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Thursday, November 23, 2023

Campaigns against corporal punishment

world political map with countries highlighted where corporal punishment is outlawed
Legal status of corporal punishment of children as of 2019:
  Illegal
  Legal (at least partially)

Campaigns against corporal punishment aim to reduce or eliminate corporal punishment of minors by instigating legal and cultural changes in the areas where such punishments are practiced. Such campaigns date mostly from the late 20th century, although occasional voices in opposition to corporal punishment existed from ancient times through to the modern era.

The UN Committee on the Rights of the Child defines "corporal punishment" as:

any punishment in which physical force is used and intended to cause some degree of pain or discomfort, however light. Most involves hitting ("smacking", "slapping", "spanking") children, with the hand or with an implement – whip, stick, belt, shoe, wooden spoon, etc. But it can also involve, for example, kicking, shaking or throwing children, scratching, pinching, biting, pulling hair or boxing ears, forcing children to stay in uncomfortable positions, burning, scalding or forced ingestion.

History

Quintilian and Plutarch, both writing in the 1st century A.D., expressed the opinion that corporal punishment was demeaning to those who were not slaves, meaning the children of the freeborn. In contrast, according to the classicist Otto Kiefer, Seneca remarked to his friend Lucilius, "Fear and love cannot live together. You seem to me to do right in refusing to be feared by your slaves and chastising them with words alone. Blows are used to correct brute beasts".

However, according to Robert McCole Wilson, "it is only in the last two hundred years that there has been a growing body of opinion" opposed to corporal punishment.

Australia

Jordan Riak began working against corporal punishment when he was residing with his children in Sydney, Australia. Corporal punishment was eventually banned in the public schools of all Australian states, and the private schools of all states except Queensland.

United Kingdom

In the United Kingdom, one of the earliest organised campaigns was that of the Humanitarian League, with its regular magazine The Humanitarian, which campaigned for several years for the abolition of the chastisement of young seamen in the Royal Navy, a goal partially achieved in 1906 when naval birching was abandoned as a summary punishment. However, it did not manage to get the Navy to abolish caning as a punishment, which continued at Naval training establishments until 1967.

The Howard League for Penal Reform campaigned in the 1930s for, among many other things, the abolition of judicial corporal punishment by cat-o'-nine-tails or birching. This was eventually achieved in the U.K. in 1948.

The Society of Teachers Opposed to Physical Punishment (STOPP) was set up in the U.K. in 1968 to campaign for the abolition of corporal punishment in UK schools.

STOPP was a very small pressure group that lobbied government, local authorities and other official institutions. It also investigated individual cases of corporal punishment and aided families wishing to pursue their cases through the UK and European courts.

The UK Parliament abolished corporal punishment in state schools in 1986. STOPP then wound itself up and ceased to exist, though some of the same individuals went on to form EPOCH to campaign to outlaw spanking, and spanking in the domestic setting.

A campaign by the name of Children Are Unbeatable! involves more than 350 separate groups, including the National Society for the Prevention of Cruelty to Children, Barnardo's, Save the Children, Action for Children (formerly NCH), and the National Children's Bureau.

Canada

In CFCYL v. Canada, the Supreme Court of Canada upheld section 43 of the Criminal Code, which allows for a defence of reasonable use of force by way of correction towards children.

United States

An early U.S. activist against corporal punishment was Horace Mann, who in the 19th century unsuccessfully opposed its use in schools.

Several organizations have been formed in the United States to advocate abolishing corporal punishment in homes and/or schools, including:

  • Parents and Teachers Against Violence in Education (PTAVE), based in California
  • The Center for Effective Discipline, now part of the Gundersen National Child Protection Training Center (NCPTC) of Winona (MN) State University
  • The U.S. Alliance to End the Hitting of Children
  • People Opposed to Paddling Students (POPS), based in Texas
  • Floridians Against Corporal Punishment in Public School, based in Florida
  • The Alliance Against Corporal Punishment
  • The National Youth Rights Association
  • We the Children Foundation

Individuals who have directly advocated against corporal punishment include, but are not limited to:

  • Kirstie Alley (born 1955), Actress - has stated her opposition to corporal punishment on numerous occasions, most notably on the Howard Stern Show
  • Nadine Block, wrote the bill which banned corporal punishment from public schools in Ohio in 2009
  • Blythe and David Daniel, Professors - advocate and teach children's rights and work for laws against corporal punishment
  • Blake Hutchison (born 1980), writer of Nobody's Property, independent filmmaker and videographer from Ohio who has made several often-controversial children's rights and anti-spanking videos on his YouTube channel. including one titled "Children's Rights Pyrotechnic Practice" where he sets fire to a copy of Michael and Debi Pearl's highly controversial book To Train Up A Child (a book which he says is a "training" book to assault kids).
  • Horace Mann, campaigned to ban corporal punishment from schools during the 19th century
  • Dr. Phil McGraw (born 1950), Television Show Host has had episodes on his show dedicated to showing the harm and/or ineffectiveness of corporal punishment.
  • Marcus Lawrence Ward (1812–1884), governor of New Jersey from 1866 to 1869, who signed into law the public and private school corporal punishment ban during his time in office, which is still in effect today.
  • Jordan Riak (1935–2016), drafted the bill which banned corporal punishment from public schools in California in the 1980s
  • Daniel Vander Ley (born 1982), using the BeatYourChildren.com campaign and the "Fundamentalism - America's Premier Child Abuse Brand" campaign, Vander Ley communicates directly with governments around the world offering their constituents research about the negative effects of corporal punishment and religious extremism.

Worldwide

An organisation called "Global Initiative To End All Corporal Punishment Of Children" was formed in 2001 to campaign for the worldwide prohibition by law of all corporal punishment of children, in homes, schools, penal institutions, and other settings. It seeks to monitor the legal situation in every country of the world. The Global Initiative has received endorsement from UNICEF, UNESCO, the United Nations High Commissioner for Human Rights, the Commissioner for Human Rights of the Council of Europe, the Parliamentary Assembly of the Council of Europe, and the European Network of Ombudsmen for Children.

In 2008, the UN Study on Violence against Children set a target date of 2009 for universal prohibition, including in the home, an aim described by The Economist the same year as "wildly unrealistic".

The Society for Prevention of Injuries & Corporal Punishment [SPIC] is an Indian organization advocating measures to stop corporal punishment in schools by making teachers and students aware of its dangers.

In Austria the White Hand Campaign for a worldwide legal ban on child corporal punishment tries to raise awareness for the topic in the German-speaking countries.

Comorbidity

From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Comorbidity

In medicine, comorbidity—from Latin morbus ("sickness"), co ("together"), -ity (as if - several sicknesses together)—is the presence of one or more additional conditions often co-occurring (that is, concomitant or concurrent) with a primary condition. Comorbidity describes the effect of all other conditions an individual patient might have other than the primary condition of interest, and can be physiological or psychological. In the context of mental health, comorbidity often refers to disorders that are often coexistent with each other, such as depression and anxiety disorders. The concept of multimorbidity is related to comorbidity but presents a different meaning and approach.

