Genuine progress indicator

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Genuine progress indicator (GPI) is a metric that has been suggested to replace, or supplement, gross domestic product (GDP). The GPI is designed to take fuller account of the well-being of a nation, only a part of which pertains to the size of the nation's economy, by incorporating environmental and social factors which are not measured by GDP. For instance, some models of GPI decrease in value when the poverty rate increases. The GPI separates the concept of societal progress from economic growth.

The GPI is used in ecological economics, "green" economics, sustainability and more inclusive types of economics. It factors in environmental and carbon footprints that businesses produce or eliminate, including in the forms of resource depletion, pollution and long-term environmental damage. GDP is increased twice when pollution is created, since it increases once upon creation (as a side-effect of some valuable process) and again when the pollution is cleaned up; in contrast, GPI counts the initial pollution as a loss rather than a gain, generally equal to the amount it will cost to clean up later plus the cost of any negative impact the pollution will have in the mean time. While quantifying costs and benefits of these environmental and social externalities is a difficult task, "Earthster-type databases could bring more precision and currency to GPI's metrics." It has been noted that such data may also be embraced by those who attempt to "internalize externalities" by making companies pay the costs of the pollution they create (rather than having the government or society at large bear those costs) "by taxing their goods proportionally to their negative ecological and social impacts".

GPI is an attempt to measure whether the environmental impact and social costs of economic production and consumption in a country are negative or positive factors in overall health and well-being. By accounting for the costs borne by the society as a whole to repair or control pollution and poverty, GPI balances GDP spending against external costs. GPI advocates claim that it can more reliably measure economic progress, as it distinguishes between the overall "shift in the 'value basis' of a product, adding its ecological impacts into the equation". Comparatively speaking, the relationship between GDP and GPI is analogous to the relationship between the gross profit of a company and the net profit; the net profit is the gross profit minus the costs incurred, while the GPI is the GDP (value of all goods and services produced) minus the environmental and social costs. Accordingly, the GPI will be zero if the financial costs of poverty and pollution equal the financial gains in production of goods and services, all other factors being constant.

Motivation

Most economists assess progress in people's welfare by comparing the gross domestic product over time—that is, by adding up the annual dollar value of all goods and services produced within a country over successive years. However, GDP was not intended to be used for such purpose. It is prone to productivism or consumerism, over-valuing production and consumption of goods, and not reflecting improvement in human well-being. It also does not distinguish between money spent for new production and money spent to repair negative outcomes from previous expenditure. For example, it would treat as equivalent one million dollars spent to build new homes and one million dollars spent in aid relief to those whose homes have been destroyed, despite these expenditures arguably not representing the same kind of progress. This is relevant for example when considering the true costs of development that destroys wetlands and hence exacerbate flood damages. Simon Kuznets, the inventor of the concept of GDP, noted in his first report to the US Congress in 1934:

the welfare of a nation can scarcely be inferred from a measure of national income. If the GDP is up, why is America down? Distinctions must be kept in mind between quantity and quality of growth, between costs and returns, and between the short and long run. Goals for more growth should specify more growth of what and for what.

Some have argued that an adequate measure must also take into account ecological yield and the ability of nature to provide services, and that these things are part of a more inclusive ideal of progress, which transcends the traditional focus on raw industrial production.

Theoretical foundation

The need for a GPI to supplement biased indicators such as GDP was highlighted by analyses of uneconomic growth in the 1980s, notably that of Marilyn Waring, who studied biases in the UN System of National Accounts.

By the early 1990s, there was a consensus in human development theory and ecological economics that growth in money supply was actually reflective of a loss of well-being: that lacks of essential natural and social services were being paid for in cash and that this was expanding the economy but degrading life.

The matter remains controversial and is a main issue between advocates of green economics and neoclassical economics. Neoclassical economists understand the limitations of GDP for measuring human well-being but nevertheless regard GDP as an important, though imperfect, measure of economic output and would be wary of too close an identification of GDP growth with aggregate human welfare. However, GDP tends to be reported as synonymous with economic progress by journalists and politicians, and the GPI seeks to correct this shorthand by providing a more encompassing measure.

Some economists, notably Herman Daly, John B. Cobb and Philip Lawn, have asserted that a country's growth, increased goods production, and expanding services have both "costs" and "benefits"—not just the "benefits" that contribute to GDP. They assert that, in some situations, expanded production facilities damage the health, culture, and welfare of people. Growth that was in excess of sustainable norms (e.g., of ecological yield) had to be considered to be uneconomic. According to the "threshold hypothesis", developed by Manfred Max-Neef, "when macroeconomic systems expand beyond a certain size, the additional benefits of growth are exceeded by the attendant costs" (Max-Neef 1995). This hypothesis is borne out in data comparing GDP/capita with GPI/capita from 17 countries. The graph demonstrates that, while GDP does increase overall well-being to a point, beyond $7,000 GDP/capita the increase in GPI is reduced or remains stagnant.^[5] Similar trends can be seen when comparing GDP to life satisfaction as well as in a Gallup Poll published in 2008.

