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Sunday, October 18, 2026

Cancer research

 


From Wikipedia, the free encyclopedia

Cancer research is research into cancer to identify causes and develop strategies for prevention, diagnosis, treatment, and cure.

Cancer research ranges from epidemiology, molecular bioscience to the performance of clinical trials to evaluate and compare applications of the various cancer treatments. These applications include surgery, radiation therapy, chemotherapy, hormone therapy, immunotherapy and combined treatment modalities such as chemo-radiotherapy. Starting in the mid-1990s, the emphasis in clinical cancer research shifted towards therapies derived from biotechnology research, such as cancer immunotherapy and gene therapy.

Cancer research is done in academia, research institutes, and corporate environments, and is largely government funded.[citation needed]

History

Sidney Farber is regarded as the father of modern chemotherapy.

Cancer research has been ongoing for centuries. Early research focused on the causes of cancer.[1] Percivall Pott identified the first environmental trigger (chimney soot) for cancer in 1775 and cigarette smoking was identified as a cause of lung cancer in 1950. Early cancer treatment focused on improving surgical techniques for removing tumors. Radiation therapy took hold in the 1900s. Chemotherapeutics were developed and refined throughout the 20th century.

The U.S. declared a "war on cancer" in the 1970s, and increased the funding and support for cancer research.[2]

Seminal papers

Some of the most highly cited and most influential research reports include:

Types of research

Cancer research encompasses a variety of types and interdisciplinary areas of research. Scientists involved in cancer research may be trained in areas such as chemistry, biochemistry, molecular biology, physiology, medical physics, epidemiology, and biomedical engineering. Research performed on a foundational level is referred to as basic research and is intended to clarify scientific principles and mechanisms. Translational research aims to elucidate mechanisms of cancer development and progression and transform basic scientific findings into concepts that can be applicable to the treatment and prevention of cancer. Clinical research is devoted to the development of pharmaceuticals, surgical procedures, and medical technologies for the eventual treatment of patients.

Prevention and epidemiology

Epidemiologic analysis indicates that at least 35% of all cancer deaths in the world could now be avoided by primary prevention.[3] According to a newer GBD systematic analysis, in 2019, ~44% of all cancer deaths — or ~4.5 million deaths or ~105 million lost disability-adjusted life years — were due to known clearly preventable risk factors, led by smoking, alcohol use and high BMI.[4]

However, one 2015 study suggested that between ~70% and ~90% of cancers are due to environmental factors and therefore potentially preventable.[5][contradictory] Furthermore, it is estimated that with further research cancer death rates could be reduced by 70% around the world even without the development of any new therapies.[3] Cancer prevention research receives only 2–9% of global cancer research funding,[3] albeit many of the options for prevention are already well-known without further cancer-specific research but are not reflected in economics and policy. Mutational signatures of various cancers, for example, could reveal further causes of cancer and support causal attribution.[6][additional citation(s) needed]

Detection

Prompt detection of cancer is important, since it is usually more difficult to treat in later stages. Accurate detection of cancer is also important because false positives can cause harm from unnecessary medical procedures. Some screening protocols are currently not accurate (such as prostate-specific antigen testing). Others such as a colonoscopy or mammogram are unpleasant and as a result some patients may opt out. Active research is underway to address all these problems, to develop novel ways of cancer screening and to increase detection rates.[citation needed][further explanation needed]

For example:

Treatment

Emerging topics of cancer treatment research include:

Cause and development of cancer

Numerous cell signaling pathways are disrupted in the development of cancer.

Research into the cause of cancer involves many different disciplines including genetics, diet, environmental factors (i.e. chemical carcinogens). In regard to investigation of causes and potential targets for therapy, the route used starts with data obtained from clinical observations, enters basic research, and, once convincing and independently confirmed results are obtained, proceeds with clinical research, involving appropriately designed trials on consenting human subjects, with the aim to test safety and efficiency of the therapeutic intervention method. An important part of basic research is characterization of the potential mechanisms of carcinogenesis, in regard to the types of genetic and epigenetic changes that are associated with cancer development. The mouse is often used as a mammalian model for manipulation of the function of genes that play a role in tumor formation, while basic aspects of tumor initiation, such as mutagenesis, are assayed on cultures of bacteria and mammalian cells.

Genes involved in cancer

The goal of oncogenomics is to identify new oncogenes or tumor suppressor genes that may provide new insights into cancer diagnosis, predicting clinical outcome of cancers, and new targets for cancer therapies. As the Cancer Genome Project stated in a 2004 review article, "a central aim of cancer research has been to identify the mutated genes that are causally implicated in oncogenesis (cancer genes)."[32] The Cancer Genome Atlas project is a related effort investigating the genomic changes associated with cancer, while the COSMIC cancer database documents acquired genetic mutations from hundreds of thousands of human cancer samples.[33]

These large scale projects, involving about 350 different types of cancer, have identified ~130,000 mutations in ~3000 genes that have been mutated in the tumors. The majority occurred in 319 genes, of which 286 were tumor suppressor genes and 33 oncogenes.

