DEPRESSION: History

What was previously known as melancholia and is now known as clinical depression, major depression, or simply depression and commonly referred to as major depressive disorder by many health care professionals, has a long history, with similar conditions being described at least as far back as classical times.

Ancient to medieval period

In ancient Greece, disease was thought due to an imbalance in the four basic bodily fluids, or humors. Personality types were similarly thought to be determined by the dominant humor in a particular person. Derived from the Ancient Greek melas, "black", and kholé, "bile", melancholia was described as a distinct disease with particular mental and physical symptoms by Hippocrates in his Aphorisms, where he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.

Aretaeus of Cappadocia later noted that sufferers were "dull or stern; dejected or unreasonably torpid, without any manifest cause". The humoral theory fell out of favor but was revived in Rome by Galen. Melancholia was a far broader concept than today's depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.

Physicians in the Persian and then the Muslim world developed ideas about melancholia during the Islamic Golden Age. Ishaq ibn Imran (d. 908) combined the concepts of melancholia and phrenitis. The 11th century Persian physician Avicenna described melancholia as a depressive type of mood disorder in which the person may become suspicious and develop certain types of phobias.

His work, The Canon of Medicine, became the standard of medical thinking in Europe alongside those of Hippocrates and Galen. Moral and spiritual observations also abounded, and in the Christian environment of medieval Europe, a malaise called acedia (sloth or absence of caring) was identified, involving a tendency of the will to low spirits and lethargy typically linked to isolation.

The seminal scholarly work of the 17th century was English scholar Robert Burton's book, The Anatomy of Melancholy, drawing on numerous theories and the author's own experiences. Burton suggested that melancholy could be combatted with a healthy diet, sufficient sleep, music, and "meaningful work", along with talking about the problem with a friend.

During the 18th century, the humoral theory of melancholia was increasingly being challenged by mechanical and electrical explanations; references to dark and gloomy states gave way to ideas of slowed circulation and depleted energy. German physician Johann Christian Heinroth, however, argued melancholia was a disturbance of the soul due to moral conflict within the patient.

Eventually, various authors proposed up to 30 different sub-types of melancholia, and alternative terms were suggested and discarded. Hypochondria came to be seen as a separate disorder. Melancholia and melancholy had been used interchangeably until the 19th century, but the former came to refer to a pathological condition and the latter to a temperament.

The term depression was derived from the Latin verb deprimere, "to press down". From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker's Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753. The term also came into use in physiology and economics.

An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function. Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and, through the 19th century, became more associated with women.

Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states. English psychiatrist Henry Maudsley proposed an overarching category of affective disorder.

20th and 21st centuries

In the 20th century, the German psychiatrist Emil Kraepelin was the first to distinguish manic depression. The influential system put forward by Kraepelin unified nearly all types of mood disorder into manic–depressive insanity. Kraepelin worked from an assumption of underlying brain pathology, but also promoted a distinction between endogenous (internally caused) and exogenous (externally caused) types.

The unitarian view became more popular in the United Kingdom, while the binary view held sway in the US, influenced by the work of Swiss psychiatrist Adolf Meyer and before him Sigmund Freud, the father of psychoanalysis.

Freud had likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic breakup, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego.

Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively, but the ego itself is compromised. The patient's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor.

Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual's life, and argued that the term depression should be used instead of melancholia.

The DSM-I (1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.

In the mid-20th century, other psycho-dynamic theories were proposed. Existential and humanistic theories represented a forceful affirmation of individualism. Austrian existential psychiatrist Viktor Frankl connected depression to feelings of futility and meaninglessness. Frankl's logotherapy addressed the filling of an "existential vacuum" associated with such feelings, and may be particularly useful for depressed adolescents.

American existential psychologist Rollo May hypothesized that "depression is the inability to construct a future". In general, May wrote that depression "occur[s] more in the dimension of time than in space," and the depressed individual fails to look ahead in time properly. Thus the "focusing upon some point in time outside the depression ... gives the patient a perspective, a view on high so to speak; and this may well break the chains of the ... depression."

Humanistic psychologists argued that depression resulted from an incongruity between society and the individual's innate drive to self-actualize, or to realize one's full potential. American humanistic psychologist Abraham Maslow theorized that depression is especially likely to arise when the world precludes a sense of "richness" or "totality" for the self-actualizer.