According to Lawn's model, the "costs" of economic activity include the following potential harmful effects:

• Cost of resource depletion
• Cost of crime
• Cost of ozone depletion
• Cost of family breakdown
• Cost of air, water, and noise pollution
• Loss of farmland
• Loss of wetlands

Analysis by Robert Costanza also around 1995 of nature's services and their value showed that a great deal of degradation of nature's ability to clear waste, prevent erosion, pollinate crops, etc., was being done in the name of monetary profit opportunity: this was adding to GDP but causing a great deal of long term risk in the form of mudslides, reduced yields, lost species, water pollution, etc. Such effects have been very marked in areas that suffered serious deforestation, notably Haiti, Indonesia, and some coastal mangrove regions of India and South America. Some of the worst land abuses for instance have been shrimp farming operations that destroyed mangroves, evicted families, left coastal lands salted and useless for agriculture, but generated a significant cash profit for those who were able to control the export market in shrimp. This has become a signal example to those who contest the idea that GDP growth is necessarily desirable.

GPI systems generally try to take account of these problems by incorporating sustainability: whether a country's economic activity over a year has left the country with a better or worse future possibility of repeating at least the same level of economic activity in the long run. For example, agricultural activity that uses replenishing water resources, such as river runoff, would score a higher GPI than the same level of agricultural activity that drastically lowers the water table by pumping irrigation water from wells.

"Income" vs. "capital depletion"

Hicks (1946) pointed out that the practical purpose of calculating income is to indicate the maximum amount that people can produce and consume without undermining their capacity to produce and consume the same amount in the future. From a national income perspective, it is necessary to answer the following question: "Can a nation's entire GDP be consumed without undermining its ability to produce and consume the same GDP in the future?" This question is largely ignored in contemporary economics but fits under the idea of sustainability.

In legislative decisions

The best-known attempts to apply the concepts of GPI to legislative decisions are probably the Atlantic indicator invented by Ronald Colman for Atlantic Canada, the Alberta GPI created by ecological economist Mark Anielski to measure the long-term economic, social and environmental sustainability of the province of Alberta and the "environmental and sustainable development indicators" used by the Government of Canada to measure its own progress to achieving well-being goals: its Environment and Sustainable Development Indicators Initiative (Canada) is an effort to justify state services in GPI terms. It assigns the Commissioner for the Environment and Sustainable Development (Canada), an officer in the Auditor-General of Canada's office, to perform the analysis and report to the House of Commons. However, Canada continues to state its overall budgetary targets in terms of reducing its debt to GDP ratio, which implies that GDP increase and debt reduction in some combination are its main priorities.

In the European Union (EU) the Metropole efforts and the London Health Observatory methods are equivalents focused mostly on urban lifestyle.

The EU and Canadian efforts are among the most advanced in any of the G8 or OECD nations, but there are parallel efforts to measure quality of life or standard of living in health (not strictly wealth) terms in all developed nations. This has also been a recent focus of the labour movement.

Calculation

The calculation of GPI presented in the simplified form is the following:

• GPI = A + B - C - D + I
• A is income weighted private consumption
• B is value of non-market services generating welfare
• C is private defensive cost of natural deterioration
• D is cost of deterioration of nature and natural resources
• I is increase in capital stock and balance of international trade

The GPI indicator is based on the concept of sustainable income, presented by economist John Hicks (1948). The sustainable income is the amount a person or an economy can consume during one period without decreasing his or her consumption during the next period. In the same manner, GPI depicts the state of welfare in the society by taking into account the ability to maintain welfare on at least the same level in the future.

Components

The Genuine Progress Indicator is measured by 26 indicators which can be divided into three main categories: Economic, Environmental, and Social. Some regions, nations, or states may adjust the verbiage slightly to accommodate their particular scenario. For example, the GPI template uses the phrase "Carbon Dioxide Emissions Damage" whereas the state of Maryland uses "Cost of Climate Change" because it also accounts for other greenhouse gases (GHG) such as methane and nitrous oxide.

Development in the United States

Non-profit organizations and universities have measured the GPI of Vermont, Maryland, Colorado, Ohio, and Utah. These efforts have incited government action in some states. As of 2014, Vermont, Maryland, Washington and Hawai'i have passed state government initiatives to consider GPI in budgeting decisions, with a focus on long-term cost and benefits.

In 2009, the state of Maryland formed a coalition of representatives from several state government departments in search of a metric that would factor social well-being into the more traditional gross product indicators of the economy. The metric would help determine the sustainability of growth and economic progress against social and environmental factors typically left out of national indicators. The GPI was chosen as a comprehensive measure of sustainability as it has a well-accepted scientific methodology that can be adopted by other states and compared over time. Maryland's GPI trends are comparable to other states and nations that have measured their GPI in that Gross State Product (GSP) and GPI have diverged over the past four decades where GSP has increased more rapidly than GPI. While economic elements of GPI have increased overall (with a significant drop off during the Great Recession), social well-being has stagnated, with any values added being cancelled out by costs deducted, and environmental indicators, while improving slightly, are always considered costs. Combined, these elements bring the GPI below GSP. However, Maryland's GPI did increase by two points from 2010 to 2011.

The calculation methodology of GPI was first adapted to US data in the late-1990s. Results show that GDP has increased substantially. At the same time, the GPI has stagnated. Thus, according to GPI theory, economic growth in the US, i.e., the growth of GDP, has not increased the welfare of the people during last 30 years. So far, GPI time-series have been calculated for the US and Australia as well as for several of their states. In addition, GPI has been calculated for Austria, Canada, Chile, France, Finland, Italy, the Netherlands, Scotland, and the rest of the UK.

