Total Cholesterol Levels
One of the readings you will see from your laboratory results is a number for “total cholesterol.” This will tell you the total number of all of the fats you have in your blood. According to the National Cholesterol Education Program:
- A desirable level is less than 200 mg/dL (5.17 mmol/L)
- Levels between 200 mg/dL and 239 mg/dL (5.17–6.18 mmol/L) are considered borderline for high cholesterol.
- Levels at or above 240 mg/dL (6.21 mmol/L ) are considered high total cholesterol levels. This may put you at an increased risk for heart disease.
It is important to note that you should not determine your cholesterol levels just by your total cholesterol level. This needs to be further broken down into LDL, HDL, and triglycerides in order to give you some insight into the types of cholesterol that are in your blood.
High Density Lipoproteins (HDL)
High density lipoproteins, or HDL, are considered to be the “good cholesterol”, because HDL’s role in the body is to take cholesterol to the liver for degredation or processing, as opposed to allowing the cholesterol to hang around in the blood. According to the National Cholesterol Education Program:
- Any HDL level above more than 60 mg/dL (1.56 mmol/L) is considered high. A high HDL level is considered very healthy, since it has a protective role in guarding against heart disease.
- An acceptable HDL range is between 40- 60 mg/dL (1.04–1.56 mmol/L).
- An undesirable level of HDL is any level below 40 mg/dL (1.04 mmol/L). In this case, low HDL levels may help to contribute to heart disease.
Elevated levels of triglycerides are also a risk factor for heart disease. According to the National Heart, Lung, and Blood Institute:
- Triglyceride levels should be below 150 mg/dL (1.69 mmol/L).
- Levels between 150 mg/dL (1.69 mmol/L ) and 199 mg/dL (2.25 mmol/L) are considered borderline high.
- Levels between 200-499 mg/dL (2.26-5.63 mmol/L) are considered high.
- Levels above 500 mg/dL (5.64 mmol/L) or considered extremely high.
Low Density Lipoproteins (LDL)
Low density lipoproteins, also known as LDLs, are considered to be the “bad cholesterol”. This type of lipoprotein circulates from the liver to other organs and tissues in the body, carrying cholesterol where it is needed. This type of cholesterol tends to linger and has been connected with various types of heart disease, including atherosclerosis, heart attack, stroke, and coronary heart disease. The current guidelines for LDL levels are:
- LDL levels less than 100 mg/dL ( 2.6 mmol/L) are considered optimal.
- LDL levels between 100 – 129 mg/dL (2.6–3.34 mmol/L) are considered near or above optimal.
- LDL levels between 130 – 159 mg/dL (3.36–4.13 mmol/L) are considered borderline high.
- LDL levels between 160 – 189 mg/dL (4.14 - 4.90 mmol/L) are considered high.
- LDL levels at or above 190 mg/dL (4.91 mmol/L) is considered very high.
Your ideal LDL level is determined by how many risk factors you have. So, although you might have an optimal LDL level, your health care provider may want it to be a little lower, based upon what types of conditions you have. For instance, a 60-year-old with diabetes and heart disease would want their LDL level much lower than a 30-year-old with no risk factors for heart disease. Although some risk factors can be modified, others cannot, such as age, gender, and family history of heart disease.
The highest risk patient group includes individuals who already have established cardiovascular disease (i.e. already had a heart attack or stroke), in addition to other conditions, such as metabolic syndrome, previous heart attack, high blood pressure, or smoking. This group of patients should have goal of having an LDL less than 70 mg/dL (1.81 mmol/L).
Individuals who have coronary artery disease(CAD) or other vascular disease (like diabetes, carotid artery disease, peripheral artery disease, or a previous abdominal aortic aneurysm) are considered at high risk. The LDL goal in these individuals is less than 100 mg/dL (2.6 mmol/L), although some health care providers may want this number below 70 mg/dL.
Individuals with two or more risk factors are considered at moderate risk of getting heart disease. Their LDL goal is less than 130 mg/dL (3.36 mmol/L).
Individuals with one or no risk factors are at low risk for getting heart disease. Their LDL goal is less than 160 mg/dL (4.14 mmol/L).