Several hereditary factors can increase the chance of cancer-causing mutations, including the activation of oncogenes or the inhibition of tumor suppressor genes. The functions of various onco- and tumor suppressor genes can be disrupted at different stages of tumor progression. Mutations in such genes can be used to classify the malignancy of a tumor.

In later stages, tumors can develop a resistance to cancer treatment. The identification of oncogenes and tumor suppressor genes is important to understand tumor progression and treatment success. The role of a given gene in cancer progression may vary tremendously, depending on the stage and type of cancer involved.[34]

Cancer epigenetics

These paragraphs are an excerpt from Cancer epigenetics.edit

Cancer epigenetics is the study of epigenetic modifications to the DNA of cancer cells that do not involve a change in the nucleotide sequence, but instead involve a change in the way the genetic code is expressed. Epigenetic mechanisms are necessary to maintain normal sequences of tissue specific gene expression and are crucial for normal development.[35] They may be just as important, if not even more important, than genetic mutations in a cell's transformation to cancer. The disturbance of epigenetic processes in cancers, can lead to a loss of expression of genes that occurs about 10 times more frequently by transcription silencing (caused by epigenetic promoter hypermethylation of CpG islands) than by mutations. As Vogelstein et al. points out, in a colorectal cancer there are usually about 3 to 6 driver mutations and 33 to 66 hitchhiker or passenger mutations.[36] However, in colon tumors compared to adjacent normal-appearing colonic mucosa, there are about 600 to 800 heavily methylated CpG islands in the promoters of genes in the tumors while these CpG islands are not methylated in the adjacent mucosa.[37][38][39] Manipulation of epigenetic alterations holds great promise for cancer prevention, detection, and therapy.[40][41] In different types of cancer, a variety of epigenetic mechanisms can be perturbed, such as the silencing of tumor suppressor genes and activation of oncogenes by altered CpG island methylation patterns, histone modifications, and dysregulation of DNA binding proteins. There are several medications which have epigenetic impact, that are now used in a number of these diseases.

Diet and cancer

This section is an excerpt from Diet and cancer.edit
Advertisement suggesting that a healthy diet helps prevent cancer

Many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence.[42][43][44] Obesity and drinking alcohol have been correlated with the incidence and progression of some cancers.[42] Lowering the consumption of sweetened beverages is recommended as a measure to address obesity.[45]

Some specific foods are linked to specific cancers. There is strong evidence that processed meat and red meat intake increases risk of colorectal cancer.[46][47][48][49] Aflatoxin B1, a frequent food contaminant, increases risk of liver cancer,[50] while drinking coffee is associated with a reduced risk.[51] Betel nut chewing causes oral cancer.[50] Stomach cancer is more common in Japan due to its high-salt diet.[50][52]

Dietary recommendations for cancer prevention typically include weight management and eating a healthy diet, consisting mainly of "vegetables, fruit, whole grains and fish, and a reduced intake of red meat, animal fat, and refined sugar."[42] A healthy dietary pattern may lower cancer risk by 10–20%.[53] There is no clinical evidence that diets or specific foods can cure cancer.[54][55]

Periods of intermittent fasting (time-restricted feeding which may not include caloric restriction) is investigated for potential usefulness in cancer prevention and treatment and as of 2021 additional trials are needed to elucidate the risks and benefits.[56][57][58][59] In some cases, "caloric restrictions could hinder both cancer growth and progression, besides enhancing the efficacy of chemotherapy and radiation therapy".[60] Caloric restriction mimetics, including some present in foods like spermidine, are also investigated for these or similar reasons.[61][62] Such and similar dietary supplements may contribute to prevention or treatment, with candidate substances including apigenin,[63][64][65] berberine,[66][67][68][69][70] jiaogulan,[71] and rhodiola rosea.[72][73]

Research funding

Cancer research is funded by government grants, charitable foundations and pharmaceutical and biotechnology companies.[74]

In the early 2000s, most funding for cancer research came from taxpayers and charities, rather than from corporations. In the US, less than 30% of all cancer research was funded by commercial researchers such as pharmaceutical companies.[75] Per capita, public spending on cancer research by taxpayers and charities in the US was five times as much in 2002–03 as public spending by taxpayers and charities in the 15 countries that were full members of the European Union.[75] As a percentage of GDP, the non-commercial funding of cancer research in the US was four times the amount dedicated to cancer research in Europe.[75] Half of Europe's non-commercial cancer research is funded by charitable organizations.[75]

The National Cancer Institute is the major funding institution in the United States. In the 2023 fiscal year, the NCI funded $7.1 billion in cancer research.[76]

Difficulties

Difficulties inherent to cancer research are shared with many types of biomedical research.

Cancer research processes have been criticised. These include, especially in the US, for the financial resources and positions required to conduct research. Other consequences of competition for research resources appear to be a substantial number of research publications whose results cannot be replicated.[77][78][79][80]

Replicability

This section is an excerpt from Replication crisis § In medicine.edit
Graphic of results and barriers. 193 experiments were designed, 87 were initiated, and 50 were completed.
Results from The Reproducibility Project: Cancer Biology suggest most studies of the cancer research sector may not be replicable.