Definition

The term "comorbid" has three definitions:

  1. to indicate a medical condition existing simultaneously but independently with another condition in a patient.
  2. to indicate a medical condition in a patient that causes, is caused by, or is otherwise related to another condition in the same patient.
  3. to indicate two or more medical conditions existing simultaneously regardless of their causal relationship.

Comorbidity can indicate either a condition existing simultaneously, but independently with another condition or a related derivative medical condition. The latter sense of the term causes some overlap with the concept of complications. For example, in longstanding diabetes mellitus, the extent to which coronary artery disease is an independent comorbidity versus a diabetic complication is not easy to measure, because both diseases are quite multivariate and there are likely aspects of both simultaneity and consequence. The same is true of intercurrent diseases in pregnancy. In other examples, the true independence or relation is not ascertainable because syndromes and associations are often identified long before pathogenetic commonalities are confirmed (and, in some examples, before they are even hypothesized). In psychiatric diagnoses it has been argued in part that this "'use of imprecise language may lead to correspondingly imprecise thinking', [and] this usage of the term 'comorbidity' should probably be avoided." However, in many medical examples, such as comorbid diabetes mellitus and coronary artery disease, it makes little difference which word is used, as long as the medical complexity is duly recognized and addressed.

Difference from multimorbidity

Comorbidity is often referred to as multimorbidity even though the two are considered distinct clinical scenarios.

Comorbidity means that one 'index' condition is the focus of attention, and others are viewed in relation to this. In contrast, multimorbidity describes someone having two or more long-term (chronic) conditions without any of them holding priority over the others. This distinction is important in how the healthcare system treats people and helps making clear the specific settings in which the use of one or the other term can be preferred. Multimorbidity offers a more general and person-centered concept that allows focusing on all of the patient's symptoms and providing a more holistic care. In other settings, for example in pharmaceutical research, comorbidity might often be the more useful term to use.

Mental health

In psychiatry, psychology, and mental health counseling, comorbidity refers to the presence of more than one diagnosis occurring in an individual at the same time. However, in psychiatric classification, comorbidity does not necessarily imply the presence of multiple diseases, but instead can reflect current inability to supply a single diagnosis accounting for all symptoms. On the DSM Axis I, major depressive disorder is a very common comorbid disorder. The Axis II personality disorders are often criticized because their comorbidity rates are excessively high, approaching 60% in some cases. Critics[who?] assert this indicates these categories of mental illness are too imprecisely distinguished to be usefully valid for diagnostic purposes, impacting treatment and resource allocation. Symptom overlap is a key component against DSM classification and serves as a note towards redefining criteria in disorders that the root cause may not be understood thoroughly. Regardless of criticisms, it stands that, annually, up to 45% of mental health patients fit the criteria for a comorbid diagnosis. A comorbid diagnosis is associated with more severe symptomatic expression and greater chance of dismal prognosis. Certain diagnoses such as ADHD, autism, OCD, and mood disorders have higher rates of co-occurring or being prevalent in separate diagnoses. "Comorbidity in OCD is the rule rather than the exception" with OCD diagnoses facing a lifetime rate of 90%. With overlapping symptoms comes overlap in treatment as well, CBT for example is common for both ADHD and OCD with pediatric onset and can be effective for both in a comorbid diagnosis. OCD and eating disorders have a high rate of occurrence, it is estimated that 20-60% of patients with an eating disorder have OCD. More often, comorbidity complicates and can prevent treatment efficacy on a varying scale depending on the circumstances.

The term 'comorbidity' was introduced in medicine by Feinstein (1970) to describe cases in which a 'distinct additional clinical entity' occurred before or during treatment for the 'index disease', the original or primary diagnosis. Since the terms were coined, meta studies have shown that criteria used to determine the index disease were flawed and subjective, and moreover, trying to identify an index disease as the cause of the others can be counterproductive to understanding and treating interdependent conditions. In response, 'multimorbidity' was introduced to describe concurrent conditions without relativity to or implied dependency on another disease, so that the complex interactions to emerge naturally under analysis of the system as a whole.

Although the term 'comorbidity' has recently become very fashionable in psychiatry, its use to indicate the concomitance of two or more psychiatric diagnoses is said to be incorrect because in most cases it is unclear whether the concomitant diagnoses actually reflect the presence of distinct clinical entities or refer to multiple manifestations of a single clinical entity. It has been argued that because "'the use of imprecise language may lead to correspondingly imprecise thinking', this usage of the term 'comorbidity' should probably be avoided".

Due to its artifactual nature, psychiatric comorbidity has been considered as a Kuhnian anomaly leading the DSM to a scientific crisis and a comprehensive review on the matter considers comorbidity as an epistemological challenge to modern psychiatry. The Hierarchical Taxonomy of Psychopathology is a leading alternative classification system that addresses these concerns about comorbidity.

History

Widespread study of physical and mental pathology found its place in psychiatry. I. Jensen (1975), J.H. Boyd (1984), W.C. Sanderson (1990), Yuri Nuller (1993), D.L. Robins (1994), A. B. Smulevich (1997), C.R. Cloninger (2002) and other psychiatrists discovered a number of comorbid conditions in those with psychiatric disorders.

The influence of comorbidity on the clinical progression of the primary (basic) physical disorder, effectiveness of the medicinal therapy and immediate and long-term prognosis of the patients was researched by physicians and scientists of various medical fields in many countries across the globe. These scientists and physicians included: M. H. Kaplan (1974), T. Pincus (1986), M. E. Charlson (1987), F. G. Schellevis (1993), H. C. Kraemer (1995), M. van den Akker (1996), A. Grimby (1997), S. Greenfield (1999), M. Fortin (2004) & A. Vanasse (2004), C. Hudon (2005), L. B. Lazebnik (2005), A. L. Vertkin (2008), G. E. Caughey (2008), F. I. Belyalov (2009), L. A. Luchikhin (2010) and many others.

Inception of the term

Many centuries ago the doctors propagated the viability of a complex approach in the diagnosis of disease and the treatment of the patient, however, modern medicine, which boasts a wide range of diagnostic methods and a variety of therapeutic procedures, stresses specification. This brought up a question: How to wholly evaluate the state of a patient who has a number of diseases simultaneously, where to start from and which disease(s) require(s) primary and subsequent treatment? For many years this question stood out unanswered, until 1970, when a renowned American doctor epidemiologist and researcher, A.R. Feinstein, who had greatly influenced the methods of clinical diagnosis and particularly methods used in the field of clinical epidemiology, came out with the term of "comorbidity". The appearance of comorbidity was demonstrated by Feinstein using the example of patients physically affected by rheumatic fever, discovering the worst state of the patients, who simultaneously had multiple diseases. In due course of time after its discovery, comorbidity was distinguished as a separate scientific-research discipline in many branches of medicine.