When you have very high LDL or other risk factors for heart disease, or when diet and exercise alone have not lowered your cholesterol levels enough, your doctor may decide it is time for you to start taking a cholesterol-lowering medication. Cholesterol-lowering medications, in addition to your healthy lifestyle, will help lower your cholesterol levels to the desired range. Sticking to your diet and exercise plan will let your doctor prescribe the lowest dose of medication possible to reach your cholesterol goals. Here is some basic information on ideal cholesterol levels, how cholesterol-lowering drugs work in your body, and the different types that are available.
What Are Ideal Cholesterol Levels?
There are four main cholesterol numbers that your doctor will monitor:
Total cholesterol: A desirable total cholesterol level is less than 200 mg/dL. Achieving and maintaining a total cholesterol level less than 200 mg/dL lowers your risk for heart disease.
LDL (“bad cholesterol”): The lower your LDL levels, the lower your risk for heart disease, heart attack, and stroke. Ideal LDL levels vary among individuals depending on several patient-specific characteristics, such as other risk factors for heart disease. However, according to the American Heart Association, an LDL level of less than 100 mg/dL is considered optimal.
HDL (“good cholesterol”): The higher your HDL levels, the better. While low HDL levels (less than 40 mg/dL for men; less than 50 mg/dL for women) put you at risk for heart disease, high HDL levels, over 60 mg/dL, may protect you from heart disease.
Triglycerides: Normal triglyceride levels are usually less than 150 mg/dL, but can vary based on age and sex.
How Do Cholesterol Drugs Work?
Some cholesterol-lowering drugs work in your liver to block the production of cholesterol. Other drugs work in your intestines to prevent cholesterol from being absorbed in your body. There are several different types of cholesterol-lowering medications. Your doctor will decide which medication, or combination of medications, is best for you depending on your cholesterol levels. There are five main classes of cholesterol-lowering medications, and each works differently to lower cholesterol.
Statins are the most effective and most commonly prescribed cholesterol-lowering class of medications. Statins work in the liver to block the production of cholesterol and are highly effective in lowering LDL levels. They can also help lower triglyceride levels and raise HDL levels. Statins have also been shown to slow the formation of sticky plaque in your arteries, which can cause heart attack and stroke.
Fibrates, also referred to as fibric acid derivatives, are effective in lowering triglyceride levels and may also increase HDL levels. Fibrates are not effective in lowering LDL levels and may actually cause a slight increase in LDL levels.
Nicotinic acid, or niacin, is primarily effective in raising HDL levels and lowering LDL and triglyceride levels. Nicotinic acid reduces the production of triglycerides and VLDL, which is converted to LDL in your blood. Nicotinic acid therapy is available in several different forms, both over the counter and by prescription. However, if treatment with niacin is right for you to lower cholesterol, you should only use it under the supervision of your doctor so you can be closely monitored for potential side effects.
Cholesterol absorption inhibitors lower cholesterol by blocking the absorption of cholesterol in your intestines. Cholesterol absorption inhibitors lower total cholesterol and LDL levels.
Bile acid sequestrants lower the amount of LDL cholesterol in your blood. Bile acid sequestrants bind with cholesterol-containing bile acids in your intestines, prevent them from being absorbed into the blood, and are eliminated from your body through the stool. Bile acid sequestrants are sometimes prescribed along with statins for certain people with high cholesterol. Bile acid sequestrants are not absorbed from the gastrointestinal tract into the body.
Remember, regardless of which cholesterol-lowering medication you have been prescribed, you must continue taking your medicine to lower your cholesterol and keep it in the recommended range. Cholesterol-lowering drugs control high cholesterol, but do not cure it. Keep taking your medication every day and stick to your diet and exercise plan.
Making sense of less conventional risk markers in your blood test results.
DR Deepak Chopra, the famous health, spirituality and wellbeing guru, once said in a TV show: “We are all on death row. The only uncertainty is the length of reprieve and the method of execution. Death makes life possible.”
Over the past 20-30 years, the “method of execution” in Malaysia, as in the rest of the world, has principally been cardiovascular diseases. This includes heart attacks and strokes.