In a 2012 paper, C. Glenn Begley, a biotech consultant working at Amgen, and Lee Ellis, a medical researcher at the University of Texas, found that only 11% of 53 pre-clinical cancer studies had replications that confirmed the original studies' conclusions.[81] In late 2021, The Reproducibility Project: Cancer Biology examined 53 top papers about cancer published between 2010 and 2012 and showed that, among studies that provided sufficient information to be redone, effect sizes were 85% smaller on average than the original findings.[82][83] A survey of cancer researchers found that half of them had been unable to reproduce a published result.[84] Another report estimated that almost half of randomized controlled trials contained flawed data (based on the analysis of anonymized individual participant data (IPD) from more than 150 trials).[85]

Public participation

Distributed computing

One can share computer time for distributed cancer research projects like Help Conquer Cancer.[86] World Community Grid also had a project called Help Defeat Cancer. Other related projects include the Folding@home and Rosetta@home projects, which focus on groundbreaking protein folding and protein structure prediction research. Vodafone has also partnered with the Garvan Institute to create the DreamLab Project, which uses distributed computing via an app on cellphones to perform cancer research.

Clinical trials

MatchMiner overview of data flow and modes of use[87]

Members of the public can also join clinical trials as healthy control subjects or for methods of cancer detection.

There could be software and data-related procedures that increase participation in trials and make them faster and less expensive. One open source platform matches genomically profiled cancer patients to precision medicine drug trials.[88][87]

MD Anderson Cancer Center is ranked as one of the top cancer research institutions.

Organizations

Breast cancer awareness ribbon statue in Kentucky

Organizations exist as associations for scientists participating in cancer research, such as the American Association for Cancer Research and American Society of Clinical Oncology, and as foundations for public awareness or raising funds for cancer research, such as Relay For Life and the American Cancer Society.

Awareness campaigns

Supporters of different types of cancer have adopted different colored awareness ribbons and promote months of the year as being dedicated to the support of specific types of cancer. The American Cancer Society began promoting October as Breast Cancer Awareness Month in the United States in the 1980s. Pink products are sold to both generate awareness and raise money to be donated for research purposes. This has led to pinkwashing, or the selling of ordinary products turned pink as a promotion for the company.

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Oxidative stress

From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Oxidative_stress
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).

Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA.

Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by the reactive oxygen species generated, e.g., O−
2 (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide).

Short-term oxidative stress is required to initiate stress response processes in plants.

Chemical and biological effects

Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione. The effects of oxidative stress depend upon the size of these changes, with a cell being able to overcome small perturbations and regain its original state. However, more severe oxidative stress can cause cell death, and even moderate oxidation can trigger apoptosis, while more intense stresses may cause necrosis.

Production of reactive oxygen species is a particularly destructive aspect of oxidative stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage. Most long-term effects are caused by damage to DNA.

DNA damage induced by ionizing radiation is similar to oxidative stress, and these lesions have been implicated in aging and cancer. Biological effects of single-base damage by radiation or oxidation, such as 8-oxoguanine and thymine glycol, have been extensively studied. Recently the focus has shifted to some of the more complex lesions. Tandem DNA lesions are formed at substantial frequency by ionizing radiation and metal-catalyzed H2O2 reactions. Under anoxic conditions, the predominant double-base lesion is a species in which C8 of guanine is linked to the 5-methyl group of an adjacent 3'-thymine (G[8,5- Me]T).

Most of these oxygen-derived species are produced by normal aerobic metabolism. Normal cellular defense mechanisms destroy most of these. Repair of oxidative damages to DNA is frequent and ongoing, largely keeping up with newly induced damages. In rat urine, about 74,000 oxidative DNA adducts per cell are excreted daily. There is also a steady state level of oxidative damages in the DNA of a cell. There are about 24,000 oxidative DNA adducts per cell in young rats and 66,000 adducts per cell in old rats. Likewise, any damage to cells is constantly repaired. However, under the severe levels of oxidative stress that cause necrosis, the damage causes ATP depletion, preventing controlled apoptotic death and causing the cell to simply fall apart.

Polyunsaturated fatty acids, particularly arachidonic acid and linoleic acid, are primary targets for free radical and singlet oxygen oxidations. For example, in tissues and cells, the free radical oxidation of linoleic acid produces racemic mixtures of 13-hydroxy-9Z,11E-octadecadienoic acid, 13-hydroxy-9E,11E-octadecadienoic acid, 9-hydroxy-10E,12-E-octadecadienoic acid (9-EE-HODE), and 11-hydroxy-9Z,12-Z-octadecadienoic acid as well as 4-Hydroxynonenal while singlet oxygen attacks linoleic acid to produce (presumed but not yet proven to be racemic mixtures of) 13-hydroxy-9Z,11E-octadecadienoic acid, 9-hydroxy-10E,12-Z-octadecadienoic acid, 10-hydroxy-8E,12Z-octadecadienoic acid, and 12-hydroxy-9Z-13-E-octadecadienoic (see 13-Hydroxyoctadecadienoic acid and 9-Hydroxyoctadecadienoic acid).