Development in Finland

The GPI time-series 1945 to 2011 for Finland have been calculated by Statistics Finland. The calculation closely followed the US methodology. The results show that in the 1970s and 1980s economic growth, as measured by GDP, clearly increased welfare, measured by the GPI. After the economic recession of the early-1990s the GDP continued to grow, but the GPI stayed on a lower level. This indicates a widening gap between the trends of GDP and GPI that began in the early-1990s. In the 1990s and 2000s the growth of GDP has not benefited the average Finn. If measured by GPI, sustainable economic welfare has actually decreased due to environmental hazards that have accumulated in the environment. The Finnish GPI time series have been updated by Dr Jukka Hoffrén at Statistics Finland.

Development in Finland regions

Within EU's Interreg IV C FRESH Project (Forwarding Regional Environmental Sustainable Hierarchies) GPI time-series were calculated to Päijät-Häme, Kainuu and South-Ostrobotnia (Etelä-Pohjanmaa) regions in 2009-2010. During 2011 these calculations were completed with GPI calculations for the Lappland, Northern Ostrobothnia (Pohjois-Pohjanmaa) and Central-Ostrobothnia (Keski-Pohjanmaa) regions.

Criticism

GDP is held up as a value neutral measure. It is relatively straightforward to measure compared to GPI. Competing measures like GPI define well-being to mean things that the definers ideologically support. Therefore, opponents of GPI claim that GPI cannot function to measure the goals of a diverse, plural society. Supporters of GDP as a measure of societal well-being claim that competing measures such as GPI are more vulnerable to political manipulation.

Finnish economists Mika Maliranta and Niku Määttänen write that the problem of alternative development indexes is their attempt to combine things that are incommensurable. It is hard to say what they exactly indicate and difficult to make decisions based on them. They can be compared to an indicator that shows the mean of a car's velocity and the amount of fuel left.

They add that it indeed seems as if the economy has to grow in order for the people to even remain as happy as they are at present. In Japan, for example, the degree of happiness expressed by the citizens in polls has been declining since the early 1990s, the period when Japan's economic growth stagnated.

Supporting countries and groups

• Canada planning applications. GDP has functioned as an "income sheet". GPI will function as a "balance sheet," taking into consideration that some income sources are very costly and contribute a negative profit overall.
• Beyond GDP is an initiative of the European Union, Club of Rome, WWF and OECD.
• Redefining Progress. Reports and analyses. A non-profit organization with headquarters in Oakland, California.

GPI and GPI-type studies completed

+/-	Indicator	Brief Explanation
Economic	Personal Consumption Expenditures	The bulk of GDP as well, consumption informs the baseline from which the rest of the indicators will be added or subtracted.
÷	Income Inequality	Using the Gini index, published by World Bank, and the Income Distribution Index (IDI), its relative change over time.
(PCE/IDI)*100	Adjusted Personal Consumption	Formula=(Personal consumption/IDI) x 100. Forms the base number from which the remaining indicators are added or subtracted.
-	Cost of Consumer Durables	Calculated as a cost to avoid double counting the value provided by the durables themselves.
+	Value of Consumer Durables	Household appliances, cars, etc. are not used up in one year and are considered a part of household capital. Their value is depreciated over a number of years.
-	Cost of Underemployment	Encompasses the chronically unemployed, discouraged workers, involuntary part-time workers and others with work-life restraints (lack of childcare or transportation).
+/-	Net Capital Investment	Capital investment in foreign markets minus incoming investments from other countries. If lending (+) if borrowing (-).
Environmental
-	Cost of Water Pollution	Damage to water quality from things such as chemicals or nutrients, and the costs of erosion/sedimentation in waterways.
-	Cost of Air Pollution	Includes damage to vegetation, degradation of materials, cost of clean-up from soot or acid rain, and resulting reduced property values, wage differentials and aesthetics.
-	Cost of Noise Pollution	Noise from traffic and factories can cause hearing loss and sleep deprivation.
-	Loss of Wetlands	Valuates the services given up when wetlands are lost to development i.e. buffering of weather, habitat, water purification.
-	Loss of farmland, soil quality or degradation	Due to urbanization, soil erosion and compaction. This indicator is measured cumulatively to account for all years of production lost as it compromises self-sufficient food supply.
-	Loss of Primary Forest and damage from logging roads	Loss of biodiversity, soil quality, water purification, carbon sequestration, recreation etc. Cumulative affect year over year.
-	CO2 Emissions	Increases in severe weather is causing billions in damages. A value of $93USD/metric ton of CO2 emitted is used, based on a meta-analysis study by Richard Tol (2005) of 103 separate studies of costs of economic damages.
-	Cost of Ozone Depletion	Our protective layer in the atmosphere. Depletion can lead to increased cases of cancer, cataracts and plant decline. Weighed at $49,669USD/ton
-	Depletion of Non-Renewables	These cannot be renewed in a lifetime. Depletion is measured against cost of implementing and substituting with renewable resources.
Social
+	Value of Housework and Parenting	Child care, repairs and maintenance are valued equivalent to the amount a household would have to pay for the service.
-	Cost of Family Changes	Social dysfunction presents itself early in family life. Care is taken to avoid double counting goods and services duplicated due to split-parent households.
-	Cost of Crime	Medical expenses, property damages, psychological care and security measures to prevent crime are all included in this indicator.
-	Cost of Household Pollution Abatement	Cost to residents to clean the air and water in their own household i.e. air and water filters.
+	Value of Volunteer Work	Valued as a contribution to social welfare. Neighborhoods and communities can find an informal safety net through their peers and volunteer work.
-	Loss of Leisure Time	Compared to 1969 hours of leisure. Recognizes that increased output of goods and services can lead to loss of valuable leisure time for family, chores or otherwise.
+	Value of Higher Education	Accounts for the contribution resulting knowledge, productivity, civic engagement, savings, and health; a "social spillover," set to $16,000 per year.
+	Value of Highways and Streets	Annual value of services contributed from the use of streets and highways. Valued at 7.5% of net stock of local, state and federal highways.
-	Cost of Commuting	Money spent to pay for the transportation and time lost in transit as opposed to other more enjoyable activities.
-	Cost of Auto Accidents	Damage and loss as a result of traffic accidents. Increased traffic densities are a direct result of industrialization and wealth accumulation.

