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What evolutionary reason is there for hemolytic disease?

What evolutionary reason is there for hemolytic disease?


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Nowawadays we have methods which allow us to overcome hemolytic disease of newborn or to prevent it to onset. The Rh or Kell conflict, but how is it possible that it is present? Why it haven't disappear due to natural selection?

A hemolytic disease occurs for example when mother have Rh- and the unborn child have Rh+ after his father. Then when the blood of the child gets to mother circulatory system she creates anti-Rh+ antybodies which will attack and eventually kill her next baby with Rh+. Thus we can assume that hemolytic disease is genetically dependent and cause lethal effect.

So i'm looking for any explanation. I know, that there can be none, i'm just asking.


Hemolytic disease is not a genetic disease. It is a drawback of how the immune system works. In general, the overall benefits of having the immune system as it is right now are way higher than sporadic disadvantages, like the Hemolytic disease, that is why it is not counter selected. If instead of being a rare condition it would be a common one, then I would expect it to be indeed counter selected.


Evidence of biological basis for religion in human evolution

An Auburn University researcher teamed up with the National Institutes of Health to study how brain networks shape an individual's religious belief, finding that brain interactions were different between religious and non-religious subjects.

Gopikrishna Deshpande, an assistant professor in the Department of Electrical and Computer Engineering in Auburn's Samuel Ginn College of Engineering, and the NIH researchers recently published their results in the journal, "Brain Connectivity."

The group found differences in brain interactions that involved the theory of mind, or ToM, brain network, which underlies the ability to relate between one's personal beliefs, intents and desires with those of others. Individuals with stronger ToM activity were found to be more religious. Deshpande says this supports the hypothesis that development of ToM abilities in humans during evolution may have given rise to religion in human societies.

"Religious belief is a unique human attribute observed across different cultures in the world, even in those cultures which evolved independently, such as Mayans in Central America and aboriginals in Australia," said Deshpande, who is also a researcher at Auburn's Magnetic Resonance Imaging Research Center. "This has led scientists to speculate that there must be a biological basis for the evolution of religion in human societies."

Deshpande and the NIH scientists were following up a study reported in the Proceedings of the National Academy of Sciences, which used functional magnetic resonance imaging, or fMRI, to scan the brains of both self-declared religious and non-religious individuals as they contemplated three psychological dimensions of religious beliefs.

The fMRI -- which allows researchers to infer specific brain regions and networks that become active when a person performs a certain mental or physical task -- showed that different brain networks were activated by the three psychological dimensions however, the amount of activation was not different in religious as compared to non-religious subjects.


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1. What is evolutionary medicine?
How I look forward to the day when no one needs to ask! Evolutionary medicine, sometimes called Darwinian medicine, is the field at the intersection of evolution and medicine. Evolution AND Medicine is a better descriptor, but that has not caught on. The field uses the basic science of evolutionary biology to find ways to prevent and treat disease, and it uses studies of disease to advance basic evolutionary biology(2).

2. What isn’t evolutionary medicine?
Evolutionary medicine is not radical or alternative. It is not a special kind of medical practice. It does not advocate any particular kind of diet, exercise, or treatment. It does not make direct clinical recommendations based on theory alone (3). If your doctor claims to practice evolutionary medicine, be sure that treatment recommendations are based on controlled scientific studies if they come directly from theory, find a better doctor. Evolutionary medicine is standard mainstream medical science, appropriately cautious about making clinical recommendations.

3. How does evolutionary medicine transform our understanding of disease?
Evolutionary medicine poses a fundamentally new kind of question about disease. Instead of only asking how bodies work and why some people get sick, evolutionary medicine also asks why natural selection has left all of us with traits that make us vulnerable to disease (1). Why do we have wisdom teeth, narrow coronary arteries, a narrow birth canal, and a food passage that crosses the windpipe? Evolution explains why we have traits that leave us vulnerable to disease, as well as why so many other aspects of the body work so well. For instance, the usual question about back pain is why it afflicts some individuals. Evolutionary medicine also asks why back problems have been a problem for all hominid species since they first walked on two legs.

4. Is evolutionary medicine mainly about diseases caused by our modern environments?
Most chronic disease results because our bodies are poorly prepared to stay healthy in modern environments(4), but this is only one of several evolutionary explanations for why we get sick(5). Vulnerability to infections persists because pathogens evolve so quickly. Not all deleterious mutations can be eliminated because there are limits to what natural selection can do. Other vulnerabilities result from inevitable tradeoffs, including the big one of maximizing reproduction even when that harms health. Also, selection has shaped many defenses, such as inflammation, whose utility comes at a substantial cost in tissue damage and suffering. These are not alternatives to standard medical explanations, they are complementary deeper explanations.