Evolution of the term

Presently there is no agreed-upon terminology of comorbidity. Some authors bring forward different meanings of comorbidity and multi-morbidity, defining the former, as the presence of a number of diseases in a patient, connected to each other through proven pathogenetic mechanisms and the latter, as the presence of a number of diseases in a patient, not having any connection to each other through any of the proven to date pathogenetic mechanisms. Others affirm that multi-morbidity is the combination of a number of chronic or acute diseases and clinical symptoms in a person and do not stress the similarities or differences in their pathogenesis. However the principle clarification of the term was given by H. C. Kraemer and M. van den Akker, determining comorbidity as the combination in a patient of 2 or more chronic diseases (disorders), pathogenetically related to each other or coexisting in a single patient independent of each disease's activity in the patient.

Synonyms

  • Polymorbidity
  • Multifactorial diseases
  • Polypathy
  • Dual diagnosis, used for mental health issues
  • Pluralpathology

Epidemiology

Comorbidity is widespread among the patients admitted at multidiscipline hospitals. During the phase of initial medical help, the patients having multiple diseases simultaneously are a norm rather than an exception. Prevention and treatment of chronic diseases declared by the World Health Organization, as a priority project for the second decade of the 20th century, are meant to better the quality of the global population. This is the reason for an overall tendency of large-scale epidemiological researches in different medical fields, carried-out using serious statistical data. In most of the carried-out, randomized, clinical researches the authors study patients with single refined pathology, making comorbidity an exclusive criterion. This is why it is hard to relate researches, directed towards the evaluation of the combination of ones or the other separate disorders, to works regarding the sole research of comorbidity. The absence of a single scientific approach to the evaluation of comorbidity leads to omissions in clinical practice. It is hard not to notice the absence of comorbidity in the taxonomy (systematics) of disease, presented in ICD-10.

Clinico-pathological comparisons

All the fundamental researches of medical documentation, directed towards the study of the spread of comorbidity and influence of its structure, were conducted until the 1990s. The sources of information, used by the researchers and scientists, working on the matter of comorbidity, were case histories, hospital records of patients and other medical documentation, kept by family doctors, insurance companies and even in the archives of patients in old houses.

The listed methods of obtaining medical information are mainly based on clinical experience and qualification of the physicians, carrying out clinically, instrumentally and laboratorially confirmed diagnosis. This is why despite their competence, they are highly subjective. No analysis of the results of postmortem of deceased patients was carried out for any of the comorbidity researches.

"It is the duty of the doctor to carry out autopsy of the patients they treat", said once professor M. Y. Mudrov. Autopsy allows you to exactly determine the structure of comorbidity and the direct cause of death of each patient independent of his/her age, gender and gender specific characteristics. Statistical data of comorbid pathology, based on these sections, are mainly devoid of subjectivism.

Research

The analysis of a decade long Australian research based on the study of patients having 6 widespread chronic diseases demonstrated that nearly half of the elderly patients with arthritis also had hypertension, 20% had cardiac disorders and 14% had type 2 diabetes. More than 60% of asthmatic patients complained of concurrent arthritis, 20% complained of cardiac problems and 16% had type 2 diabetes.

In patients with chronic kidney disease (renal insufficiency) the frequency of coronary heart disease is 22% higher and new coronary events 3.4 times higher compared to patients without kidney function disorders. Progression of CKD towards end stage renal disease requiring renal replacement therapy is accompanied by increasing prevalence of Coronary Heart Disease and sudden death from cardiac arrest.

A Canadian research conducted upon 483 obesity patients, it was determined that spread of obesity related accompanying diseases was higher among females than males. The researchers discovered that nearly 75% of obesity patients had accompanying diseases, which mostly included dyslipidemia, hypertension and type 2 diabetes. Among the young obesity patients (from 18 to 29) more than two chronic diseases were found in 22% males and 43% females.

Fibromyalgia is a condition which is comorbid with several others, including but not limited to; depression, anxiety, headache, irritable bowel syndrome, chronic fatigue syndrome, systemic lupus erythematosus, rheumatoid arthritis, migraine, and panic disorder.

The number of comorbid diseases increases with age. Comorbidity increases by 10% in ages up to 19 years, up to 80% in people of ages 80 and older. According to data by M. Fortin, based on the analysis of 980 case histories, taken from daily practice of a family doctor, the spread of comorbidity is from 69% in young patients, up to 93% among middle aged people and up to 98% patients of older age groups. At the same time the number of chronic diseases varies from 2.8 in young patients and 6.4 among older patients.

According to Russian data, based on the study of more than three thousand postmortem reports (n=3239) of patients of physical pathologies, admitted at multidisciplinary hospitals for the treatment of chronic disorders (average age 67.8 ± 11.6 years), the frequency of comorbidity is 94.2%. Doctors mostly come across a combination of two to three disorders, but in rare cases (up to 2.7%) a single patient carried a combination of 6–8 diseases simultaneously.

The fourteen-year research conducted on 883 patients of idiopathic thrombocytopenic purpura (Werlhof disease), conducted in Great Britain, shows that the given disease is related to a wide range of physical pathologies. In the comorbid structure of these patients, most frequently present are malignant neoplasms, locomotorium disorders, skin and genitourinary system disorders, as well as haemorrhagic complications and other autoimmune diseases, the risk of whose progression during the first five years of the primary disease exceeds the limit of 5%.

In a research conducted on 196 larynx cancer patients, it was determined that the survival rate of patients at various stages of cancer differs depending upon the presence or absence of comorbidity. At the first stage of cancer the survival rate in the presence of comorbidity is 17% and in its absence it is 83%, in the second stage of cancer the rate of survivability is 14% and 76%, in the third stage it is 28% and 66% and in the fourth stage of cancer it is 0% and 50% respectively. Overall the survivability rate of comorbid larynx cancer patients is 59% lower than the survivability rate of patients without comorbidity.

Except for therapists and general physicians, the problem of comorbidity is also often faced by specialists. Regretfully they seldom pay attention to the coexistence of a whole range of disorders in a single patient and mostly conduct the treatment of specific to their specialization diseases. In current practice urologists, gynecologists, ENT specialists, eye specialists, surgeons and other specialists all too often mention only the diseases related to "own" field of specialization, passing on the discovery of other accompanying pathologies "under the control" of other specialists. It has become an unspoken rule for any specialized department to carry out consultations of the therapist, who feels obliged to carry out symptomatic analysis of the patient, as well as to the form the diagnostic and therapeutic concept, taking in view the potential risks for the patient and his long-term prognosis.

Based on the available clinical and scientific data it is possible to conclude that comorbidity has a range of undoubted properties, which characterize it as a heterogeneous and often encountered event, which enhances the seriousness of the condition and worsens the patient's prospects. The heterogeneous character of comorbidity is due to the wide range of reasons causing it.