Cognitive psychologists offered theories on depression in the mid-twentieth century. Starting in the 1950s, Albert Ellis argued that depression stemmed from irrational "should" and "musts" leading to inappropriate self-blame, self-pity, or other-pity in times of adversity. Starting in the 1960s, Aaron Beck developed the theory that depression results from a "cognitive triad" of negative thinking patterns, or "schemas," about oneself, one's future, and the world.

In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms. During the 1960s and 70s, manic-depression came to refer to just one type of mood disorder (now most commonly known as bipolar disorder) which was distinguished from (unipolar) depression. The terms unipolar and bipolar had been coined by German psychiatrist Karl Kleist.

The term major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the Research Diagnostic Criteria, building on earlier Feighner Criteria), and was incorporated into the DSM-III in 1980. To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes.

DSM-IV-TR excluded cases where the symptoms are a result of bereavement, although it was possible for normal bereavement to evolve into a depressive episode if the mood persisted and the characteristic features of a major depressive episode developed. The criteria were criticized because they do not take into account any other aspects of the personal and social context in which depression can occur. In addition, some studies found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration.

The ancient idea of melancholia still survives in the notion of a melancholic sub-type. The new definitions of depression were widely accepted, albeit with some conflicting findings and views, and the nomenclature continues in DSM-IV-TR, published in 2000.

There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.

SOURCE: https://en.wikipedia.org/wiki/History_of_depression

PANDEMICS IN HISTORY

Historical accounts of epidemics are often vague or contradictory in describing how victims were affected. A rash accompanied by a fever might be smallpox, measles, scarlet fever, or varicella, and it is possible that epidemics overlapped, with multiple infections striking the same population at once. It is often impossible to know the exact causes of mortality, although ancient DNA studies can sometimes detect residues of certain pathogens.

It is assumed that, prior to the Neolithic Revolution around 10,000 BC, disease outbreaks were limited to a single family or clan, and did not spread widely before dying out. The domestication of animals increased human-animal contact, increasing the possibility of zoonotic infections. The advent of agriculture, and trade between settled groups, made it possible for pathogens to spread widely. As population increased, contact between groups became more frequent. A history of epidemics maintained by the Chinese Empire from 243 B.C. to 1911 A.C. shows an approximate correlation between the frequency of epidemics and the growth of the population.

The incomplete list of known epidemics which spread widely enough to merit the title "pandemic".

Plague of Athens (430 to 426 BC): During the Peloponnesian War, an epidemic killed a quarter of the Athenian troops and a quarter of the population. This disease fatally weakened the dominance of Athens, but the sheer virulence of the disease prevented its wider spread. The exact cause of the plague was unknown for many years. In January 2006, researchers from the University of Athens analyzed teeth recovered from a mass grave underneath the city and confirmed the presence of bacteria responsible for typhoid fever.

Antonine Plague (165 to 180 AD): Possibly measles or smallpox brought to the Italian peninsula by soldiers returning from the Near East, it killed a quarter of those infected, up to five million in total.

Plague of Cyprian (251–266 AD): A second outbreak of what may have been the same disease as the Antonine Plague killed (it was said) 5,000 people a day in Rome.

Plague of Justinian (541 to 549 AD): Also known as the First Plague Pandemic. This epidemic started in Egypt and reached Constantinople the following spring, killing (according to the Byzantine chronicler Procopius) 10,000 a day at its height, and perhaps 40% of the city's inhabitants. The plague went on to eliminate a quarter to half the human population of the known world and was identified in 2013 as being caused by bubonic plague.

Black Death (1331 to 1353): Also known as the Second Plague Pandemic. The total number of deaths worldwide is estimated at 75 to 200 million. Starting in Asia, the disease reached the Mediterranean and western Europe in 1348 (possibly from Italian merchants fleeing fighting in Crimea) and killed an estimated 20 to 30 million Europeans in six years; a third of the total population, and up to a half in the worst-affected urban areas. It was the first of a cycle of European plague epidemics that continued until the 18th century; there were more than 100 plague epidemics in Europe during this period, including the Great Plague of London of 1665–66 which killed approximately 100,000 people, 20% of London's population.

1817–1824 cholera pandemic. Previously endemic in the Indian subcontinent, the pandemic began in Bengal, then spread across India by 1820. The deaths of 10,000 British troops were documented - it is assumed that tens of thousands of Indians must have died. The disease spread as far as China, Indonesia (where more than 100,000 people succumbed on the island of Java alone) and the Caspian Sea before receding. Subsequent cholera pandemics during the 19th century are estimated to have caused many millions of deaths globally.