Statistics in 2009 from the Health Ministry estimated that about one in four deaths in government hospitals are attributed to either heart or strokes.
Such grim statistics are not likely to improve in the coming years. Instead, the numbers are poised to worsen given the rising trend of risk factors that contribute to cardiovascular diseases. The recently completed fourth National Health and Morbidity Survey revealed an increasing incidence of non-communicable diseases. Approximately 15% of adult Malaysians are obese and nearly one in every two Malaysians are either overweight or obese. About 20% of us are diabetics, and more than one in three have high blood pressure.
Related to these embarrassing statistics are our poor lifestyle habits, eg low intake of adequate servings of vegetable and inadequate exercise (only 65% claim to exercise regularly).
A large international trial involving nearly 30,000 subjects, the INTERHEART study, showed very clearly that 90-95% of the risks attributable to the causation of heart attacks can be explained by nine potentially modifiable risk factors (smoking, apoprotein B/apoprotein A1 ratio, hypertension, diabetes, abdominal obesity, psychosocial factors, daily consumption of fruits and vegetables, regular alcohol intake, and regular physical activity).
This association is generic as it applies to men and women, old and young, and in all regions of the world.
Atherosclerosis: basis of cardiovascular diseases
The term atherosclerosis refers to the build-up of plaque – a predominantly cholesterol deposit with an overlying cap of fibrous tissue – in the wall of the arteries in the body. It is now clear that the development of the plaque is a chronic process that often begins in childhood and adolescence. This is an active inflammatory process involving the body’s immune cells and mechanisms, but remains silent for decades until a late stage of advanced plaque accumulation or plaque rupture.
The manifestation of disease may be the development of chest pain on effort (angina pectoris) or the more risky situation of threatened or established heart attack.
All too often, we hear stories of apparently healthy and even fit young persons collapsing suddenly in the midst of their regular activities. In fact, statistics reveal that 40-60% of persons with heart disease first manifest in the form of a heart attack or sudden death.
Detecting early disease
The prospect for such an outcome is scary, and this has led to intense efforts by clinicians and scientists to develop methods and tests to detect heart disease in asymptomatic individuals. The potential to prevent such catastrophic events through early detection and treatment is enticing.
The detection of early disease or increased risk entails more aggressive treatment of risk factors, and sometimes, initiation of cardioprotective medications.
In general, there are a number of ways that your doctor employs to estimate an asymptomatic person’s cardiovascular risk. The simplest, inexpensive and rather useful way is to identify the presence of established traditional risk factors. These include high cholesterol levels, high blood pressure, diabetes, smoking, age and gender.
Through various validated risk prediction models, estimated risk – expressed as percentage risk of a cardiovascular event over a number of years, may be obtained.
One of the most popular models is the Framingham Risk Score. A low risk is conventionally defined as having a 5% or less chance of cardiovascular event in the next 10 years. Intermediate risk is between 6-20%, and a high risk individual has more than 20% risk projection of a cardiovascular event in the next 10 years.
However, no single risk prediction model is perfect. Hence, the search for better ways to improve the stratification of risks in asymptomatic individuals.
This may be in the form of imaging tools, blood markers or ankle-brachial index (ABI) test. The former are methods to directly identify the presence of plaque, and include cardiac CT (computed tomography) angiography scans, heart MRI (magnetic resonance imaging), carotid intimal medial thickness (CIMT) measurements with ultrasound and invasive tests (eg intravascular ultrasound), and optical coherence tomography (OCT).
Investigators have identified new and novel markers in the blood that appear to predict cardiovascular risks. The detection of peripheral arterial disease – narrowing of arteries of the lower limb via conducting an ABI test has also been shown to predict risks.
These new tests are available to the Malaysian public and are often recommended in enterprising ways. Confronted by the confusion and anxiety that often arises from such tests, this writer hopes to briefly put into perspective the indications and current scientific opinion for some of these novel blood tests.
The use of ABI and imaging modalities, is by large, a sometimes controversial topic and will not be covered in this article.
Current paradigm and use of new blood markers
We need to understand that no single test is definitive in risk estimation. The approach that most clinicians use combines the global clinical evaluation of an individual based on the traditional risk scores and refining the risk estimates with additional selected tests.