Causes

  • Anatomic proximity of diseased organs
  • Singular pathogenetic mechanism of a number of diseases
  • Terminable cause-effect relation between the diseases
  • One disease resulting from complications of another
  • Pleiotropy

The factors responsible for the development of comorbidity can be chronic infections, inflammations, involutional and systematic metabolic changes, iatrogenesis, social status, ecology and genetic susceptibility.

Types

  • Trans-syndromal comorbidity: coexistence, in a single patient, of two and/or more syndromes, pathogenetically related to each other.
  • Trans-nosological comorbidity: coexistence, in a single patient, of two and/or more syndromes, pathogenetically not related to each other.

The division of comorbidity as per syndromal and nosological principles is mainly preliminary and inaccurate, however it allows us to understand that comorbidity can be connected to a singular cause or common mechanisms of pathogenesis of the conditions, which sometimes explains the similarity in their clinical aspects, which makes it difficult to differentiate between nosologies.

  • Etiological comorbidity: It is caused by concurrent damage to different organs and systems, which is caused by a singular pathological agent (for example due to alcoholism in patients with chronic alcohol intoxication; pathologies associated with smoking; systematic damage due to collagenoses).
  • Complicated comorbidity: It is the result of the primary disease and often subsequent after sometime after its destabilization appears in the shape of target lesions (for example chronic nephratony resulting from diabetic nephropathy (Kimmelstiel-Wilson disease) in patients with type 2 diabetes; development of brain infarction resulting from complications due to hypertensive crisis in patients with hypertension).
  • Iatrogenic comorbidity: It appears as a result of necessitated negative effect of the doctor on the patient, under the conditions of pre determine danger of one or the other medical procedure (for example, glucocorticosteroid osteoporosis in patients treated for a long time using systematic hormonal agents (preparations); drug-induced hepatitis resulting from chemotherapy against TB, prescribed due to the conversion of tubercular tests).
  • Unspecified (NOS) comorbidity: This type assumes the presence of singular pathogenetic mechanisms of development of diseases, comprising this combination, but require a number of tests, proving the hypothesis of the researcher or physician (for example, erectile dysfunction as an early sign of general atherosclerosis (ASVD); occurrence of erosive-ulcerative lesions in the mucous membrane of the upper gastrointestinal tract in "vascular" patients).
  • "Arbitrary" comorbidity: initial alogism of the combination of diseases is not proven, but soon can be explained with clinical and scientific point of view (for example, combination of coronary heart disease (CHD) and choledocholithiasis; combination of acquired heart valvular disease and psoriasis).

Structure

There are a number of rules for the formulation of clinical diagnosis for comorbid patients, which must be followed by a practitioner. The main principle is to distinguish in diagnosis the primary and background diseases, as well as their complications and accompanying pathologies.

  • Primary disease: This is the nosological form, which itself or as a result of complications calls for the foremost necessity for treatment at the time due to threat to the patient's life and danger of disability. Primary is the disease, which becomes the cause of seeking medical help or the reason for the patient's death. If the patient has several primary diseases it is important to first of all understand the combined primary diseases (rival or concomitant).
  • Rival diseases: These are the concurrent nosological forms in a patient, interdependent in etiologies and pathogenesis, but equally sharing the criterion of a primary disease (for example, transmural myocardial infarction and massive thromboembolism of pulmonary artery, caused by phlebemphraxis of lower limbs). For practicing pathologist rival are two or more diseases, exhibited in a single patient, each of which by itself or through its complications could cause the patient's death.
  • Polypathia: Diseases with different etiologies and pathogenesis, each of which separately could not cause death, but, concurring during development and reciprocally exacerbating each other, they cause the patient's death (for example, osteoporotic fracture of the surgical neck of the femur and hypostatic pneumonia).
  • Background disease: This helps in the occurrence of or adverse development of the primary disease increases its dangers and helps in the development of complications. This disease as well as the primary one requires immediate treatment (for example, type 2 diabetes).
  • Complications: Nosologies having pathogenetic relation to the primary disease, supporting the adverse progression of the disorder, causing acute worsening of the patient's conditions (are a part of the complicated comorbidity). In a number of cases the complications of the primary disease and related to it etiological and pathogenetic factors, are indicated as conjugated disease. In this case they must be identified as the cause of comorbidity. Complications are listed in a descending order of prognostic or disabling significance.
  • Associating diseases: Nosological units not connected etiologically and pathogenetically with the primary disease (Listed in the order of significance).

Diagnosis

Many tests attempt to standardize the "weight" or value of comorbid conditions, whether they are secondary or tertiary illnesses. Each test attempts to consolidate each individual comorbid condition into a single, predictive variable that measures mortality or other outcomes. Researchers have validated such tests because of their predictive value, but no one test is as yet recognized as a standard.

Charlson Comorbidity Index (CCI)

The Charlson Comorbidity Index predicts the mortality for a patient who may have a range of comorbid conditions, such as heart disease, AIDS, or cancer (a total of 17 conditions). Each condition is assigned a score of 1, 2, 3, or 6, depending on the risk of dying associated with each one. Scores are summed to provide a total score to predict mortality. Many variations of the Charlson comorbidity index have been presented, including the Charlson/Deyo, Charlson/Romano, Charlson/Manitoba, and Charlson/D'Hoores comorbidity indices.

For a physician, this score is helpful in deciding how aggressively to treat a condition. For example, a patient may have cancer with comorbid heart disease and diabetes. These comorbidities may be so severe that the costs and risks of cancer treatment would outweigh its short-term benefit.

Since patients often do not know how severe their conditions are, nurses were originally supposed to review a patient's chart and determine whether a particular condition was present in order to calculate the index. Subsequent studies have adapted the comorbidity index into a questionnaire for patients.

The Charlson index, especially the Charlson/Deyo, followed by the Elixhauser have been most commonly referred by the comparative studies of comorbidity and multimorbidity measures.

Comorbidity–Polypharmacy Score (CPS)

The comorbidity–polypharmacy score (CPS) is a simple measure that consists of the sum of all known comorbid conditions and all associated medications. There is no specific matching between comorbid conditions and corresponding medications. Instead, the number of medications is assumed to be a reflection of the "intensity" of the associated comorbid conditions. This score has been tested and validated extensively in the trauma population, demonstrating good correlation with mortality, morbidity, triage, and hospital readmissions. Of interest, increasing levels of CPS were associated with significantly lower 90-day survival in the original study of the score in trauma population.