5. Is evolutionary medicine only about vulnerabilities?
No, questions about vulnerability are only one part of evolutionary medicine. Some scientists use DNA evidence to trace the evolutionary history of humans and pathogens. Some use evolution to discover new ways to prevent resistance to antibiotics and cancer chemotherapy drugs. Others study why selection cannot remove some genetic variations that cause disease. Evolutionary medicine includes all aspects of evolutionary biology applied to all problems in medicine and public health.

6. Evolutionary medicine shows how diseases are useful, right?
Wrong. Diseases are not adaptations shaped by selection. There is nothing useful about pneumonia, schizophrenia, epilepsy, or cancer. Trying to understand diseases as if they are adaptations is a mistake, one that is unfortunately as common as it is serious (6). However, many symptoms of disease, such as pain, fever, vomiting, cough, and fatigue, are adaptations. The systems that regulate such defenses are, for good evolutionary reasons, prone to failures that cause chronic pain, anxiety disorders, and many other diseases.

7. Is evolutionary medicine useful?
It sure is! Some applications are relatively direct — doctors who understand how selection shaped regulation mechanisms can make better decisions about when it is safe to use drugs to block fever and cough(2,3). However, like genetics and microbiology, evolution is a basic science that mainly provides new understanding that lead to new treatments(1,7,8). Evolutionary models that analyze the evolutionary competition between cells in a malignancy have led to new chemotherapy strategies that greatly extend the lives of mice with cancer(9). Models of antibiotic resistance suggest that “take every pill in the bottle” may be bad advice(10). We must find out what in our modern environment is causing the new epidemic of autoimmune diseases like diabetes, multiple sclerosis, and Crohn’s disease(11).

8. Don’t most doctors already know all about evolution?
No, most doctors would likely fail the midterm in an introductory evolution class(13,14). Even medical leaders often have gross misconceptions. A famous geneticist once suggested at a big Darwin meeting that selection keeps mutations happening for the good of the species, an idea has been recognized as a mistake for 50 years. The belief that long association with a host makes viruses milder remains common among physicians, decades after Paul Ewald and others pointed out that selection maximizes transmission of pathogens even if that kills the host. Engineers learn the principles of thermodynamics so they don’t make mistakes like trying to build perpetual motion machines. Doctors never learn the principles of evolutionary biology, so major misconceptions persist in medicine(15).

9. Why don’t medical schools teach evolution the same way they teach other sciences?
Most medical schools have no evolutionary biologists on faculty, few doctors who know much about evolution, and some who think bodies are products of intelligent design. Even the core idea that evolutionary explanations are needed to complement descriptions of mechanisms is unfamiliar to most doctors. Some display their naiveté of methods for testing evolutionary hypotheses by spouting the phrase “just so stories,” as if that is a devastating critique. Some actually teach “just so stories.” That evolution in the medical curriculum remains in the 19th century is shameful.

10. How long will it take for medicine and public health to make full use of evolutionary biology?

Progress is now rapid(16). The International Society for Evolution, Medicine and Public Health has created a network of evolutionarily sophisticated researchers, educators, and clinicians, and new education resources, including EvMedEd.org. Several new textbooks are available (8,17,18) along with a new journal, Evolution, Medicine, & Public Health, and The Evolution and Medicine Review. The evolution questions recently added to medical school entrance examinations are spurring enrollment in evolution courses. Students who have taken an undergraduate evolutionary medicine course are arriving at medical school full of new questions. They will grow up to be medical school deans. When they do, evolutionary biology will finally be recognized widely as an essential basic science for medicine.

Literature Cited

1. Nesse RM, Williams GC. Why we get sick : the new science of Darwinian medicine. 1st Vintage Books. New York: Vintage Books 1996. xi, 290 p.

2. Nesse RM, Stearns SC. The great opportunity: Evolutionary applications to medicine and public health. Evol Appl. 20081(1):28–48.

3. Nesse RM. Ten questions for evolutionary studies of disease vulnerability. Evol Appl [Internet]. 20114(2):264–77. Available from: http://dx.doi.org/10.1111/j.1752-4571.2010.00181.x

4. Gluckman PD, Hanson M. Mismatch: why our world no longer fits our bodies. New York: Oxford University Press, USA 2006.