Similar attacks on arachidonic acid produce a far larger set of products including various isoprostanes, hydroperoxy- and hydroxy- eicosatetraenoates, and 4-hydroxyalkenals. While many of these products are used as markers of oxidative stress, the products derived from linoleic acid appear far more predominant than arachidonic acid products and therefore easier to identify and quantify in, for example, atheromatous plaques.

Certain linoleic acid products have also been proposed to be markers for specific types of oxidative stress. For example, the presence of racemic 9-HODE and 9-EE-HODE mixtures reflects free radical oxidation of linoleic acid whereas the presence of racemic 10-hydroxy-8E,12Z-octadecadienoic acid and 12-hydroxy-9Z-13-E-octadecadienoic acid reflects singlet oxygen attack on linoleic acid.

In addition to serving as markers, the linoleic and arachidonic acid products can contribute to tissue and/or DNA damage but also act as signals to stimulate pathways which function to combat oxidative stress.

OxidantDescription
•O−
2, superoxide anion		 One-electron reduction state of O2, formed in many autoxidation reactions and by the electron transport chain. Rather unreactive but can release Fe2+
 from iron-sulfur proteins and ferritin. Undergoes dismutation to form H2O2 spontaneously or by enzymatic catalysis and is a precursor for metal-catalyzed •OH formation.
H2O2, hydrogen peroxide Two-electron reduction state, formed by dismutation of •O−
2 or by direct reduction of O2. Lipid-soluble and thus able to diffuse across membranes.
•OH, hydroxyl radical Three-electron reduction state, formed by Fenton reaction and decomposition of peroxynitrite. Extremely reactive, will attack most cellular components
ROOH, organic hydroperoxide Formed by radical reactions with cellular components such as lipids and nucleobases.
RO•, alkoxy and ROO•, peroxy radicals Oxygen centred organic radicals. Lipid forms participate in lipid peroxidation reactions. Produced in the presence of oxygen by radical addition to double bonds or hydrogen abstraction.
HOCl, hypochlorous acid Formed from H2O2 by myeloperoxidase. Lipid-soluble and highly reactive. Will readily oxidize protein constituents, including thiol groups, amino groups and methionine.
ONOO-, peroxynitrite Formed in a rapid reaction between •O−
2 and NO•. Lipid-soluble and similar in reactivity to hypochlorous acid. Protonation forms peroxynitrous acid, which can undergo homolytic cleavage to form hydroxyl radical and nitrogen dioxide.

Production and consumption of oxidants

One source of reactive oxygen under normal conditions in humans is the leakage of activated oxygen from mitochondria during oxidative phosphorylation. E. coli mutants that lack an active electron transport chain produce as much hydrogen peroxide as wild-type cells, indicating that other enzymes contribute the bulk of oxidants in these organisms. One possibility is that multiple redox-active flavoproteins all contribute a small portion to the overall production of oxidants under normal conditions.

Other enzymes capable of producing superoxide are xanthine oxidase, NADPH oxidases and cytochromes P450. Hydrogen peroxide is produced by a wide variety of enzymes including several oxidases. Reactive oxygen species play important roles in cell signalling, a process termed redox signaling. Thus, to maintain proper cellular homeostasis, a balance must be struck between reactive oxygen production and consumption.

The best studied cellular antioxidants are the enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase. Less well studied (but probably just as important) enzymatic antioxidants are the peroxiredoxins and the recently discovered sulfiredoxin. Other enzymes that have antioxidant properties (though this is not their primary role) include paraoxonase, glutathione-S transferases, and aldehyde dehydrogenases.

The amino acid methionine is prone to oxidation, but oxidation of methionine can be reversible. Oxidation of methionine is shown to inhibit the phosphorylation of adjacent Ser/Thr/Tyr sites in proteins. This gives a plausible mechanism for cells to couple oxidative stress signals with mainstream cellular signaling such as phosphorylation.

Antioxidants as supplements

The use of antioxidants to prevent some diseases is controversial. In a high-risk group like smokers, high doses of beta carotene increased the rate of lung cancer since high doses of beta-carotene in conjunction with high oxygen tension due to smoking results in a pro-oxidant effect and an antioxidant effect when oxygen tension is not high. In less high-risk groups, the use of vitamin E appears to reduce the risk of heart disease. However, while consumption of food rich in vitamin E may reduce the risk of coronary heart disease in middle-aged to older men and women, using vitamin E supplements also appears to result in an increase in total mortality, heart failure, and hemorrhagic stroke. The American Heart Association therefore recommends the consumption of food rich in antioxidant vitamins and other nutrients, but does not recommend the use of vitamin E supplements to prevent cardiovascular disease. In other diseases, such as Alzheimer's, the evidence on vitamin E supplementation is also mixed. Since dietary sources contain a wider range of carotenoids and vitamin E tocopherols and tocotrienols from whole foods, ex post facto epidemiological studies can have differing conclusions than artificial experiments using isolated compounds. The nitrone radical scavenger NXY-059 was investigated for acute ischemic stroke, but a large phase III trial failed to confirm its efficacy.