Elixhauser Comorbidity Index

The Elixhauser comorbidity measure was developed using administrative data from a statewide California inpatient database from all non-federal inpatient community hospital stays in California (n = 1,779,167). The Elixhauser comorbidity measure developed a list of 30 comorbidities relying on the ICD-9-CM coding manual. The comorbidities were not simplified as an index because each comorbidity affected outcomes (length of hospital stay, hospital changes, and mortality) differently among different patients groups. The comorbidities identified by the Elixhauser comorbidity measure are significantly associated with in-hospital mortality and include both acute and chronic conditions. van Walraven et al. have derived and validated an Elixhauser comorbidity index that summarizes disease burden and can discriminate for in-hospital mortality. In addition, a systematic review and comparative analysis shows that among various comorbidities indices, Elixhauser index is a better predictor of the risk especially beyond 30 days of hospitalization.

Diagnosis-related group

Patients who are more seriously ill tend to require more hospital resources than patients who are less seriously ill, even though they are admitted to the hospital for the same reason. Recognizing this, the diagnosis-related group (DRG) manually splits certain DRGs based on the presence of secondary diagnoses for specific complications or comorbidities (CC). The same applies to Healthcare Resource Groups (HRGs) in the UK.

Clinical example of evaluation

Patient S., 73 years, called an ambulance because of a sudden pressing pain in the chest. It was known from the case history that the patient had CHD for many years. Such chest pains were experienced by her earlier as well, but they always disappeared after a few minutes of sublingual administration of organic nitrates. This time taking three tablets of nitroglycerine did not kill the pain. It was also known from the case history that the patient had twice had myocardial infarctions during the last ten years, as well as had an Acute Cerebrovascular Event with sinistral hemiplegia more than 15 years ago. Apart from that the patient had hypertension, type 2 diabetes with diabetic nephropathy, hysteromyoma, cholelithiasis, osteoporosis and varicose pedi-vein disease. It was also learned that the patient regularly takes a number of antihypertensive drugs, urinatives and oral antihyperglycemic remedies, as well as statins, antiplatelet and nootropics. In the past the patient had undergone cholecystectomy due to cholelithiasis more than 20 years ago, as well as the extraction of a cataract of the right eye 4 years ago. The patient was admitted to cardiac intensive care unit at a general hospital diagnosed for acute transmural myocardial infarction. During the check-up moderate azotemia, mild erythronormoblastic anemia, proteinuria and lowering of left vascular ejection fraction were also identified.

Methods of evaluation

There are currently several generally accepted methods of evaluating (measuring) comorbidity:

  1. Cumulative Illness Rating Scale (CIRS): Developed in 1968 by B. S. Linn, it became a revolutionary discovery, because it gave the practicing doctors a chance to calculate the number and severity of chronic illnesses in the structure of the comorbid state of their patients. The proper use of CIRS means separate cumulative evaluation of each of the biological systems: "0" The selected system corresponds to the absence of disorders, "1": Slight (mild) abnormalities or previously had disorders, "2": Illness requiring the prescription of medicinal therapy, "3": Disease, which caused disability and "4": Acute organ insufficiency requiring emergency therapy. The CIRS system evaluates comorbidity in cumulative score, which can be from 0 to 56. As per its developers, the maximum score is not compatible with the patient's life.
  2. Cumulative Illness Rating Scale for Geriatrics (CIRS-G): This system is similar to CIRS, but for aged patients, offered by M. D. Miller in 1991. This system takes into account the age of the patient and the peculiarities of the old age disorders.
  3. The Kaplan–Feinstein Index: This index was created in 1973 based on the study of the effect of the associated diseases on patients with type 2 diabetes during a period of 5 years. In this system of comorbidity evaluation all the present (in a patient) diseases and their complications, depending on the level of their damaging effect on body organs, are classified as mild, moderate and severe. In this case the conclusion about cumulative comorbidity is drawn on the basis of the most decompensated biological system. This index gives cumulative, but less detailed as compared to CIRS, assessment of the condition of each of the biological systems: "0": Absence of disease, "1": Mild course of the disease, "2": Moderate disease, "3": Severe disease. The Kaplan–Feinstein Index evaluates comorbidity by cumulative score, which can vary from 0 to 36. Apart from that the notable deficiency of this method of evaluating comorbidity is the excessive generalization of diseases (nosologies) and the absence of a large number of illnesses in the scale, which, probably, should be noted in the "miscellaneous" column, which undermines (decreases) this method's objectivity and productivity of this method. However the indisputable advantage of the Kaplan–Feinstein Index as compared to CIRS is in the capability of independent analysis of malignant neoplasms and their severities. Using this method patient S's, age 73, comorbidity can be evaluated as of moderate severity (16 out of 36 points), however its prognostic value is unclear, because of the absence of the interpretation of the overall score, resulting from the accumulation of the patient's diseases.
  4. Charlson Index: This index is meant for the long-term prognosis of comorbid patients and was developed by M. E. Charlson in 1987. This index is based on a point scoring system (from 0 to 40) for the presence of specific associated diseases and is used for prognosis of lethality. For its calculation the points are accumulated, according to associated diseases, as well as the addition of a single point for each 10 years of age for patients of ages above forty years (in 50 years 1 point, 60 years 2 points etc.). The distinguishing feature and undisputed advantage of the Charlson Index is the capability of evaluating the patient's age and determination of the patient's mortality rate, which in the absence of comorbidity is 12%, at 1–2 points it is 26%; at 3–4 points it is 52% and with the accumulation of more than 5 points it is 85%. Regretfully this method has some deficiencies: Evaluating comorbidity severity of many diseases is not considered, as well as the absence of many important for prognosis disorders. Apart from that it is doubtful that possible prognosis for a patient with bronchial asthma and chronic leukemia is comparable to the prognosis for the patient ailing from myocardial infarction and cerebral infarction. In this case comorbidity of patient S, 73 years of age according to this method, is equivalent to mild state (9 out of 40 points).
  5. Modified Charlson Index: R. A. Deyo, D. C. Cherkin, and Marcia Ciol added chronic forms of ischemic cardiac disorder and the stages of chronic cardiac insufficiency to this index in 1992.
  6. Elixhauser Index: The Elixhauser comorbidity measure include 30 comorbidities, which are not simplified as an index. Elixhauser shows a better predictive performance for mortality risk especially beyond 30 days of hospitalization.
  7. Index of Co-Existent Disease (ICED): This Index was first developed in 1993 by S. Greenfield to evaluate comorbidity in patients with malignant neoplasms, later it also became useful for other categories of patients. This method helps in calculating the duration of a patient's stay at a hospital and the risks of repeated admittance of the same at a hospital after going through surgical procedures. For the evaluation of comorbidity the ICED index suggests to evaluate the patient's condition separately as per two different components: Physiological functional characteristics. The first component comprises 19 associated disorders, each of which is assessed on a 4-point scale, where "0" indicates the absence of disease and "3" indicates the disease's severe form. The second component evaluates the effect of associated diseases on the physical condition of the patient. It assesses 11 physical functions using a 3-point scale, where "0" means normal functionality and "2" means the impossibility of functionality.
  8. Geriatric Index of Comorbidity (GIC): Developed in 2002
  9. Functional Comorbidity Index (FCI): Developed in 2005.
  10. Total Illness Burden Index (TIBI): Developed in 2007.