Importantly, a test should not be conducted just for the sake of testing. For example, a person already deemed to be at high risk for a cardiovascular event based on global risk estimates will have little to gain from doing further tests as his/her risk profile remains elevated, regardless of the test results.
Requesting a whole battery of tests would hence be a waste of funds, with little additional information to gain.
Similarly, a person with very low risk may not benefit from additional testing as his/her risk category is not likely to change. However, a physician may, in selected cases, recommend additional tests based on professional knowledge of limitations of certain risk models.
An example would be an often underestimation of risks with the Framingham model for women with a family history of premature coronary heart disease.
The best category of persons to gain from these additional tests are those in the intermediate risk group. Selecting appropriate tests may reclassify the prevailing risk estimate either upwards or downgrade the risk projection.
Another misconception that needs to be addressed is the understanding that certain blood markers are good only to predict risk. The relationship between marker and risk does not necessarily mean a causative link. This means that although an elevated blood marker predicts greater cardiovascular risk, the logic that reducing the level of such a marker will reduce risk may not necessarily apply.
Highly sensitive C-reactive protein (hs-CRP)
C-reactive protein is a circulating protein involved in immunity, and elevated levels are indicative of inflammation, including that of the vessel wall. It has been implicated in the development of atherosclerotic plaques and also in the conversion of the quiescent plaque to an unstable ruptured one that is liable to cause a heart attack.
Multiple large scale studies have shown elevated hs-CRP to independently predict risk of a heart attack, stroke, or death from cardiovascular disease.
The incorporation of hs-CRP in the Framingham calculation of cardiovascular risk (ie Reynold’s Risk Score) has further improved its risk-predictive ability.
The general categories of hs-CRP levels are 3 mg/l (high). However, these cut-off levels are arbitrary, and even lower levels have been shown to correlate with further lowered risks.
The best value of this test, however, comes from the potential for some medications, especially cholesterol-lowering medications (statins), to lower hs-CRP.
A study called the JUPITER trial investigated the use of statins in asymptomatic patients with fairly normal cholesterol levels but elevated hs-CRP levels. This trial was prematurely stopped owing to resounding benefits seen in individuals actively treated with a statin, as the study safety committee found it unethical to withhold such benefits from the placebo-treated study group.
However, there are many caveats to the use of this test. There are many factors that may increase hs-CRP levels, eg smoking, any infection, inflammatory conditions, etc.
Apo-lipoprotein A and B
The conventional lipid profile measures the total cholesterol level, HDL-cholesterol level (good cholesterol), triglyceride level and the mathematical calculation-derived LDL-cholesterol level (bad cholesterol).
LDL-cholesterol is recognised as the major culprit in the development of cholesterol plaques.
The cholesterol particles are, however, not a simple lump of cholesterol travelling in the blood stream to be deposited in the arterial walls. Cholesterol is packaged as a lipoprotein particle that has a protein component called apo-lipoprotein (Apo-A or Apo-B), and the cholesterol/lipid component.
Apo-A1 is the major apo-lipoprotein in HDL-cholesterol and apo-B in LDL-cholesterol. HDL-C cholesterol, we know, are the “reverse-transporters”. It collects cholesterol from the vessel walls and brings them back to the liver for excretion.
In certain situations like diabetes mellitus or metabolic syndrome (combined presence of obesity, abnormal blood sugars, hypertension, abnormal lipid profile), the LDL-cholesterol particles are predominantly small and dense. These LDL particles are more pro-atherogenic. The increased numbers of these small dense-LDLs are not reflected in the conventional calculation of LDL-C cholesterol.
Hence, one may get a false impression of normal LDL-C cholesterol levels in these subjects. By measuring apo-B level, we are able to directly assess the number of LDL-C cholesterol particles and give a better assessment of risk associated with LDL-C cholesterol.
Therefore, conceptually, apo-B reflects the total amount of pro-atherosclerotic lipid particles and apo-A reflects the total protective lipid fraction. The ratio of apo-B/apo-A1 tells us the balance of cholesterol transport – the lower the value, the better the risk.