5. Nesse RM. Maladaptation and natural selection. Q Rev Biol [Internet]. 2005 Mar80(1):62–70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15884737

6. Nesse RM. Ten questions for evolutionary studies of disease vulnerability. Evol Appl [Internet]. 20114(2):264–77. Available from: http://dx.doi.org/10.1111/j.1752-4571.2010.00181.x

7. Stearns SC. Evolutionary medicine: its scope, interest and potential. Proc Biol Sci [Internet]. 2012 Nov 7279(1746):4305–21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22933370

8. Stearns SC, Medzhitov R. Evolutionary medicine. Sunderland, MA: Sinauer Associates, Inc., Publishers 2016.

9. Gatenby RA, Silva AS, Gillies RJ, Frieden BR. Adaptive therapy. Cancer Res [Internet]. 2009 [cited 2016 Jun 3]69(11):4894–903. Available from: http://cancerres.aacrjournals.org/content/69/11/4894.short

10. Read AF, Day T, Huijben S. The evolution of drug resistance and the curious orthodoxy of aggressive chemotherapy. Proc Natl Acad Sci. 2011108(Supplement 2):10871–7.

11. Blaser MJ. Missing microbes: how the overuse of antibiotics is fueling our modern plagues [Internet]. Macmillan 2014 [cited 2016 Jun 3]. Available from: https://books.google.com/books?hl=en&lr=lang_en&id=iB5OAwAAQBAJ&oi=fnd&p.

12. Nesse RM. Natural Selection and the Regulation of Defenses: A Signal Detection Analysis of the Smoke Detector Principle. Evol Hum Behav. 200526:88–105.

13. Nesse RM, Schiffman JD. Evolutionary Biology in the Medical School Curriculum. Bioscience. 200353(6):585–7.

14. Hidaka BH, Asghar A, Aktipis CA, Nesse RM, Wolpaw TM, Skursky NK, et al. The status of evolutionary medicine education in North American medical schools. BMC Med Educ [Internet]. 2015 [cited 2016 Feb 1]15(1):1. Available from: http://bmcmededuc.biomedcentral.com/articles/10.1186/s12909-015-0322-5

15. Antolin MF, Jenkins KP, Bergstrom CT, Crespi BJ, De S, Hancock A, et al. Evolution and medicine in undergraduate education: a prescription for all biology students. Evolution [Internet]. 2012 Jun66(6):1991–2006. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22671563

16. Nesse RM, Bergstrom CT, Ellison PT, Flier JS, Gluckman P, Govindaraju DR, et al. Making evolutionary biology a basic science for medicine. Proc Natl Acad Sci USA [Internet]. 2010 Jan 26107 Suppl 1:1800–7. Available from: www.pnas.org/cgi/doi/10.1073/pnas.0906224106

17. Perlman RL. Evolution and medicine. First edition. Oxford, United Kingdom: Oxford University Press 2013. 162 p.

18. Gluckman P, Beedle A, Hanson M. Principles of Evolutionary Medicine. Oxford, UK: Oxford University Press 2009.

19. Kruger DJ, Nesse RM. An Evolutionary Life-History Framework for Understanding Sex Differences in Human Mortality Rates. Hum Nat. 200617(1):74–97.


Prognosis Prognosis

If you need medical advice, you can look for doctors or other healthcare professionals who have experience with this disease. You may find these specialists through advocacy organizations, clinical trials, or articles published in medical journals. You may also want to contact a university or tertiary medical center in your area, because these centers tend to see more complex cases and have the latest technology and treatments.

If you can’t find a specialist in your local area, try contacting national or international specialists. They may be able to refer you to someone they know through conferences or research efforts. Some specialists may be willing to consult with you or your local doctors over the phone or by email if you can't travel to them for care.

You can find more tips in our guide, How to Find a Disease Specialist. We also encourage you to explore the rest of this page to find resources that can help you find specialists.


What evolutionary reason is there for hemolytic disease? - Biology

Huntington's Chorea: Evolution and Genetic Disease

How is it possible that such a devastating genetic disease is so common in some populations? Shouldn't natural selection remove genetic defects from human populations? Research on the evolutionary genetics of this disease suggests that there are two main reasons for the persistence of Huntington's in human populations: mutation coupled with weak selection.

The diagram at left shows how the Huntington's allele is passed down. Since it is the dominant allele, individuals with just one parent with Huntingtons's chorea have a 50-50 chance of developing the disease themselves.