The USDA removed the table showing the Oxygen Radical Absorbance Capacity (ORAC) of Selected Foods Release 2 (2010) table due to the lack of evidence that the antioxidant level present in a food translated into a related antioxidant effect in the body.

Metal catalysts

Metals such as iron, copper, chromium, vanadium, and cobalt are capable of redox cycling in which a single electron may be accepted or donated by the metal. This action catalyzes production of reactive radicals and reactive oxygen species. The presence of such metals in biological systems in an uncomplexed form (not in a protein or other protective metal complex) can significantly increase the level of oxidative stress. These metals are thought to induce Fenton reactions and the Haber-Weiss reaction, in which hydroxyl radical is generated from hydrogen peroxide. The hydroxyl radical then can modify amino acids. For example, meta-tyrosine and ortho-tyrosine form by hydroxylation of phenylalanine. Other reactions include lipid peroxidation and oxidation of nucleobases. Metal-catalyzed oxidations also lead to irreversible modification of arginine, lysine, proline, and threonine. Excessive oxidative-damage leads to protein degradation or aggregation.

The reaction of transition metals with proteins oxidized by reactive oxygen or nitrogen species can yield reactive products that accumulate and contribute to aging and disease. For example, in Alzheimer's patients, peroxidized lipids and proteins accumulate in lysosomes of the brain cells.

Origin of eukaryotes

The great oxygenation event began with the biologically induced appearance of oxygen in the Earth's atmosphere about 2.45 billion years ago. The rise of oxygen levels due to cyanobacterial photosynthesis in ancient microenvironments was probably highly toxic to the surrounding biota. Under these conditions, the selective pressure of oxidative stress is thought to have driven the evolutionary transformation of an archaeal lineage into the first eukaryotes. Oxidative stress might have acted in synergy with other environmental stresses (such as ultraviolet radiation and/or desiccation) to drive this selection. Selective pressure for efficient repair of oxidative DNA damages may have promoted the evolution of eukaryotic sex involving such features as cell-cell fusions, cytoskeleton-mediated chromosome movements and emergence of the nuclear membrane. Thus, the evolution of meiotic sex and eukaryogenesis may have been inseparable processes that evolved in large part to facilitate repair of oxidative DNA damages.

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Hispanic paradox

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

The Hispanic paradox is an epidemiological finding that Hispanic Americans tend to have health outcomes that paradoxically are comparable to, or in some cases better than, those of their U.S. non-Hispanic White counterparts, even though Hispanics have lower average income and education, higher rates of disability, as well as a higher incidence of various cardiovascular risk factors and metabolic diseases.

Low socioeconomic status is almost universally associated with worse population health and higher death rates everywhere in the world. The paradox usually refers in particular to low mortality among Hispanics in the United States relative to non-Hispanic Whites. According to the Centers for Disease Control's 2015 Vital Signs report, Hispanics in the United States had a 24% lower risk of mortality, as well as lower risk for nine of the fifteen leading causes of death as compared to Whites.

Researchers attribute the phenomenon to the cultural values, interpersonal context, and community context of the Hispanic population. Hispanics tend to be less stressed economically, since they tend to compare themselves to individuals in their country of origin. There is also strong social and communal support in Hispanic communities, especially for elders. Some health researchers attribute the Hispanic paradox to different eating habits, especially the relatively high intake of legumes such as beans and lentils.

Statistical biases such as the "salmon bias", which suggests that Hispanics tend to return to their country of origin towards the end of their lives, or the "healthy migrant bias", which assumes that the healthiest and strongest members of a population are most likely to migrate, have been largely refuted by researchers.

Since the 2010s, research has indicated that the Hispanic paradox is disappearing, as Latino mortality increases relative to white Americans, and cardiovascular risk factors are increasing in the Hispanic population. In 2023, a study found that the mortality advantage of Hispanics was largely erased during the COVID-19 pandemic, during which Hispanic death rates disproportionately increased.

History

Life expectancy in the US by race, 2006 to 2024.

First coined as the Hispanic Epidemiological Paradox in 1986 by Kyriakos Markides, the phenomenon is also known as the Latino Epidemiological Paradox. According to Markides, a professor of sociomedical sciences at the University of Texas Medical Branch in Galveston, this paradox was ignored by past generations, but is now "the leading theme in the health of the Hispanic population in the United States."

The specific cause of the phenomenon is poorly understood, although the decisive factor appears to be place of birth. It appears that the Hispanic paradox cannot be explained by either the "salmon bias hypothesis" or the "healthy migrant effect", two theories that posit low mortality among immigrants due to, respectively, a possible tendency for sick immigrants to return to their home country before death and a possible tendency for new immigrants to be unusually healthy compared to the rest of their home-country population. Historical differences in smoking habits by ethnicity and place of birth may explain much of the paradox, at least at adult ages.