This lipoprotein basically has an apolipoprotein (a) of unknown significance attached to the lipid particle. This apolipoprotein (a) may have properties that enhance oxidation of LDL-cholesterol, which encourages deposition of cholesterol in vessel walls and also promotes clot formation.
This test is not recommended for routine screening but may be most useful for individuals with high cholesterol and a family history of premature coronary artery disease.
The homocysteine story is an interesting one. The correlation between elevated homocysteine level and cardiovascular risk is well established. It has also been shown to increase risk prediction capability of the Framingham risk score.
We also know that supplementation with folic acid and vitamin B6 or B12 can lower homocysteine level. It was based on this observation that some have recommended this therapy as a means to prevent cardiovascular events.
Despite lowering homocysteine by 25%, folic acid supplementation did not result in less cardiovascular events. A recent large study (compilation of eight trials involving 37,485 individuals in 2010) reaffirms the lack of benefit from lowering homocysteine with vitamin B therapy.
Homocysteine seems to be a marker for cardiovascular disease, but may not be involved in disease development. Hence, an individual with intermediate risk may choose to perform this test for better classification of his/her risk, but there is no further treatment advocated to lower the level even if it is elevated. There has been much progress in our understanding of the causation of heart disease. The number of persons with known cases of heart disease are only the tip of the iceberg. There is a large pool of individuals with silent, “smouldering” coronary heart disease, waiting for a cardiac event to occur.
Not uncommonly, the outcome is catastrophic, with sudden death or major heart attack as the first presentation of cardiac disease.
Medical science has achieved much success in treating heart disease. However, success will be greater if we can prevent heart disease, or at least detect disease earlier to allow preventive treatment.
The conventional global risk scoring methods based on traditional risk factors stratify individuals to different categories of risk. Intermediate risk patients, however, will benefit from refinement of their risk using selected blood tests or imaging methods.
Beyond conventional blood tests that identify the presence of risk factors that contribute to heart disease like cholesterol levels, sugar levels, etc, there are many new emerging markers that help to improve risk prediction.
However, not all tests are necessary nor useful. Though some of these tests are easily available at your disposal, performing unnecessary tests may create undue distress without incremental useful information. You are encouraged to consult your personal physician on the appropriate tests.
n This article is contributed by The Star Health & Ageing Panel, which comprises a group of panellists who are not just opinion leaders in their respective fields of medical expertise, but have wide experience in medical health education for the public. The members of the panel include: Datuk Prof Dr Tan Hui Meng, consultant urologist; Dr Yap Piang Kian, consultant endocrinologist; Datuk Dr Azhari Rosman, consultant cardiologist; A/Prof Dr Philip Poi, consultant geriatrician; Dr Hew Fen Lee, consultant endocrinologist; Prof Dr Low Wah Yun, psychologist; Datuk Dr Nor Ashikin Mokhtar, consultant obstetrician and gynaecologist; Dr Lee Moon Keen, consultant neurologist; Dr Ting Hoon Chin, consultant dermatologist; Prof Khoo Ee Ming, primary care physician; Dr Ng Soo Chin, consultant haematologist. For more information, e-mail email@example.com. The Star Health & Ageing Advisory Panel provides this information for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care. The Star Health & Ageing Advisory Panel disclaims any and all liability for injury or other damages that could result from use of the information obtained from this article.
Many people have lent their names to well-known medical conditions.
THERE is a certain thrill to discovering something new that no one else has ever seen or heard or quite put together before.
This is especially so for those who are explorers by heart, whether physically – like Portuguese sea captain Ferdinand Magellan, astronaut Neil Armstrong or undersea explorer Robert Ballard – or through research, like many scientists, famous or not, around the world.
Aside from the excitement and pleasure of coming across something previously unknown, explorers also have the chance to name that thing, whether it be an island, animal or disease.
Hence, the Philippines was named after the then-Spanish crown prince Philip, a subspecies of marsh rabbit (Sylvilagus palustris hefneri) is named after Playboy founder Hugh Hefner for his donations to support the bunny’s conservation, and Lyme disease is named after the American town in which researchers first identified it.