Mutation
In 1993, a collaborative research group discovered the culprit responsible for Huntington's: a stretch of DNA that repeats itself over and over again, CAGCAGCAGCAG. and so on. People carrying too many CAGs in the Huntington's gene (more than about 35 repeats) develop the disease. In most cases, those affected by Huntington's inherited a disease-causing allele from a parent. Others may have no family history of the disease, but may have new mutations which cause Huntington's.

If a mutation ends up inserting extra CAGs into the Huntington's gene, new Huntington's alleles may be created. Of course it's also possible for a mutation to remove CAGs. But research suggests that for Huntington's, mutation is biased additions of CAGs are more likely than losses of CAGs.

Selection
As though that weren't bad enough, Huntington's belongs to a class of genetic diseases that largely escape natural selection. Huntington's is often "invisible" to natural selection for a very simple reason: it generally does not affect people until after they've reproduced. In this way, the alleles for late-onset Huntington's may evade natural selection, "sneaking" into the next generation, despite its deleterious effects. Early-onset cases of Huntington's are rare these are an exception, and are strongly selected against.

Dr. Nancy Wexler (shown at right tracking geneologies) has been studying the remarkably high frequency of Huntington's in Lake Maracaibo since the 1970s. She has found that the high incidence of this disease there is explained by an evolutionary event called the founder effect. About 200 years ago, a single woman who happened to carry the Huntington's allele bore 10 children — and today, many residents of Lake Maracaibo trace their ancestry (and their disease-causing gene) back to this lineage. A simple fluke of history, high-birth rates, and weak selection are responsible for the genetic burden shouldered by this population.

Solutions?


Comparing the banding patterns in a genetic test can tell researchers whether a person carries an allele that is likely to cause Huntington's.
Currently, physicians don't have any cures for Huntington's disease — there's no miracle pill that will stop the progress of the disease. However, understanding the evolutionary history of the disease — a recurrent mutation that is often "missed" by natural selection — points out a way to reduce the frequency of the disease in the long term: allowing people to make more informed reproductive choices.

Today, genetic testing can identify people who carry a Huntington's allele long before the onset of the disease and before they have made their reproductive choices. The genetic test that identifies the Huntington's allele works sort of like DNA fingerprinting. A DNA sample is copied and cut into pieces. The pieces are then spread out on a gel (see right). The banding pattern can tell researchers whether a person carries an allele that is likely to cause Huntington's.

Having this information could allow people to make more-informed reproductive decisions. For example, at Lake Maracaibo, researchers and health workers have tried to make contraception available to the local population so that they can make reproductive choices based on their own family history with the disease. But whatever people eventually decide to do with this knowledge, a deep understanding of the disease would not be possible without the historical perspective offered by evolution.

Photo of Venezuelan familiy © 1983 by Steve Uzzell Dr. Wexler photo © 1986 by Steve Uzzell


NON-ADAPTIVE EVOLUTION INDUCED BY THE RELAXATION OF NATURAL SELECTION

The primary rationale for arguing that human evolution has stopped is that human culture has relaxed or even completely eliminated natural selection on certain traits. What is not generally appreciated is that the relaxation of selection on one trait can actually lead to its evolution by natural selection on other traits. All too often traits are regarded one-by-one, as if each trait could evolve independently of all other traits. However, the biological reality is that traits are correlated through developmental processes, pleiotropic genetic effects, and physiological connections. Consequently, it is commonplace that evolution of one trait induces correlated evolution on another trait. If the nature of these inherent correlations are known or estimated, then one test for natural selection on a set of traits is that they violate these inherent correlations over evolutionary time. If one trait is evolving due to natural selection, but a second trait is no longer being selected, selection on the first trait is expected to cause evolutionary change at the second trait in a manner consistent with the inherent correlations.

For example, there is no controversy that the human lineage has been strongly selected for increased brain size over the past 2 million years,38 and that one of the primary driving forces for this evolution of brain size has been our increasing use of learned culture as a means of dealing with the environment and social interactions. As the cultural sophistication of the human lineage increased, it perhaps did indeed reduce or eliminate selection on some traits. For example, most animals adapt to their diet through their teeth and jaws, but humans increasingly used tools and fire to prepare their food, thereby reducing the importance of jaw and tooth evolution as a means of adapting to the dietary environment.