Analyzing the comorbid state of patient S, 73 years of age, using the most used international comorbidity assessment scales, a doctor would come across totally different evaluation. The uncertainty of these results would somewhat complicate the doctors judgment about the factual level of severity of the patient's condition and would complicate the process of prescribing rational medicinal therapy for the identified disorders. Such problems are faced by doctors on everyday basis, despite all their knowledge about medical science. The main hurdle in the way of inducting comorbidity evaluation systems in broad based diagnostic-therapeutic process is their inconsistency and narrow focus. Despite the variety of methods of evaluation of comorbidity, the absence of a singular generally accepted method, devoid of the deficiencies of the available methods of its evaluation, causes disturbance. The absence of a unified instrument, developed on the basis of colossal international experience, as well as the methodology of its use does not allow comorbidity to become doctor "friendly". At the same time due to the inconsistency in approach to the analysis of comorbid state and absence of components of comorbidity in medical university courses, the practitioner is unclear about its prognostic effect, which makes the generally available systems of associated pathology evaluation unreasoned and therefore un-needed as well.

Treatment of comorbid patient

The effect of comorbid pathologies on clinical implications, diagnosis, prognosis and therapy of many diseases is polyhedral and patient-specific. The interrelation of the disease, age and drug pathomorphism greatly affect the clinical presentation and progress of the primary nosology, character and severity of the complications, worsens the patient's life quality and limit or make difficult the remedial-diagnostic process. Comorbidity affects life prognosis and increases the chances of fatality. The presence of comorbid disorders increases bed days, disability, hinders rehabilitation, increases the number of complications after surgical procedures, and increases the chances of decline in aged people.

The presence of comorbidity must be taken into account when selecting the algorithm of diagnosis and treatment plans for any given disease. It is important to enquire comorbid patients about the level of functional disorders and anatomic status of all the identified nosological forms (diseases). Whenever a new, as well as mildly notable symptom appears, it is necessary to conduct a deep examination to uncover its causes. It is also necessary to be remembered that comorbidity leads to polypragmasy (polypharmacy), i.e. simultaneous prescription of a large number of medicines, which renders impossible the control over the effectiveness of the therapy, increases monetary expenses and therefore reduces compliance. At the same time, polypragmasy, especially in aged patients, renders possible the sudden development of local and systematic, unwanted medicinal side-effects. These side-effects are not always considered by the doctors, because they are considered as the appearance of comorbidity and as a result become the reason for the prescription of even more drugs, sealing-in the vicious circle. Simultaneous treatment of multiple disorders requires strict consideration of compatibility of drugs and detailed adherence of rules of rational drug therapy, based on E. M. Tareev's principles, which state: "Each non-indicated drug is contraindicated" and B. E. Votchal said: "If the drug does not have any side-effects, one must think if there is any effect at all".

A study of inpatient hospital data in the United States in 2011 showed that the presence of a major complication or comorbidity was associated with a great risk of intensive-care unit utilization, ranging from a negligible change for acute myocardial infarction with major complication or comorbidity to nearly nine times more likely for a major joint replacement with major complication or comorbidity.

Drug interaction

From Wikipedia, the free encyclopedia
Grapefruit juice can act as an enzyme inhibitor, affecting the metabolism of drugs.

In pharmaceutical sciences, drug interactions occur when a drug's mechanism of action is affected by the concomitant administration of substances such as foods, beverages, or other drugs. A popular example of drug-food interaction is the effect of grapefruit in the metabolism of drugs.

Interactions may occur by simultaneous targeting of receptors, directly or indirectly. For example, both Zolpidem and alcohol affect GABAA receptors, and their simultaneous consumption results in the overstimulation of the receptor, which can lead to loss of consciousness. When two drugs affect each other, it receives the name of a drug-drug interaction. The risk of a drug-drug interaction (DDI) increases with the number of drugs used.

A large share of elderly people regularly use five or more medications or supplements, with a significant sharte risk of side-effects from drug-drug interactions.

Drug interactions can be of three kinds:

  • additive (the result is what you expect when you add together the effect of each drug taken independently),
  • synergistic (combining the drugs leads to a larger effect than expected), or
  • antagonistic (combining the drugs leads to a smaller effect than expected).

It may be difficult to distinguish between synergistic or additive interactions, as individual effects of drugs may vary.

Direct interactions between drugs are also possible and may occur when two drugs are mixed before intravenous injection. For example, mixing thiopentone and suxamethonium can lead to the precipitation of thiopentone.

Interactions based on pharmacodynamics

Pharmacodynamic interactions are the drug-drug interactions that occur at a biochemical level and depend mainly on the biological processes of organisms. These interactions occur due to action on the same targets, for example the same receptor or signaling pathway.

Effects of the competitive inhibition of an agonist by increases in the concentration of an antagonist. A drug's potency can be affected (the response curve shifted to the right) by the presence of an antagonistic interaction.

Pharmacodynamic interactions can occur on protein receptors. Two drugs can be considered to be Homodynamic, if they act on the same receptor. Homodynamic effects include drugs that act as (1) pure agonists, if they bind to the main locus of the receptor, causing a similar effect to that of the main drug, (2) partial agonists if, on binding to a secondary site, they have the same effect as the main drug, but with a lower intensity and (3) antagonists, if they bind directly to the receptor's main locus but their effect is opposite to that of the main drug. These may be competitive antagonists, if they compete with the main drug to bind with the receptor. or uncompetitive antagonists, when the antagonist binds to the receptor irreversibly. The drugs can be considered Heterodynamic competitors, if they act on distinct receptor with similar downstream pathways.

The interaction my also occur via signal transduction mechanisms. For example, low blood glucose leads to a release of catecholamines, triggering symptoms that hint the organism to take action, including the eating sugar. If a patient is on insulin, which reduces blood sugar, and also beta-blockers, the body is less able to cope with an insulin overdose.

Interactions based on pharmacokinetics

Pharmacokinetics is the field of research studying the chemical and biochemical factors that directly affect dosage and the half-life of drugs in an organism, including absorption, transport, distribution, metabolism and excretion. Compounds may affect any of those process, ultimately interfering with the flux of drugs in the human body, increasing or reducing drug availability.

Based on absorption

Drugs that change intestinal motility may impact the level of other drugs taken. For example, prokinetic agents increase the intestinal motility, which may cause drugs to go through the digestive system too fast, reducing absorption.

The pharmacological modification of pH can also affect other compounds. Drugs can be present in ionized or non-ionized forms depending on pKa, and neutral compounds are usually better absorbed by membranes. Medication like antacids can increase pH and inhibit the absorption of other drugs such as zalcitabine, tipranavir and amprenavir. The opposite is more common, with, for example, the antacid cimetidine stimulating the absorption of didanosine. Some resources describe that a gap of two to four hours between taking the two drugs is needed to avoid the interaction.

