killed Bruce Lee?

The balance of water in the body is regulated by plasma osmolarity: increased plasma osmolarity (hypertonicity) is sensed by osmoreceptors in the hypothalamus that regulate both antidiuretic hormone (ADH) release and thirst.

Researchers state that it is unusual to develop hyponatraemia (i.e. water intoxication) unless the rate of water intake is clearly superior to this rate of water excretion or there are predisposing factors that limit the kidney’s ability to excrete water. However, this high volume may be surpassed by excessive free water drinking over short periods of time: urinating 20 L/day would translate into being able to handle an excess free water intake of around 0.8 L/h.

Acute or hyperacute water loading during ‘dare’ activities involving ingestion of large amounts of water over a short period of time is a cause of cerebral oedema and death within a few hours, even for individuals without risk factors for hyponatraemia.

Death due to hyponatraemia leading to cerebral oedema can occur within a few hours of greatly exceeding this rate of water intake, as in recent cases in which 7–8 L of water were ingested within a few hours during ‘dare activities’. These persons are usually young and healthy.

However, even if a reasonable water intake limit is not exceeded, there are factors that limit the kidneys’ ability to excrete a water load, further decreasing the safe amounts of water intake when water intake is not needed. These factors may result in severe hyponatraemia from drinking a much lower water load. Could hyponatraemia have occurred in an apparently healthy young sportsman like Lee?

The existence of predisposing factors that interfere with water excretion by the kidneys is the most common cause of hyponatraemia and Lee did not appear to have drunk 6–8 L of free water as in some case reports of excessive water ingestion by healthy people. So, did Lee have factors predisposing to hyponatraemia? A brief overview of publicly available information suggested that Lee had the following predisposing factors in his medical history.

Researchers conclude that the answer to the question of whether Lee had factors predisposing to hyponatraemia is yes, not only one, but multiple factors that predispose to hyponatraemia:

They further concluded that Lee had multiple risk factors predisposing to hyponatraemia resulting from interference with water homeostasis mechanisms that regulate both water intake and water excretion, a clinical presentation consistent with hyponatraemia and a necropsy finding of cerebral oedema which is the cause of death in severe hyponatraemia. This predisposition may have caused pre-existing asymptomatic hyponatraemia, which is associated with a high risk for the development of worsening hyponatraemia with altered mental status.

Pre-existing hyponatraemia was found in over 70% of all patients admitted with symptomatic hyponatraemia and represented the most common risk factor identified.

Additionally, in patients with a baseline risk of hyponatraemia due to other factors, an increase in the number of prescription drugs that predispose to hyponatraemia synergistically increases the risk of hyponatraemia. Thus, even if some of the risk factors identified in the present report were not actually present or had a mild influence by themselves, the presence of multiple risk factors may explain the sequence of events that led to Lee’s demise.

In summary, researchers hypothesized that Bruce Lee died from a specific form of kidney dysfunction: the inability to excrete enough water to maintain water homeostasis, which is mainly a tubular function. This could have lead to hyponatraemia, cerebral oedema and death within hours if excess water intake was not matched by water excretion in urine, which is in line with the timeline of Lee’s demise.

Given that hyponatraemia is frequent, as is found in up to 40% of hospitalized persons and may cause death due to excessive water ingestion even in young healthy persons, researchers believe that there is a need for a wider dissemination of the concept that excessive water intake can kill.

The fact that we are 60% water does not protect us from the potentially lethal consequences of drinking water at a faster rate than our kidneys can excrete excess water. Ironically, Lee made famous the quote ‘Be water my friend’, but excess water appears to have ultimately killed him.

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