Ackerman and Cheverud39 tested the hypotheses of selected versus neutral evolution of human teeth and jaws by comparing various hominid fossil measurements to the expected correlations among relative brain size, tooth size, and jaw size as inferred from modern-day humans, chimpanzees and gorillas, which all have remarkably similar developmental correlations for these traits. The results are shown in Figure 1 . At the base of this figure is a skull of a gracile australopithecine, and stemming off that ancestral form are two lineages. The lineage on the left represents the robust australopithecines, and the lineage on the right is the one that led to modern humans. The arrows indicating the lineages are shaded to indicate the strength of the estimated selection on the face (mostly teeth and jaws measurements), such that the darker the shading, the more intense the selection. As can be seen, the robust australopithecine lineage was subject to very intense natural selection on their faces, indicating that they primarily adapted to their dietary environment through adaptive evolution of the teeth and jaws. In contrast, in the lineage leading to modern humans, the intensity of selection on the face diminishes with time, and by 1.5 million years ago there is no longer any detectable selection on human teeth and jaws. Ackerman and Cheverud39 interpreted this as being consistent with the hypothesis that cultural evolution in the human lineage had indeed eliminated natural selection on human teeth and jaws. However, this does not mean that human teeth and jaws have not evolved over the last 1.5 million years. During the last 1.5 million years, there was a large increase in brain size in the human lineage driven by natural selection, and given the developmental constraints common to humans, chimpanzees, and gorillas, human jaws and teeth would continue to evolve as a correlated effect of brain size evolution. In particular, jaws and teeth were predicted to become relatively smaller for our body size as a correlated response to increased brain size, with the jaw becoming relatively smaller more rapidly than the teeth. Hence, the elimination of natural selection directly upon teeth and jaws did not eliminate evolution on these traits because of natural selection for increased brain size. The result of this correlated evolution is that humans have a small, flat face compared to chimpanzees and gorillas, and that our jaws tend to be too small for our teeth, thereby giving rise to the modern profession of orthodontics.

Natural selection on facial characteristics and diversity in early human evolution are shown in a temporal context. The two arrows indicate the robust austra-lopithecine lineage on the left and the lineage leading to modern humans on the right. The darker the shading, the more intense the selection on facial features. Reprinted from Ackermann and Cheverud39 with permission. Copyright (2004) National Academy of Sciences, USA.


Differential Diagnoses (Other Causes of Anemia) in Dogs

It is crucial that the diagnosis of IMHA be confirmed, because there are many causes of anemia other than IMHA. Both treatment and prognosis for these other causes are often quite different that that of IMHA. Other potential cause of anemia include:

  • Blood loss. Bleeding results in anemia, and the site of bleeding may not always be obvious. For example, an animal can lose a tremendous amount of blood through the gastrointestinal tract with the only evidence of bleeding being dark, tarry colored stools.
  • Decreased production of red blood cells. The bone marrow is responsible for producing a continuous supply of new red blood cells. Sometimes this production of new cells falls behind, either due to disease inside the bone marrow or from other diseases with affect the signals or materials needed for production of new red cells. Examples of disease within the marrow might include cancer, toxic damage to the marrow, and infection in the marrow. Examples of other diseases that might affect the production of new red blood cells include kidney failure, iron deficiency, or chronic infections anywhere in the body.
  • Hemolytic anemia is not always due to an immune system attack. Other causes of hemolytic anemia are possible.
    Infection of the red blood cells can lead to hemolytic anemia. Examples of such infections would include Babesiosis or Hemobartonellosis.
  • Certain toxins can lead to hemolytic anemia. The metal zinc and certain foods (like onion and garlic) are examples of such toxins.
  • The mechanical destruction of red blood cells results in hemolytic anemia. Examples would include a twisted spleen, a severe form of heartworm disease in which a clump of worms occludes the major blood vessels, or widespread formation of tiny blood clots (disseminated intravascular coagulation).
  • Certain hereditary diseases result in the formation of abnormal red blood cells. These abnormal cells are more likely to be destroyed, potentially resulting in hemolytic anemia.

A systematic approach to evolutionary medicine

Nesse, together with Williams (Nesse and Williams 1995), and later Stephen Stearns (Nesse and Stearns 2008), has posed the primary question: why has selection and related processes left the human body vulnerable to disease? They identified several major explanatory pathways that, at the most integrated level, can be summarized by three factors: the inability of selection, because of its inherently slow nature, to cope with fast-evolving pathogens or with novel environments the constraints of natural selection and downsides of trade-offs and the potential consequences of selection acting to improve fitness rather than health. Gluckman and colleagues (Gluckman et al. 2009) expanded this categorization to take account of the overlap between evolutionary processes and population genetics, and this is the classification we shall follow here ( Table 1 ).