Indicator name	Region	Beginning year in study	End year in study	Year of publication	Authors
MEW -(A/S)	United States of America	1929	1965	1972	Nordhaus and Tobin
ISEW	United States of America	1951	1986	1989	Daly and Cobb
ISEW	Germany	1950	1990	1994	Diefenbacher
ISEW	Scotland	1980	1991	1994	Moffatt and Wilson
ISEW	Netherlands	1950	1992	1995	Oegema and Rosenberg
ISEW	Netherlands	1950	1992	1995	Rosenberg, Oegema, Bovy
ISEW	Sweden	1950	1992	1996	Jackson and Stymne
ISEW	Austria	1955	1992	1997	Stockhammer et al.
ISEW	UK	1950	1996	1997	Jackson, et al.
ISEW	Austria	1955	1992	1997	Stockhammer, Hochreiter, Obermayr, Steiner
ISEW	Italy	1960	1991	1998	Giogio Guenno, Silvia Tiezzi
ISEW	Chile	1965	1995	1999	Castañeda
GPI	United States of America	1950	1998	1999	Cobb, Goodman, Wackernagel
GPI	Australia	1950	1996	1999	Clive Hamilton
SNBI	Australia	1966	1967	1999	Lawn and Sanders
SNBI	Australia	1994	1995	1999	Lawn and Sanders
ISEW	Scotland	1980	1993	1999	Hanley
GPI	Australia	1950	2000	2000	Hamilton and Dennis
GPI	Minnesota	1960	1995	2000	Minnesota Planning Agency
GPI	Alberta, Canada	1961	1999	2001	Mark Anielski
ISEW	Czech Republic	1988	1998	2002	Scasny
ISEW	Poland	1980	1997	2003	Gil and Sleszynski
ISEW	Wales	1990	2000	2003	Matthews, Williams, Roberts, Munday
GPI	United States of America	1950	2002	2004	Venetoulis and Cobb
GPI	San Francisco Bay Area	2000	2000	2004	Venetoulis and Cobb
GPI	Vermont, Chittenton County, and Burlington	1950	2000	2004	Costanza, Erickson et al.
ISEW	Thailand	1975	1999	2005	Matthew Clarke, Sardar M.N. Islam
GPI	United States of America	1950	2004	2006	John Talberth, Clifford Cobb, and Noah Slattery
ISEW	Siena, Italy	1999	1999	2006	Pulselli, Ciampalini, Tiezzi, Zappia
ISEW	Belgium	1970	2000	2006	Brent Bleys
GPI	Victoria, Australia	1986	2003	2006	Clarke and Lawn
ISEW	Netherlands	1971	2004	2007	Brent Bleys
IBES/ISEW	Puerto Rico	1970	2006	2007	Alameda-Lozada and Diaz-Rodriguez
GPI	China (4 regions)	1991	2001	2007	Zongguo Wen, Kunmin Zhanf, Bin Du, Yadong Li, Wei Li
GPI	Northern Vermont (7 counties)	1950	2000	2007	Bagstad and Ceroni
ISEW	Belgium	1970	2004	2008	Brent Bleys
R-ISEW	England (regions)	1994	2005	2008	Tim Jackson, Nat McBride, Saamah Abdallah and Nic Marks
ISEW	France	1990	2002	2008	Nourry
ISEW	Modena and Rimini, Italy	?	?	2008	Pulselli, F.M., Tiezzi, E., Marchettini, N., Bastiononi, S.
GPI	India	1987	2003	2008	Ed: Philip Lawn and Matthew Clarke (Book)
GPI	Australia	1967	2006	2008	Ed: Philip Lawn and Matthew Clarke (Book)
GPI	New Zealand	1970	2005	2008	Ed: Philip Lawn and Matthew Clarke (Book)
GPI	Japan	1970	2003	2008	Ed: Philip Lawn and Matthew Clarke (Book)
GPI	China	1970	2005	2008	Ed: Philip Lawn and Matthew Clarke (Book)
GPI	Thailand	1975	2004	2008	Ed: Philip Lawn and Matthew Clarke (Book)
GPI	Vietnam	1992	2004	2008	Ed: Philip Lawn and Matthew Clarke (Book)
Edmonton Wellbeing Index	Edmonton, Canada	1981	2008	2009	Anielski and Johannessen
ISEW	Tuscany, Italy	1971	2006	2009	Pulselli, F., Bravi, M., Tiezzi, E.
GPI	Utah	1990	2007	2011	Berik, G. and E. Gaddis.
GPI	Baltimore City, County, and the State of Maryland	1950	2005	2011	Posner, S. and R. Costanza
GPI	Vermont	1960	2010	2011	Zencey, Eric, Sebastian Castro, Marigo Farr, Mark Isselhardt, Brian Kelly, Katharine Lucas, Julie Nash, Matt Pescatore, Meagan Pharis, Vinson Pierce, Tarah Rose, Daniel Sanchez, Aaron Witham, Zach Zimmerman.
GPI & ISEW	Päijät-Häme, 'CEDESO', and Kainuu, Finland	1960	2009	2011	Hoffren
GPI	Vermont	1960	2011	2013	Jon D. Erickson, Eric Zencey, Matthew J. Burke, Sam Carlson, and Zachary Zimmerman
GPI	Maryland	1950	2004	2012	MacGuire, S., S. Posner, H. Haake
ISEW	Netherlands	1970	2010	2012	Bob van Moerkerk
GPI	Northern Ohio	1990	2005	2012	Kenneth Bagstad and Md Rumi Shammin
ISEW	Flanders, Belgium	1990	2009	2013	Brent Bleys
GPI	Austria	1955	1992	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Belgium	1970	2005	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Netherlands	1950	1992	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Poland	1980	1998	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Italy	1960	1990	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Sweden	1950	1992	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	United Kingdom	1950	2001	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	United States	1950	2005	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Chile	1950	1992	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Australia	1965	2006	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	New Zealand	1970	2005	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	China	1970	2006	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	India	1985	2003	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Japan	1970	2003	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Thailand	1975	2005	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Vietnam	1990	2005	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
GPI	Global	1950	2005	2013	Kubiszewski, Costanza, Franco, Lawn, Talberth, Jackson, Aylmer
ISEW	Tuscany and Marche, Italy	1999	2009	2013	Chelli, Ciommi, Gigliarano
GPI	Maryland	1960	2013	2014	Hans Haake
GPI	Hawaii	2000	2009	2014	Regina Ostergaard-Klem, Kirsten Oleson
ISEW	Flanders, Belgium	1990	2012	2014	Brent Bleys
GPI	Brazil	1970	2010	2015	Daniel Caixeta Andrade, Junior Ruiz Garcia
GPI	Hong Kong	1968	2010	2015	Claudio O Delang (Book)
GPI	Singapore	1968	2010	2015	Claudio O Delang (Book)
GPI	Massachuesetts	1960	2012	2015	Jon D. Erickson, Eric Zencey, and Zachary Zimmerman
GPI	Oregon	1960	2010	2015	Ida Kubiszewski, Robert Costanza, Nicole E. Gorko, Michael A. Weisdorf, Austin W. Carnes, Cathrine E. Collins, Carol Franco, Lillian R. Gehres, Jenna M. Knobloch, Gayle E. Matson, Joan D. Schoepfer
ISEW	Flanders, Belgium	1990	2014	2016	Brent Bleys
GPI	Missouri	2000	2014	2016	Zencey, Eric
ISEW	Flanders, Belgium	1990	2015	2017	Brent Bleys
GPI	US, 50 States	2010	2011	2017	Mairi-Jane Fox
GPI	California	2010	2014	2017	Brown and Lazarus
ISEW	Turkey	2001	2012	2018	Angeliki Menegaki
N/RWI	Germany, Bavaria, Hamburg, North Rhine/Westphalia, Rhineland-Palantinate, Saxonia, Thuringia	1991	2014	2018	Held, Rodenhäuser, Diefenbacher, Zieschank
GPI	Vermont	2000	2015	2018	Eric Zencey
GPI	10 megacities (Beijing, Tianjin, Nanjing, Shanghai, Guangzhou, Chongqing, Chengdu, Xi'an, Wuhan, Shenyang), China	199x	201x	2018	Lu Huang