Factors such as food with high-fat content may also alter the solubility of drugs and impact its absorption. This is the case for oral anticoagulants and avocado. The formation of non-absorbable complexes may occur also via chelation, when cations can make certain drugs harder to absorb, for example between tetracycline or the fluoroquinolones and dairy products, due to the presence of calcium ions. Other drugs Binding with proteins. Some drugs such as sucralfate binds to proteins, especially if they have a high bioavailability. For this reason its administration is contraindicated in enteral feeding.

Some drugs also alter absorption by acting on the P-glycoprotein of the enterocytes. This appears to be one of the mechanisms by which grapefruit juice increases the bioavailability of various drugs beyond its inhibitory activity on first pass metabolism.

Based on transport and distribution

Drugs also may affect each other by competing for transport proteins in plasma, such as albumin. In these cases the drug that arrives first binds with the plasma protein, leaving the other drug dissolved in the plasma, modifying its expected concentration. The organism has mechanisms to counteract these situations (by, for example, increasing plasma clearance), and thus they are not usually clinically relevant. They may become relevant if other problems are present, such as issues with drug excretion.

Based on metabolism

Diagram of cytochrome P450 isoenzyme 2C9 with the haem group in the centre of the enzyme.

Many drug interactions are due to alterations in drug metabolism. Further, human drug-metabolizing enzymes are typically activated through the engagement of nuclear receptors. One notable system involved in metabolic drug interactions is the enzyme system comprising the cytochrome P450 oxidases.

CYP450

Cytochrome P450 is a very large family of haemoproteins (hemoproteins) that are characterized by their enzymatic activity and their role in the metabolism of a large number of drugs. Of the various families that are present in humans, the most interesting in this respect are the 1, 2 and 3, and the most important enzymes are CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4. The majority of the enzymes are also involved in the metabolism of endogenous substances, such as steroids or sex hormones, which is also important should there be interference with these substances. The function of the enzymes can either be stimulated (enzyme induction) or inhibited (enzyme inhibition).

Through enzymatic inhibition and induction

If a drug is metabolized by a CYP450 enzyme and drug B blocks the activity of these enzymes, it can lead to pharmacokinetic alterations. A. This alteration results in drug A remaining in the bloodstream for an extended duration, and eventually increase in concentration.

In some instances, the inhibition may reduce the therapeutic effect, if instead the metabolites of the drug is responsible for the effect.

Compounds that increase the efficiency of the enzymes, on the other hand, may have the opposite effect and increase the rate of metabolism.

Examples of metabolism-based interactions

An example of this is shown in the following table for the CYP1A2 enzyme, showing the substrates (drugs metabolized by this enzyme) and some inductors and inhibitors of its activity:

Drugs related to CYP1A2
Substrates Inhibitors Inductors

Some foods also act as inductors or inhibitors of enzymatic activity. The following table shows the most common:

Foods and their influence on drug metabolism
Food Mechanism Drugs affected
Enzymatic inductor Acenocoumarol, warfarin
Grapefruit juice Enzymatic inhibition
Soya Enzymatic inhibition Clozapine, haloperidol, olanzapine, caffeine, NSAIDs, phenytoin, zafirlukast, warfarin
Garlic Increases antiplatelet activity
Ginseng To be determined Warfarin, heparin, aspirin and NSAIDs
Ginkgo biloba Strong inhibitor of platelet aggregation factor Warfarin, aspirin and NSAIDs
Hypericum perforatum (St John's wort) Enzymatic inductor (CYP450) Warfarin, digoxin, theophylline, cyclosporine, phenytoin and antiretrovirals
Ephedra Receptor level agonist MAOI, central nervous system stimulants, alkaloids ergotamines and xanthines
Kava (Piper methysticum) Unknown Levodopa
Ginger Inhibits thromboxane synthetase (in vitro) Anticoagulants
Chamomile Unknown Benzodiazepines, barbiturates and opioids
Hawthorn Unknown Beta-adrenergic antagonists, cisapride, digoxin, quinidine

Based on excretion

Renal and biliary excretion

Drugs tightly bound to proteins (i.e. not in the free fraction) are not available for renal excretion. Filtration depends on a number of factors including the pH of the urine. Drug interactions may affect those points.

With herbal medicines

Herb-drug interactions are drug interactions that occur between herbal medicines and conventional drugs. These types of interactions may be more common than drug-drug interactions because herbal medicines often contain multiple pharmacologically active ingredients, while conventional drugs typically contain only one. Some such interactions are clinically significant, although most herbal remedies are not associated with drug interactions causing serious consequences. Most catalogued herb-drug interactions are moderate in severity. The most commonly implicated conventional drugs in herb-drug interactions are warfarin, insulin, aspirin, digoxin, and ticlopidine, due to their narrow therapeutic indices. The most commonly implicated herbs involved in such interactions are those containing St. John’s Wort, magnesium, calcium, iron, or ginkgo.

Examples

Examples of herb-drug interactions include, but are not limited to:

Mechanisms

The mechanisms underlying most herb-drug interactions are not fully understood. Interactions between herbal medicines and anticancer drugs typically involve enzymes that metabolize cytochrome P450. For example, St. John's Wort has been shown to induce CYP3A4 and P-glycoprotein in vitro and in vivo.

Underlying factors

The factors or conditions that predispose the appearance of interactions include factors Old age: factors relating to how human physiology changes with age may affect the interaction of drugs. For example, liver metabolism, kidney function, nerve transmission, or the functioning of bone marrow all decrease with age. In addition, in old age, there is a sensory decrease that increases the chances of errors being made in the administration of drugs. The elderly are also more vulnerable to polypharmacy, and the more drugs a patient takes, higher is the chance of an interaction.

Genetic factors may also affect the enzymes and receptors, thus altering the possibilities of interactions.

Parients with hepatic or renal diseases already may have difficulties metabolizing and excreding drugs, what may exacerbate the effect of interactions.

Some drugs present an intrinsic increased risk for a harmful interaction, including drugs with a narrow therapeutic index, where the difference between the effective dose and the toxic dose is small. The drug digoxin is an example of this type of drug.

Risks are also increased when the drug presents a steep dose-response curve, and small changes in the dosage produce large changes in the drug's concentration in the blood plasma.

Epidemiology

As of 2008, among adults in the United States of America older than 56, 4% were taking medication and or supplements that put them at risk of a major drug interaction. Potential drug-drug interactions have increased over time and are more common in the less-educated elderly even after controlling for age, sex, place of residence, and comorbidity.

Just-so story

From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Just-so_story

In science and philosophy, a just-so story is an untestable narrative explanation for a cultural practice, a biological trait, or behavior of humans or other animals. The pejorative nature of the expression is an implicit criticism that reminds the listener of the fictional and unprovable nature of such an explanation. Such tales are common in folklore genres like mythology (where they are known as etiological myths – see etiology). A less pejorative term is a pourquoi story, which has been used to describe usually more mythological or otherwise traditional examples of this genre, aimed at children.