Great Plague of Marseille in 1720 killed a total of 100,000 people

Third plague pandemic (1855–1960): Starting in China, it is estimated to have caused over 12 million deaths in total, the majority of them in India. During this pandemic, the United States saw its first outbreak: the San Francisco plague of 1900–1904. The causative bacterium, Yersinia pestis, was identified in 1894. The association with fleas, and in particular rat fleas in urban environments, led to effective control measures. The pandemic was considered to be over in 1959 when annual deaths due to plague dropped below 200. The disease is nevertheless present in the rat population worldwide and isolated human cases still occur.

The 1918–1920 Spanish flu infected half a billion people around the world, including on remote Pacific islands and in the Arctic—killing 20 to 100 million. Most influenza outbreaks disproportionately kill the very young and the very old, but the 1918 pandemic had an unusually high mortality rate for young adults. Mass troop movements and close quarters during World War I caused it to spread and mutate faster, and the susceptibility of soldiers to the flu may have been increased by stress, malnourishment and chemical attacks. Improved transportation systems made it easier for soldiers, sailors and civilian travelers to spread the disease.

Pandemics in indigenous populations

Beginning from the Middle Ages, encounters between European settlers and native populations in the rest of the world often introduced epidemics of extraordinary virulence. Settlers introduced novel diseases which were endemic in Europe, such as smallpox, measles, pertussis and influenza, to which the indigenous peoples had no immunity. The Europeans infected with such diseases typically carried them in a dormant state, were actively infected but asymptomatic, or had only mild symptoms.

Smallpox was the most destructive disease that was brought by Europeans to the Native Americans, both in terms of morbidity and mortality. The first well-documented smallpox epidemic in the Americas began in Hispaniola in late 1518 and soon spread to Mexico. Estimates of mortality range from one-quarter to one-half of the population of central Mexico. It is estimated that over the 100 years after European arrival in 1492, the indigenous population of the Americas dropped from 60 million to only 6 million, due to a combination of disease, war, and famine. The majority these deaths are attributed to successive waves of introduced diseases such as smallpox, measles, and typhoid fever.

In Australia, smallpox was introduced by European settlers in 1789 devastating the Australian Aboriginal population, killing an estimated 50% of those infected with the disease during the first decades of colonization. In the early 1800s, measles, smallpox and intertribal warfare killed an estimated 20,000 New Zealand Maori.

In 1848–49, as many as 40,000 out of 150,000 Hawaiians are estimated to have died of measles, whooping cough and influenza. Measles killed more than 40,000 Fijians, approximately one-third of the population, in 1875, and in the early 19th century devastated the Great Andamanese population.[110] In Hokkaido, an epidemic of smallpox introduced by Japanese settlers is estimated to have killed 34% of the native Ainu population in 1845.

SOURCE: https://en.wikipedia.org/wiki/Pandemic

DIABETES HISTORY

The condition known today as diabetes (diabetes mellitus) is thought to have been described in the Ebers Papyrus (c. 1550 BC) Ayurvedic physicians (5th/6th century BC) first noted the sweet taste of diabetic urine, and called the condition madhumeha ("honey urine"). The term diabetes traces back to Demetrius of Apamea (1st century BC). For a long time, the condition was described and treated in traditional Chinese medicine as xiāo kě (wasting-thirst). Physicians of the medieval Islamic world, including Avicenna, have also written on diabetes. Early accounts often referred to diabetes as a disease of the kidneys. In 1674, Thomas Willis suggested that diabetes may be a disease of the blood. Johann Peter Frank is credited with distinguishing diabetes mellitus and diabetes insipidus in 1794.

 

In regard to diabetes mellitus, Joseph von Mering and Oskar Minkowski are commonly credited with the formal discovery (1889) of a role for the pancreas in causing the condition. In 1893, Édouard Laguesse suggested that the islet cells of the pancreas, described as "little heaps of cells" by Paul Langerhans in 1869, might play a regulatory role in digestion. These cells were named islets of Langerhans after the original discoverer. In the beginning of the 20th century, physicians hypothesized that the islets secrete a substance (named "insulin") that metabolises carbohydrates. The first to isolate the extract used, called insulin, was Nicolae Paulescu. In 1916, he succeeded in developing an aqueous pancreatic extract which, when injected into a diabetic dog, proved to have a normalizing effect on blood sugar levels. Then, while Paulescu served in army, during World War I, the discovery and purification of insulin for clinical use in 1921–1922 was achieved by a group of researchers in Toronto—Frederick Banting, John Macleod, Charles Best, and James Collip—paved the way for treatment. The patent for insulin was assigned to the University of Toronto in 1923 for a symbolic dollar to keep treatment accessible.