Cortisol

From Wikipedia, the free encyclopedia

Cortisol

Properties
Chemical formula	C21H30O5
Molar mass	362.460 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Cortisol is a steroid hormone, in the glucocorticoid class of hormones. When used as a medication, it is known as hydrocortisone.

It is produced in humans by the zona fasciculata of the adrenal cortex within the adrenal gland. It is released in response to stress and low blood-glucose concentration. It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates. It also decreases bone formation.

Health effects

Metabolic response

In the early fasting state, cortisol stimulates gluconeogenesis (the formation of glucose), and activates antistress and anti-inflammatory pathways. Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis, the breaking down of glycogen to glucose-1-phosphate and glucose. This is done through its passive influence on glucagon. Additionally, cortisol facilitates the activation of glycogen phosphorylase, which is necessary for epinephrine to have an effect on glycogenolysis.

In the late fasting state, the function of cortisol changes slightly and increases glycogenesis. This response allows the liver to take up glucose not being used by the peripheral tissue and turn it into liver glycogen stores to be used if the body moves into the starvation state.

Elevated levels of cortisol, if prolonged, can lead to proteolysis (breakdown of proteins) and muscle wasting. Several studies have shown that cortisol can have a lipolytic effect (promote the breakdown of fat). Under some conditions, however, cortisol may somewhat suppress lipolysis.