This phrase is a reference to Rudyard Kipling's 1902 Just So Stories, containing fictional and deliberately fanciful tales for children, in which the stories pretend to explain animal characteristics, such as the origin of the spots on the leopard. It has been used to criticize evolutionary explanations of traits that have been proposed to be adaptations, particularly in the evolution–creation debates and in debates regarding research methods in sociobiology and evolutionary psychology.

However, the first widely acknowledged use of the phrase in the modern and pejorative sense seems to have originated in 1978 with Stephen Jay Gould, a prominent paleontologist and popular science writer. Gould expressed deep skepticism as to whether evolutionary psychology could ever provide objective explanations for human behavior, even in principle; additionally, even if it were possible to do so, Gould did not think that it could be proven in a properly scientific way.

Critique

Academics such as David Barash say that the term just-so story, when applied to a proposed evolutionary adaptation, is simply a derogatory term for a hypothesis. Hypotheses, by definition, require further empirical assessment, and are a part of normal science. Similarly, Robert Kurzban suggested that "The goal should not be to expel stories from science, but rather to identify the stories that are also good explanations." In his book The Triumph of Sociobiology, John Alcock suggested that the term just-so story as applied to proposed evolved adaptations is "one of the most successful derogatory labels ever invented". In a response to Gould's criticism, John Tooby and Leda Cosmides argued that the "just-so" accusation is unsubstantiated as it claims evolutionary psychologists are only interested in facts already known, when in reality evolutionary psychology is interested in what can be predicted from already known information as a means of pursuing unknown avenues of research. Thus evolutionary psychology has predictive utility, meaning it is not composed of just-so stories. Steve Stewart-Williams argues that all scientific hypotheses are just-so stories prior to being tested, yet the accusation is seldom levelled at other fields. Stewart-Williams also agrees with the idea that evolutionary explanations can potentially be made up for almost anything, but argues the same could be said of competing approaches, such as sociocultural explanations, so in the view of Stewart-Williams this is not a useful criticism. In 2001 interview, Leda Cosmides argued:

There is nothing wrong with explaining facts that are already known: no one faults a physicist for explaining why stars shine or apples fall toward earth. But evolutionary psychology would not be very useful if it were only capable of providing explanations after the fact, because almost nothing about the mind is known or understood: there are few facts, at the moment, to be explained! The strength of an evolutionary approach is that it can aid discovery: it allows you to generate predictions about what programs the mind might contain, so that you can conduct experiments to see if they in fact exist.....[W]hat about evolutionary explanations of phenomena that are already known? Those who have a professional knowledge of evolutionary biology know that it is not possible to cook up after the fact explanations of just any trait. There are important constraints on evolutionary explanation. More to the point, every decent evolutionary explanation has testable predictions about the design of the trait. For example, the hypothesis that pregnancy sickness is a byproduct of prenatal hormones predicts different patterns of food aversions than the hypothesis that it is an adaptation that evolved to protect the fetus from pathogens and plant toxins in food at the point in embryogenesis when the fetus is most vulnerable – during the first trimester. Evolutionary hypotheses – whether generated to discover a new trait or to explain one that is already known – carry predictions about the design of that trait. The alternative – having no hypothesis about adaptive function – carries no predictions whatsoever. So which is the more constrained and sober scientific approach?

Al-Shawaf et al. argue that many evolutionary psychology hypotheses are formed in a "top-down" approach; a theory is used to generate a hypothesis and predictions are then made from this hypothesis. This method makes it generally impossible to engage in just-so storytelling because the hypothesis and predictions are made a priori, based on the theory. By contrast, the "bottom-up" approach, whereby an observation is made and a hypothesis is generated to explain the observation, could potentially be a form of just-so storytelling if no novel predictions were developed from the hypothesis. Provided novel, testable predictions are made from the hypothesis, then it cannot be argued that the hypothesis is a just-so story. Al-Shawaf et al. argue that the just-so accusation is a result of the fact that, like other evolutionary sciences, evolutionary psychology is partially a historical discipline. However, the authors argue that if this made evolutionary psychology nothing but just-so storytelling, then other partially historical scientific disciplines such as astrophysics, geology or cosmology would also be just-so storytelling. What makes any scientific discipline, not just partially historical ones, valid is their ability to make testable novel predictions in the present day. Evolutionary psychologists do not need to travel back in time to test their hypotheses, as their hypotheses yield predictions about what we would expect to see in the modern world.

Lisa DeBruine argues that evolutionary psychology can generate testable, novel predictions. She gives an example of evolved navigation theory, which hypothesised that people would overestimate vertical distances relative to horizontal ones and that vertical distances are overestimated more from the top than from the bottom, due to the risks of falling from a greater height leading to a greater chance of injury or death encouraging people to be more cautious when assessing the risks of vertical distances. The predictions of the theory were confirmed and the facts were previously unknown until evolved navigation theory tested them, demonstrating that evolutionary psychology can make novel predictions of previously unknown facts.

Berry et al. argue that critics of adaptationist "just so stories" are often guilty of creating "just not so stories", uncritically accepting any alternative explanation provided it is not the adaptationist one. Furthermore, the authors argue that Gould's use of the term "adaptive function" is overly restrictive, as they insist it must refer to the original adaptive function the trait evolved for. According to the authors, this is a nonsensical requirement, because if an adaptation was then used for a new, different, adaptive function, then this makes the trait an adaptation because it remains in the population because it helps organisms with this new function. Thus the trait's original purpose is irrelevant because it has been co-opted for a new purpose and maintains itself within the species because it increases reproductive success of members of the species who have it (versus those who may have lost it for some reason); nature is blind to the original "intended" function of the trait.

David Buss argued that while Gould's "just-so story" criticism is that the data that an evolutionary psychology adaptationist hypothesis explains could be equally explained by different hypotheses (such as exaptationist or co-opted spandrel hypotheses), Gould failed to meet the relevant evidentiary burdens with regards to these alternative hypotheses. According to Buss, co-opted exaptationist and spandrel hypotheses have an additional evidentiary burden compared to adaptationist hypotheses, as they must identify both the later co-opted functionality and the original adaptational functionality, while proposals that something is a co-opted byproduct must identify what the trait was a byproduct of and what caused it to be co-opted; it is not sufficient simply to propose an alternative exaptationist, functionless byproduct or spandrel hypotheses to the adaptationist one, rather these evidentiary burdens must be met. Buss argues that Gould's failure to do this meant that his assertion that apparent adaptations were actually exaptations was itself nothing more than a just-so story.

Alternatives in evolutionary developmental biology

How the Snake Lost Its Legs: Curious Tales from the Frontier of Evo-Devo is a 2014 book on evolutionary developmental biology by Lewis I. Held, Jr. The title pays a “factual homage to Rudyard Kipling's fanciful Just So Stories."

Politics of Europe

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