While most diseases tend to be given descriptive names – for example, polycystic renal disease, which is an illness affecting the kidneys (renal, from the Latin word for kidney, renes) caused by the growth of multiple (poly, a Greek combining form meaning “much, many”) cysts – some have been named after the doctor, or doctors, who first described them.
Although there has been some controversy over whether this naming convention should be maintained – oftentimes there are doubts over whether the named doctor is indeed the original discoverer of the disease, and unlike descriptive names, eponyms really say nothing at all about the disease – there are still quite a few diseases that are known by someone’s name.
This chronic degenerative brain disease was first presented at a lecture in 1905 by German psychiatrist and neuropathologist Dr Alois Alzheimer.
While working at the Frankfurt Asylum, the doctor became very interested in the symptoms shown by one of his patients, 51-year-old Auguste Deter.
Deter exhibited short-term memory loss, aphasia, hallucinations, disorientation and the inability to take care of herself – common signs of the disease.
After her death at the age of 55, Dr Alzheimer conducted a microscopic examination of her brain, noting down organic changes like amyloid plaques and neurofibrillary tangles, which are the hallmark signs of the disease that bears his name.
His findings were included in a textbook Psychiatrie by his colleague Dr Emil Kraepelin, who called the condition Alzheimer’s disease in the book.
In 1981, English psychiatrist Dr Lorna Wing first introduced the name Asperger’s syndrome in association with the particular set of behavioural patterns shown by patients with this form of high-functioning autism.
Dr Hans Asperger was an Austrian paediatrician, who was particularly interested in what he called “autistic psychopathy”.
Although he published some 359 articles, mainly on this topic, during his lifetime, it was mostly in German.
As his works were mostly untranslated, his research on the syndrome that bears his name went little noticed until Dr Wing, one of the co-founders of the National Autistic Society in the United Kingdom, included it in her paper published in Psychological Medicine.
No, this form of the inherited blood disorder haemophilia is not named after the festive holiday. And unlike the first two conditions, it is not named after the doctor who discovered it either.
Although it is more commonly referred to as haemophilia B, Christmas disease is so called after the patient in whom this condition was first observed in detail – a boy named Stephen Christmas.
Coincidentally, the British Medical Journal edition that contained the paper describing this disease was published on Dec 27, 1952 – just two days after Christmas day.
Sometimes, having a surname that comes early in the alphabet pays off.
In 1932, three New York physicians, Drs Burrill Bernard Crohn, Leon Ginzburg and Gordon Oppenheimer, jointly published a paper describing a newly identified form of inflammatory bowel disease in the Mount Sinai Journal of Medicine.
Originally called terminal ileitis by the three doctors, the disease came to be popularly called Crohn’s disease after the first author as listed alphabetically.
Cushing’s syndrome and Cushing’s disease are actually two slightly different conditions that are both named after American neurosurgeon Dr Harvey Cushing.
In 1912, Dr Cushing described a condition caused by the body’s constant exposure to too much of the hormone cortisol due to excessive production by the pituitary gland.
This illness, described in his book The Pituitary Body and its Disorders, is now known as Cushing’s disease.
Cushing’s syndrome refers to the same condition of constant exposure to excessive cortisol, but not necessarily caused by the pituitary gland.
The syndrome encompasses various causes including iatrogenic ones – usually due to side effects of medications for other conditions, adrenal tumours and adrenocorticotropic hormone-producing tumours.
This well-known chromosomal disorder is named after Dr John Langdon Down, the English physician who first described the features of the syndrome in detail in his 1866 paper published in the London Hospital Reports.
His observations mainly centred on the distinctive facial characteristics of Down syndrome patients, which he described as being similar to that of the Mongoloid race.
(This description was based on German physician and anthropologist Johann Friedrich Blumenbach’s 1779 racial classification system, which considered all East Asians and some Central Asians, as part of the Mongoloid, or yellow, race.)
Initially, the condition was known as mongolism, but as the term evolved to gather negative connotations in the 1960s, the medical community soon began referring to it as Down’s syndrome, with the possessive eventually being dropped as well.
The condition is also called Trisomy 21, after its chromosomal cause was discovered by French geneticist Dr Jerome Lejeune in 1958.