Others have proposed that the lower mortality of Hispanics could reflect a slower biological aging rate of Hispanics. Some believe that there is no Hispanic paradox, and that inaccurate counting of Hispanic deaths in the United States leads to an underestimate of Hispanic mortality.

Statistical findings

Percentage surviving to certain ages in the US in 2024 by Hispanic origin and race for male and for female
 
Probability of dying at various ages in the US in 2024 by Hispanic origin and race for male and for female

Mortality

Despite having lower socioeconomic status, higher rates of disability, obesity, cardiovascular disease and type 2 diabetes, most Hispanic groups, excepting Puerto Ricans, demonstrate lower or equal levels of mortality to their non-Hispanic White counterparts. The Centers for Disease Control reported in 2003 that Hispanic's mortality rate was 25 percent lower than non-Hispanic whites and 43 percent lower than African Americans. This mortality advantage most commonly found among middle-aged and elderly Hispanics. The death rates of Hispanics to non-Hispanic whites was found to exceed 1.00 in the twenties, decreases by age 45, then is severely reduced to 0.75–.90 by at age 65, persisting until death. When controlling for socioeconomic factors, the health advantage gap for Mexican Americans, the largest Hispanic population in the US, increases noticeably.

Hispanics do not have a mortality advantage over non-Hispanic Whites in all mortality rates. In 1999, they had higher rates for mortality from liver disease, cervical cancer, AIDS, homicide (males), and diabetes.

Infant mortality

Another important indicator of health is the infant mortality rate, which is also either equal to or lower than that of non-Hispanic Americans. A 2007 study by Hummer, et al. found that infants born to Mexican immigrant women in the United States have about a 10 percent lower mortality in the first hour, first day, and first week than that of infants born to non-Hispanic white, U.S.-born women. In 2003, the national Hispanic infant mortality rate was 5.7, nearly equal to that of non-Hispanic white Americans and 58 percent lower than that of African Americans.

In 2014, the children of Mexican immigrant women had a lower infant mortality rate than that of U.S.-born Mexican-American women, even though the latter population usually has a higher income and education, and are much more likely to have health insurance.

Reasons for the paradox

Socio-economic factors

According to Alder and Estrove (2006), the more socioeconomically advantaged individuals are, the better their health. Access to health insurance and preventative medical services are one of the main reasons for socioeconomic health disparities. Economic hardship within the household can cause distress and affect parenting, causing health problems among children leading to depression, substance abuse, and behavior problems. Low socioeconomic status is correlated with increased rates of morbidity and mortality. Mental health disorders are an important health problem for those of low socioeconomic status; they are two to five times more likely to develop a diagnosable disorder than those of high socioeconomic status, and are more likely to face barriers to getting treatment. This lack of treatment for mental disorders can affect educational and employment opportunities and achievement.

Residential segregation

Important to the understanding of migrant community health is the increasingly stratified American society, manifested in residential segregation. Beginning in the 1970s, the low to moderate levels of income segregation in the United States began to degrade. As the rich became richer, so did their neighborhoods. This trend was inversely reflected in the poor, as their neighborhoods became poorer. As sociologist Douglas Massey explains, "As a result, poverty and affluence both became more concentrated geographically."

In 2009, Professor of public administration and economics John Yinger wrote that "one way for poor people to win the spatial competition for housing is to rent small or low-quality housing." However, he continues, low-quality housing often features serious health risks such as lead paint and animal pests. Though lead-based paint was deemed illegal in 1978, it remains on the walls of older apartments and houses, posing a serious neurological risk to children. Asthma, a possible serious health risk, also has a clear link to poverty. Asthma attacks have been associated with certain aspects of poor housing quality such as the presence of cockroaches, mice, dust, dust mites, mold, and mildew. The 1997 American Housing Survey found that signs of rats or mice are almost twice as likely to be detected in poor households as in non-poor households.

Cultural values

Speculation of a sociocultural advantage stems from the idea that many traditional Hispanic cultural values are protective in health. One such value is that of simpatia, a drive toward social harmony, which may serve to ameliorate social conflict and the negative stress-related health implications that come with it. Familismo (family-centeredness) and allocentrismo (valuing the group) are both values which emphasize the needs of the group in accordance to those of the individual.

Respeto is another familial value in which family members are largely invested in care of their elders. Emphasis on family attachment in the Latino culture is believed to foster social cohesion and a sturdy social support network, which is protective of health during adverse circumstances. Familial support has been associated with higher likelihood of taking preventative health measures and of seeking medical attention when ill. Overall psychological and physical well-being has been found to be better in individuals who come from a supportive family than those who experience family conflict, which is why the family-centered culture of Hispanics may be advantageous in health.