Immune response

Cortisol prevents the release of substances in the body that cause inflammation. It is used to treat conditions resulting from overactivity of the B-cell-mediated antibody response. Examples include inflammatory and rheumatoid diseases, as well as allergies. Low-potency hydrocortisone, available as a nonprescription medicine in some countries, is used to treat skin problems such as rashes and eczema.

It inhibits production of interleukin (IL)-12, interferon (IFN)-gamma, IFN-alpha, and tumor-necrosis-factor (TNF)-alpha by antigen-presenting cells (APCs) and T helper (Th)1 cells, but upregulates IL-4, IL-10, and IL-13 by Th2 cells. This results in a shift toward a Th2 immune response rather than general immunosuppression. The activation of the stress system (and resulting increase in cortisol and Th2 shift) seen during an infection is believed to be a protective mechanism which prevents an over-activation of the inflammatory response.

Cortisol can weaken the activity of the immune system. It prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor (IL-2). Cortisol also has a negative-feedback effect on interleukin-1.

Though IL-1 is useful in combating some diseases, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels (forcing the secretion of corticotropin-releasing hormone, thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor, so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes (reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of corticosterone (the endogenous type I and type II receptor agonist) or RU28362 (a specific type II receptor agonist) to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are affected by cortisol.

Cortisol stimulates many copper enzymes (often to 50% of their total potential), probably to increase copper availability for immune purposes. This includes lysyl oxidase, an enzyme that cross-links collagen, and elastin. Especially valuable for immune response is cortisol's stimulation of the superoxide dismutase, since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria.

Other effects

Metabolism

Glucose

Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis and inhibits the peripheral use of glucose (insulin resistance) by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane. Cortisol also increases glycogen synthesis (glycogenesis) in the liver, storing glucose in easily accessible form. The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown.

Bone and collagen

Cortisol reduces bone formation, favoring long-term development of osteoporosis (progressive bone disease). It transports potassium out of cells in exchange for an equal number of sodium ions (see above). This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine.

Collagen is an important component of connective tissue. It is vital for structural support and is found in muscles, tendons, and joints, as well as throughout the entire body. Cortisol down-regulates the synthesis of collagen.

Amino acid

Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis. Cortisol (as opticortinol) may inversely inhibit IgA precursor cells in the intestines of calves. Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE.

Wound healing

Cortisol and the stress response have known deleterious effects on the immune system. High levels of perceived stress and increases in cortisol have been found to lengthen wound-healing time in healthy, male adults. Those who had the lowest levels of cortisol the day following a 4 mm punch biopsy had the fastest healing time. In dental students, wounds from punch biopsies took an average of 40% longer to heal when performed three days before an examination as opposed to biopsies performed on the same students during summer vacation. This is in line with previous animal studies that show similar detrimental effects on wound healing, notably the primary reports showing that turtles recoil from cortisol.

Electrolyte balance

Cortisol acts as a diuretic, increasing water diuresis, glomerular filtration rate, and renal plasma flow from the kidneys, as well as increasing sodium retention and potassium excretion. It also increases sodium and water absorption and potassium excretion in the intestines.

Sodium

Cortisol promotes sodium absorption through the small intestine of mammals. Sodium depletion, however, does not affect cortisol levels so cortisol cannot be used to regulate serum sodium. Cortisol's original purpose may have been sodium transport. This hypothesis is supported by the fact that freshwater fish use cortisol to stimulate sodium inward, while saltwater fish have a cortisol-based system for expelling excess sodium.

Potassium

A sodium load augments the intense potassium excretion by cortisol. Corticosterone is comparable to cortisol in this case. For potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell. This should make pH regulation much easier (unlike the normal potassium-deficiency situation, in which two sodium ions move in for each three potassium ions that move out—closer to the deoxycorticosterone effect).

Stomach and kidneys

Cortisol stimulates gastric-acid secretion. Cortisol's only direct effect on the hydrogen-ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme.

Memory

Cortisol works with adrenaline (epinephrine) to create memories of short-term emotional events; this is the proposed mechanism for storage of flash bulb memories, and may originate as a means to remember what to avoid in the future. However, long-term exposure to cortisol damages cells in the hippocampus; this damage results in impaired learning. Furthermore, cortisol inhibits memory retrieval of already stored information.

Sleep, stress, and mood

Diurnal cycles of cortisol levels are found in humans. In humans, the amount of cortisol present in the blood undergoes diurnal variation; the level peaks in the early morning (around 8 am) and reaches its lowest level at about midnight-4 am, or three to five hours after the onset of sleep. Information about the light/dark cycle is transmitted from the retina to the paired suprachiasmatic nuclei in the hypothalamus. This pattern is not present at birth; estimates of when it begins vary from two weeks to nine months of age.

Sustained stress can lead to high levels of circulating cortisol, which can create an allostatic load. An allostatic load can lead to various physical modifications in the body's regulatory networks. Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, mood disorders such as major depressive disorder, anxiety disorders, psychological stress, and physiological stressors such as hypoglycemia, illness, fever, trauma, surgery, fear, pain, physical exertion, or temperature extremes. Cortisol levels may also differ for individuals with autism or Asperger's syndrome. Also, significant individual variation is seen, although a given person tends to have consistent rhythms.