In an example of a disease not being named after its original “discoverer”, this cancer of the white blood cells called lymphocytes is actually named after British pathologist Dr Thomas Hodgkin.
In his 1832 paper published in Medico-Chirurgical Transactions, Dr Hodgkin had described the condition that now bears his name. He also noted that the earliest reference to this condition had been made by Italian doctor Marcello Malphigi in 1666.
However, Dr Hodgkin’s paper went largely unnoticed, and in 1856, his successor at Guy’s Hospital, London, Dr Samuel Wilks, published a paper describing the same condition, unaware of Dr Hodgkin’s previous work on the disease.
Their mutual colleague Dr Richard Bright informed Dr Wilks of Dr Hodgkins’ prior paper, and in 1865, Dr Wilks proposed the name Hodgkin’s disease in another paper detailing further information about the disease.
The condition was also called Hodgkin’s lymphoma, and in 2001, the World Health Organization’s International Classification of Diseases used the latter in preference to the former.
As there are two main types of lymphomas, by default, the other type of lymphoma is called non-Hodgkin’s lymphoma.
This inherited progressive neurodegenerative disorder is another example of a disease that is rather arbitrarily named after only one of many medical practitioners who have described it in one form or the other over the past few centuries.
The most likely reason that American physician Dr George Huntington has his name attached to this disease is because he was the first doctor to thoroughly describe the disease in a presentation, and subsequent published paper, in 1872.
This paper even impressed renowned American physician Sir William Osler, one of the four founding professors of the Johns Hopkins University School of Medicine, in its detail.
It was originally called Huntington’s chorea (from the Greek word choreia, which means dance), after the characteristic jerky, random and uncontrollable physical movements of the condition.
However, the name was eventually changed to Huntington’s disease as chorea is not always seen in patients with the illness.
Lou Gehrig’s disease
This is another disease named after a patient, in this case, a well-known patient, rather than the first one found to have the disease.
Lou Gehrig was a famous and well-loved American baseball player, who played for the New York Yankees from 1923 to 1939.
He had to quit his successful career, which included several major league baseball records, after developing this fatal progressive neurodegenerative disease.
Due to his fame, this condition, also called amyotrophic lateral sclerosis, is primarily known as Lou Gehrig’s disease in North America.
In the United Kingdom, this illness is usually referred to as motor neurone disease.
One of the most common nervous disorders in the elderly, Parkinson’s disease is named after English doctor James Parkinson.
Even though there has been mention of this disease ever since the 10th century BCE, it was not until Dr Parkinson’s 1817 paper entitled An Essay on the Shaking Palsy, that the condition was clearly described.
At that time, the disease was known as paralysis agitans (Latin for shaking palsy).
It was French neurologist Dr Jean-Martin Charcot, who not only produced groundbreaking research on the disease between 1868 and 1881, but also promoted the renaming of the disease to honour Dr Parkinson.
This infectious foodborne illness can actually be considered as being named after a person by secondhand.
Salmonellosis is named after the bacteria that causes it, Salmonella sp. The Salmonella bacteria however, is named after American veterinary pathologist Dr Daniel Elmer Salmon.
Although the bacteria was actually discovered by Dr Salmon’s research assistant Dr Theobald Smith, the two had been working together to isolate the bacteria from pigs with hog cholera, and Dr Smith decided to name the new bacteria after his boss.
The genus name Salmonella was officially adopted in 1900 by Dr J. Lignières.
This condition, which causes repeated quick movements or sounds called tics that are uncontrollable, was first described as a clinical entity by French neurologist Dr Georges Albert Édouard Brutus Gilles de la Tourette.
He had been assigned to study patients with repetitive behaviours at the Salpêtrière Hospital by his mentor Dr Charcot (the same one mentioned under Parkinson’s disease), with the idea of establishing a condition separate from hysteria and chorea.
Dr Tourette subsequently published a paper entitled Study of a Nervous Affliction in 1885 reporting on nine patients with the syndrome, and concluding that a new clinical category should be defined.
It was Dr Charcot who named the disease Tourette syndrome in honour of Dr Tourette.