Interpersonal context

Social comparison theory

Social comparison theory proposes that individuals make comparisons with others, most often those of a similar group, to evaluate their own well-being and worth. The psychological implications that these comparisons present depend on the nature of the comparisons. Upward comparisons often result in negative psychological effects due to feelings of disadvantage when being compared to those higher in the hierarchy. Conversely, lateral and downward comparisons often result in satisfaction when one sees himself as better off than those lower in the hierarchy.

Latino Americans and noncitizen Latinos are expected to make lateral or downward comparisons, either to other low-economic status Latinos and/or to relatives and friends in their home country. Such downward comparisons would result in boosted self-esteem and less psychological stress, resulting in better health.

Social networks and support

Social capital is thought to be a significant moderator in the advantageous health outcomes of Latinos. It has been found that the magnitude of the effect of social integration on mortality is greater than smoking fifteen cigarettes a day. Characteristic values of Latino culture such as familismo and allocentrismo contribute to greater social cohesion and social support networks. This tight social fabric is a mechanism which fosters resilience through social support. Resilience is the ability to adapt to a disadvantageous experience and high resilience is protective in health.

Hypotheses

Barrio advantage

One hypothesis for the Hispanic paradox proposes that living in the same neighborhood as people with similar ethnic backgrounds confers significant advantages to one's health. In a study of elderly Mexican-Americans, those living in areas with a higher percentage of Mexican-Americans had lower seven-year mortality as well as a decreased prevalence of medical conditions, including stroke, cancer, and hip fracture. Despite these neighborhoods' relatively high rates of poverty due to lack of formal education and a preponderance of low paying service sector jobs, residents do not have the same mortality and morbidity levels seen in similarly disadvantaged socioeconomic neighborhoods.

These neighborhoods have intact family structures, community institutions, and kinship structures that span households, all of which are thought to provide significant benefits to an individual's health. These social network support structures are especially important to the health of the elderly population as they deal with declining physical function. Another reason for this phenomenon could be that those Hispanic-Americans that live among those of similar cultural and social backgrounds are shielded from some of the negative effects of assimilation to American culture.

Characteristics of the community in which one lives can also affect health. Latino immigrants living in communities with a large proportion of Latinos experience better health than immigrants who live in communities with a smaller proportion of Latinos. This is thought to be at least in part due to greater levels of social ties within majority-Latino communities which have been associated with greater social integration and social support. While strong family ties definitively promote psychological and physical well-being, weaker ties such as those formed with other members of the community are thought to have similar health-promoting effects.

High collective efficacy, trust within the community which engenders mutually beneficial action, within Latino communities has also been shown to be protective of health, particularly in ameliorating asthma and breathing problems. Better health outcomes for those living in communities with a high proportion of Latinos have been hypothesized to result from increased information exchange facilitated through a common language and ethnicity, as well as from benefits conferred through greater social support within the community.

Acculturation

Acculturation, a phenomenon whereby individuals internalize habits and beliefs of a new culture upon being immersed in its social institutions, is also believed to influence the health of Latinos in the United States. In this case, acculturation of Latino immigrants would mean the relinquishment of the characteristic sociocultural aspects of Latino culture listed above in favor of characteristics which are more representative of the American lifestyle. Research has given mixed results regarding the idea that the health of Latino immigrants worsen as length of stay in the United States increases.

As Latinos adopt American tendencies, for example, it is thought that the strong social support networks of tight-knit Latino communities are eroded, and the resulting stress begets worse health outcomes. On the other hand, greater acculturation to the United States has been associated with worsening in some health behaviors, including higher rates of smoking and alcohol use, but improvement in others, such as physical activity.

Measurements of acculturation, such as length of time in the United States, proportion of Latino friends, and language use are proxy measures and as such are not completely precise. It is possible that confounding factors such as socioeconomic status influence the mixed effects of acculturation seen in health outcomes and behaviors.

The extent of a Hispanic American's acculturation in the United States, or their assimilation to mainstream American culture, is relative to his or her health. One of the main negative effects of acculturation on health has been on substance abuse. More assimilated Latinos have higher rates of illicit drug use, alcohol consumption, and smoking, especially among women. Another negative effect of acculturation is changes in diet and nutrition. More acculturated Latinos eat fewer/less fruits, vegetables, vitamins, fiber and protein and consume more fat than their less acculturated counterparts.

One of the most significant impacts of acculturation on Latino health is birth outcomes. Studies have found that more acculturated Latinas have higher rates of low birthweight, premature births, teenage pregnancy and undesirable prenatal and postnatal behaviors such as smoking or drinking during pregnancy, and lower rates of breastfeeding. Acculturation and greater time in the United States has also been associated with negative mental health impacts. US-born Latinos or long-term residents of the United States had higher rates of mental illness than recent Latino immigrants.

Foreign-born Mexican Americans are at significantly lower risk of suicide and depression than those born in the United States. The increased rates of mental illness is thought to be due to increased distress associated with alienation, discrimination and Mexican Americans attempting to advance themselves economically and socially stripping themselves of traditional resources and ethnically based social support.