Effects during pregnancy

During human pregnancy, increased fetal production of cortisol between weeks 30 and 32 initiates production of fetal lung surfactant to promote maturation of the lungs. In fetal lambs, glucocorticoids (principally cortisol) increase after about day 130, with lung surfactant increasing greatly, in response, by about day 135, and although lamb fetal cortisol is mostly of maternal origin during the first 122 days, 88% or more is of fetal origin by day 136 of gestation. Although the timing of fetal cortisol concentration elevation in sheep may vary somewhat, it averages about 11.8 days before the onset of labor. In several livestock species (e.g. cattle, sheep, goats, and pigs), the surge of fetal cortisol late in gestation triggers the onset of parturition by removing the progesterone block of cervical dilation and myometrial contraction. The mechanisms yielding this effect on progesterone differ among species. In the sheep, where progesterone sufficient for maintaining pregnancy is produced by the placenta after about day 70 of gestation, the prepartum fetal cortisol surge induces placental enzymatic conversion of progesterone to estrogen. (The elevated level of estrogen stimulates prostaglandin secretion and oxytocin receptor development.)

Exposure of fetuses to cortisol during gestation can have a variety of developmental outcomes, including alterations in prenatal and postnatal growth patterns. In marmosets, a species of New World primates, pregnant females have varying levels of cortisol during gestation, both within and between females. Infants born to mothers with high gestational cortisol during the first trimester of pregnancy had lower rates of growth in body mass indices than infants born to mothers with low gestational cortisol (about 20% lower). However, postnatal growth rates in these high-cortisol infants was more rapid than low-cortisol infants later in postnatal periods, and complete catch-up in growth had occurred by 540 days of age. These results suggest that gestational exposure to cortisol in fetuses has important potential fetal programming effects on both pre- and postnatal growth in primates.

Synthesis and release

Cortisol is produced in the human body by the adrenal gland in the zona fasciculata, the second of three layers comprising the adrenal cortex. The cortex forms the outer "bark" of each adrenal gland, situated atop the kidneys. The release of cortisol is controlled by the hypothalamus, a part of the brain. The secretion of corticotropin-releasing hormone by the hypothalamus triggers cells in the neighboring anterior pituitary to secrete another hormone, the adrenocorticotropic hormone (ACTH), into the vascular system, through which blood carries it to the adrenal cortex. ACTH stimulates the synthesis of cortisol and other glucocorticoids, mineralocorticoids, and dehydroepiandrosterone.

Normal levels

Normal values indicated in the following tables pertain to humans (normal levels vary among species). Measured cortisol levels, and therefore reference ranges, depend on the analytical method used and factors such as age and sex. Test results should, therefore, always be interpreted using the reference range from the laboratory that produced the result.

Reference ranges for blood plasma content of free cortisol

Time	Lower limit	Upper limit	Unit
09:00 am	140	700	nmol/L
	5	25	μg/dL
Midnight	80	350	nmol/l
	2.9	13	μg/dl

Using the molecular weight of 362.460 g/mole, the conversion factor from µg/dl to nmol/l is approximately 27.6; thus, 10 µg/dl is about 276 nmol/l.

Reference ranges for urinalysis of free cortisol

Lower limit	Upper limit	Unit
28 or 30	280 or 490	nmol/24h
10 or 11	100 or 176	µg/24 h

Disorders of cortisol production

• Cushing's syndrome or hypercortisolism: Excessive levels of cortisol in the blood
• Hypocortisolism: Insufficient levels of cortisol in the blood

Disorders of cortisol production, and some consequent conditions, are:

• Primary hypercortisolism (Cushing's syndrome)
• Primary hypocortisolism (Addison's disease, Nelson's syndrome)
  • Secondary hypercortisolism (pituitary tumor resulting in Cushing's disease, pseudo-Cushing's syndrome)
  • Secondary hypocortisolism (pituitary tumor, Sheehan's syndrome)

Regulation

The primary control of cortisol is the pituitary gland peptide, ACTH, which probably controls cortisol by controlling the movement of calcium into the cortisol-secreting target cells. ACTH is in turn controlled by the hypothalamic peptide corticotropin-releasing hormone (CRH), which is under nervous control. CRH acts synergistically with arginine vasopressin, angiotensin II, and epinephrine. (In swine, which do not produce arginine vasopressin, lysine vasopressin acts synergistically with CRH.)

When activated macrophages start to secrete IL-1, which synergistically with CRH increases ACTH, T-cells also secrete glucosteroid response modifying factor (GRMF), as well as IL-1; both increase the amount of cortisol required to inhibit almost all the immune cells. Immune cells then assume their own regulation, but at a higher cortisol setpoint. The increase in cortisol in diarrheic calves is minimal over healthy calves, however, and falls over time. The cells do not lose all their fight-or-flight override because of interleukin-1's synergism with CRH. Cortisol even has a negative feedback effect on interleukin-1—especially useful to treat diseases that force the hypothalamus to secrete too much CRH, such as those caused by endotoxic bacteria. The suppressor immune cells are not affected by GRMF, so the immune cells' effective setpoint may be even higher than the setpoint for physiological processes. GRMF affects primarily the liver (rather than the kidneys) for some physiological processes.