 

In regard to diabetes insipidus, treatment became available before the causes of the disease were clarified. The discovery of an antidiuretic substance extracted from the pituitary gland by researchers in Italy (A. Farini and B. Ceccaroni) and Germany (R. Von den Velden) in 1913 paved the way for treatment. By the 1920s, accumulated findings defined diabetes insipidus as a disorder of the pituitary. The main question now became whether the cause of diabetes insipidus lay in the pituitary gland or the hypothalamus, given their intimate connection. In 1954, Berta and Ernst Scharrer concluded that the hormones were produced by the nuclei of cells in the hypothalamus.

SOURCE: https://en.wikipedia.org/wiki/History_of_diabetes

HYPERTENSION HISTORY

The modern history of hypertension begins with the understanding of the cardiovascular system based on the work of physician William Harvey (1578–1657), who described the circulation of blood in his book De motu cordis. The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733. Descriptions of what would come to be called hypertension came from, among others, Thomas Young in 1808 and especially Richard Bright in 1836. Bright noted a link between cardiac hypertrophy and kidney disease, and subsequently kidney disease was often termed Bright's disease in this period. In 1850 George Johnson suggested that the thickened blood vessels seen in the kidney in Bright's disease might be an adaptation to elevated blood pressure. William Senhouse Kirkes in 1855 and Ludwig Traube in 1856 also proposed, based on pathological observations, that elevated pressure could account for the association between left ventricular hypertrophy to kidney damage in Bright's disease. Samuel Wilks observed that left ventricular hypertrophy and diseased arteries were not necessarily associated with diseased kidneys, implying that high blood pressure might occur in people with healthy kidneys; however, the first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed in 1874 using a sphygmograph. The concept of hypertensive disease as a generalized circulatory disease was taken up by Sir Clifford Allbutt, who termed the condition "hyperpiesia". However, hypertension as a medical entity really came into being in 1896 with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896, which allowed blood pressure to be measured in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculted with a stethoscope while the sphygmomanometer cuff is deflated. Tracking serial blood pressure measurements was further enhanced when Donal Nunn invented an accurate fully automated oscillometric sphygmomanometer device in 1981.

 

The term essential hypertension ('Essentielle Hypertonie') was coined by Eberhard Frank in 1911 to describe elevated blood pressure for which no cause could be found. In 1928, the term malignant hypertension was coined by physicians from the Mayo Clinic to describe a syndrome of very high blood pressure, severe retinopathy and inadequate kidney function which usually resulted in death within a year from strokes, heart failure or kidney failure. A prominent individual with severe hypertension was Franklin D. Roosevelt. However, while the menace of severe or malignant hypertension was well recognised, the risks of more moderate elevations of blood pressure were uncertain and the benefits of treatment doubtful. Consequently, hypertension was often classified into "malignant" and "benign". In 1931, John Hay, Professor of Medicine at Liverpool University, wrote that "there is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery, because then some fool is certain to try and reduce it". This view was echoed in 1937 by US cardiologist Paul Dudley White, who suggested that "hypertension may be an important compensatory mechanism which should not be tampered with, even if we were certain that we could control it". Charles Friedberg's 1949 classic textbook "Diseases of the Heart", stated that "people with 'mild benign' hypertension ... [defined as blood pressures up to levels of 210/100 mm Hg] ... need not be treated". However, the tide of medical opinion was turning: it was increasingly recognised in the 1950s that "benign" hypertension was not harmless. Over the next decade increasing evidence accumulated from actuarial reports and longitudinal studies, such as the Framingham Heart Study, that "benign" hypertension increased death and cardiovascular disease, and that these risks increased in a graded manner with increasing blood pressure across the whole spectrum of population blood pressures. Subsequently, the National Institutes of Health also sponsored other population studies, which additionally showed that African Americans had a higher burden of hypertension and its complications.

SOURCE: https://en.wikipedia.org/wiki/History_of_hypertension