Healthy migrant effect

The "healthy migrant effect" hypothesizes that the selection of healthy Hispanic immigrants into the United States is reason for the paradox. International immigration statistics demonstrate that the mortality rate of immigrants is lower than in their country of origin. In the United States, foreign-born individuals have better self-reported health than American-born respondents. Hispanic immigrants have better health than those living in the US for a long amount of time.

Salmon Bias

A second popular hypothesis, called the "Salmon Bias", attempts to factor in the occurrence of returning home. This hypothesis purports that many Hispanic people return home after temporary employment, retirement, or severe illness, meaning that their deaths occur in their native land and are not taken into account by mortality reports in the United States. This hypothesis considers those people as "statistically immortal" because they artificially lower the Hispanic mortality rate.

Certain studies hint that it could be reasonable. These studies report that though return migration, both temporary and permanent, depend upon specific economic and social situations in communities, up to 75 percent of households in immigrant neighborhoods do some kind of return migration from the U.S. However, Abraido-Lanza, et al. found in 1999 that the "Salmon Hypothesis" cannot account for the lower mortality of Hispanics in the US because, according to their findings, the Hispanic paradox is still present when non-returning migrants are observed (e.g. Cubans).

Slow biological aging

Horvath et al. (2013) have proposed that the lower mortality of Hispanics could reflect a slower biological aging rate of Hispanics. This hypothesis is based on the finding that blood and saliva from Hispanics ages more slowly than that of non-Hispanic whites, African Americans, and other populations according to a biomarker of tissue age known as epigenetic clock.

Comparison with other ethnicities

One of the most important aspects of this phenomenon is the comparison of Hispanics' health to non-Hispanic African Americans' health. Both the current and historical poverty rates for Hispanic and non-Hispanic African American populations in the United States are consistently starkly higher than that of non-Hispanic white and non-Hispanic Asian Americans. Dr. Hector Flores explains that "You can predict in the African–American population, for example, a high infant-mortality rate, so we would think a [similar] poor minority would have the same health outcomes." However, he said, the health poor outcomes are not present in the Hispanic population. For example, the age-adjusted mortality rate for Hispanics living in Los Angeles County was 52 percent less than the blacks living in the same county.

Comparison to non-Hispanic white Americans

Although Hispanic Americans are twice more likely to be living under the poverty line and three times more likely to not have health insurance than non-Hispanic white Americans, they have a longer life span than them by 3 years. More Hispanics, than any other racial group, are uninsured and are in general less likely to use medical care. The median life span of Hispanic Americans is an average of 81.8 years and non-Hispanic white Americans have an average of 78.8 years. This could be explained from scientist taking DNA samples from multiple ethnic groups, the blood from Latino aged more slowly than any other group.

In 2012, new cancer cases of all sites among Hispanic men and Non-Hispanic men had a ratio of 0.7, Hispanic men having 362.2 and Non-Hispanic men having 489.9. In comparison to non-Hispanic Whites, Hispanic men are 10 percent less likely to be diagnosed with prostate cancer. Hispanic women, compared to NHW, were found to be 30 percent less likely to be diagnosed with breast cancer.

21st century waning of the paradox

Since the 21st century, a number of studies have published results which contradict the Hispanic paradox, suggesting that the health status of Hispanic Americans is declining. These findings include a higher incidence of cardiovascular disease risk factors among Hispanics, higher rates or obesity, increasing deaths from stroke even as white deaths remain stable, and a larger increase in deaths from heart failure.

Other researchers have predicted that the paradox will disappear as obesity rates rise rapidly among Hispanic males, in particular. A 2023 study published found that the Hispanic mortality advantage had been erased by the COVID-19 pandemic. Hispanic death rates increased at a much higher rate than White Americans death rates, during this period.

Criticism

Some public health researchers have argued that the Hispanic paradox is not actually a national phenomenon in the United States. In 2006, Smith and Bradshaw argued that no Hispanic paradox exists. They maintain that life expectancy was nearly equal for non-Hispanic White and Hispanic females, but less close for non-Hispanic White and Hispanic males.

In 2007, Turra and Goldman argued that the paradox is concentrated among the foreign born from specific national origins, and is only present in those of middle to older ages. At younger ages, they explain, deaths are highly related to environmental factors such as homicides and accidents. Deaths at older ages, they maintain, are more related to detrimental health-related behaviors and health status at younger ages. Therefore, immigration-related processes only offer survival protection to those at middle and older ages; the negative impact of assimilation into poor neighborhoods is higher on the mortality of immigrants at a younger age.

In contrast, Palloni and Arias in 2004 hypothesized that this phenomenon is most likely caused by across-the-board bias in underestimating mortality rates, caused by ethnic misidentification or an overstatement of ages. These errors could also be related to mistakes in matching death records to the National Health Interview Survey, missing security numbers, or complex surnames.

Although it may not mean progress for all Hispanics, as of 2019, some Hispanic migrants' lifestyles were drastically improving within the United States due to Latino unemployment being at an all-time low of 4.2%. The low unemployment rates have enabled families to have multiple streams of income by individuals working more than one job.

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