High-potassium media (which stimulates aldosterone secretion in vitro) also stimulate cortisol secretion from the fasciculata zone of canine adrenals — unlike corticosterone, upon which potassium has no effect.

Potassium loading also increases ACTH and cortisol in humans. This is probably the reason why potassium deficiency causes cortisol to decline (as mentioned) and causes a decrease in conversion of 11-deoxycortisol to cortisol. This may also have a role in rheumatoid-arthritis pain; cell potassium is always low in RA.

Ascorbic acid presence, particularly in high doses has also been shown to mediate response to psychological stress and speed the decrease of the levels of circulating cortisol in the body post stress. This can be evidenced through a decrease in systolic and diastolic blood pressures and decreased salivary cortisol level after treatment with ascorbic acid.

Factors reducing cortisol levels

• Magnesium supplementation decreases serum cortisol levels after aerobic exercise, but not after resistance training;
• Omega-3 fatty acids have a dose-dependent effect in slightly reducing cortisol release influenced by mental stress, suppressing the synthesis of interleukin-1 and -6 and enhancing the synthesis of interleukin-2; the former promotes higher CRH release. Omega-6 fatty acids, though, have an inverse effect on interleukin synthesis;
• Music therapy can reduce cortisol levels in certain situations;
• Massage therapy can reduce cortisol;
• Laughing, and the experience of humor, can lower cortisol levels;
• Soy-derived phosphatidylserine interacts with cortisol; the correct dose, however, is unclear;
• Regular dancing has been shown to lead to significant decreases in salivary cortisol concentrations;
• Withania somnifera (ashwagandha) root extract;
• High-dosage treatment with ascorbic acid (vitamin C) has been shown to decrease circulating cortisol levels during and shortly after the treatment period.

Factors increasing cortisol levels

• Viral infections increase cortisol levels through activation of the HPA axis by cytokines;
• Caffeine may increase cortisol levels;
• Sleep deprivation;
• Intense (high VO₂ max) or prolonged aerobic exercise transiently increases cortisol levels to increase gluconeogenesis and maintain blood glucose; however, cortisol declines to normal levels after eating (i.e., restoring a neutral energy balance);
• The Val/Val variation of the BDNF gene in men and the Val/Met variation in women are associated with increased salivary cortisol in a stressful situation;
• Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods;
• Subcutaneous adipose tissue regenerates cortisol from cortisone by the enzyme 11-beta HSD1;
• Anorexia nervosa may be associated with increased cortisol levels;
• The serotonin receptor gene 5HTR2C is associated with increased cortisol production in men;
• Smelling androstadienone has been found in one study to raise cortisol levels in women, as well as, in other studies, to affect mood;
• Excessive or problematic drinking has been linked to increased cortisol levels, especially in college students.

Biochemistry

Biosynthesis

   

Steroidogenesis, showing cortisol at right

Cortisol is synthesized from cholesterol. Synthesis takes place in the zona fasciculata of the adrenal cortex. (The name cortisol is derived from cortex.) While the adrenal cortex also produces aldosterone (in the zona glomerulosa) and some sex hormones (in the zona reticularis), cortisol is its main secretion in humans and several other species. (However, in cattle, corticosterone levels may approach or exceed cortisol levels.). The medulla of the adrenal gland lies under the cortex, mainly secreting the catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine) under sympathetic stimulation.

The synthesis of cortisol in the adrenal gland is stimulated by the anterior lobe of the pituitary gland with ACTH; ACTH production is, in turn, stimulated by CRH, which is released by the hypothalamus. ACTH increases the concentration of cholesterol in the inner mitochondrial membrane, via regulation of the steroidogenic acute regulatory protein. It also stimulates the main rate-limiting step in cortisol synthesis, in which cholesterol is converted to pregnenolone and catalyzed by cytochrome P450SCC (side-chain cleavage enzyme).

Metabolism

Cortisol is metabolized by the 11-beta hydroxysteroid dehydrogenase system (11-beta HSD), which consists of two enzymes: 11-beta HSD1 and 11-beta HSD2:

• 11-beta HSD1 uses the cofactor NADPH to convert biologically inert cortisone to biologically active cortisol;
• 11-beta HSD2 uses the cofactor NAD+ to convert cortisol to cortisone.

Overall, the net effect is that 11-beta HSD1 serves to increase the local concentrations of biologically active cortisol in a given tissue; 11-beta HSD2 serves to decrease local concentrations of biologically active cortisol.

Cortisol is also metabolized into 5-alpha tetrahydrocortisol (5-alpha THF) and 5-beta tetrahydrocortisol (5-beta THF), reactions for which 5-alpha reductase and 5-beta reductase are the rate-limiting factors, respectively. 5-Beta reductase is also the rate-limiting factor in the conversion of cortisone to tetrahydrocortisone.

An alteration in 11-beta HSD1 has been suggested to play a role in the pathogenesis of obesity, hypertension, and insulin resistance known as metabolic syndrome.

An alteration in 11-beta HSD2 has been implicated in essential hypertension and is known to lead to the syndrome of apparent mineralocorticoid excess (SAME).

Chemistry

Cortisol is a naturally occurring pregnane corticosteroid and is also known as 11β,17α,21-trihydroxypregn-4-ene-3,20-dione.

Animals

In animals, cortisol is often used as an indicator of stress and can be measured in blood, saliva, urine, hair, and faeces.