Table 1

Pathways that mediate the influence of evolutionary processes on disease vulnerability

1Mismatch: exposure to an evolutionarily mismatched or novel environment
2Life history factors
3Excessive defence mechanisms: inappropriate deployment of processes that evolved as an adaptation
4Co-evolutionary considerations: losing the evolutionary arms race against microbes
5Constraints imposed by our evolutionary history
6Sexual selection and its consequences
7Balancing selection maintaining an allele that raises disease risk
8Demographic history and its outcomes

Mismatch

Increased disease risk can emerge, because the individual has been exposed to an environment that is beyond their evolved capacity to adapt, is entirely novel or that poses a challenge. At its simplest level, diabetes mellitus type 2 can be envisaged as the response of the individual to a nutritional environment that gives them a metabolic load beyond their capacity to cope. While there are developmental and genetic factors that influence the adaptive metabolic capacity of an individual, ultimately, it is the exposure to high glycemic foods and a very different mix of macronutrient intakes, which is thought to be the basis of the diabetes epidemic. Even in populations such as the Pima Indian, for which it has been argued that genetic factors are critical for the high incidence of diabetes mellitus type 2, maintenance of higher energy expenditure and more fundamental nutrition in those villages that maintain a traditional subsistence lifestyle is associated with a lower incidence of diabetes (Schulz et al. 2006).

Scurvy can be considered as another example of mismatch. Only some primates, including humans, have lost the capacity to synthesize vitamin C (Chatterjee et al. 1975). It is assumed that the enzyme responsible for its synthesis, L-gulonolactone oxidase, underwent neutral mutations in a frugivorous ancestor and that it was only with exposure to environments without access to fresh fruits—such as extreme famine and sailing ships—that our inability to make vitamin C is exposed.

Myopia, or short-sightedness, is caused by the inappropriate growth of the eyeball in its sagittal dimension, leading to the light being focused in front of the retina. Eyeball growth occurs in childhood and is regulated by growth factors that are induced by light exposure, so that the growth can be affected by the dominant focal length of vision. Close range indoor activities such as reading may result in the tendency of the growing child's eyes to focus at only the distance of a page, and indeed, an association between incidence of myopia and increased education has been noted (Milinski 1999). While there may be a genetic predisposition to myopia in some populations, exposure of children in those populations to the outdoors leads to a lower incidence of this condition (Dirani et al. 2009). Thus, myopia can be seen as a mismatch between the environment in which we evolved—outdoors in natural light𠅊nd the modern day largely indoor life.

Robin Dunbar proposed, from the association between neocortical size and group size across different species of primate, that humans evolved to live in social groups of 100� (Dunbar 2003). There is indeed much evidence in support of that proposition. But humans now live in much larger groups than in the Paleolithic—groups that rely predominantly on verbal or even electronic communication, with less emphasis on the bonding effect of body language. If we add to that the complexity of modern society and its structures compared to those of the Paleolithic or even the modern hunter-gatherer social organizations, it is reasonable to speculate that some forms of mental illness simply reflect individuals living in a social environment beyond their evolved capacity to cope. This is a fertile area for research (Brüne 2008).

With the development of animal husbandry and agriculture and the associated shift to a more concentrated way of living following the invention of agriculture, humans became much more exposed to parasitic loads from each other and proximity to animals. Pandemic influenza outbreaks generally arise from this association. Other infectious patterns reflect the changing environments: the historical distribution of malaria is directly linked to patterns of swamplands and land use. Similarly, increased irrigation following the development of canals in Africa led to a considerable increase in schistosomiasis (Steinmann et al. 2006). The implications of the development of antibiotics are discussed later.

Life history factors

This category combines several related evolutionary concepts that account for how the evolved human life course strategy and changed way of living have led to increased susceptibility to disease. There is necessarily some overlap with the other pathways discussed in this paper, and it includes multiple possible mechanisms such as life history trade-offs and antagonistic pleiotropy however, we find it a useful heuristic for considering a number of evolutionary explanations.

In life history, there are two basic kinds of trade-off that may arise as a result of adaptive developmental responses to environmental influences. The first occurs when such responses are made to confer immediate advantage, such as the early metamorphosis of the tadpole of the spadefoot toad in response to pond desiccation, which promotes immediate survival but results in smaller adult size that is more susceptible to predation. The second type of trade-off arises from responses that result in an advantage that is manifest later, such as the presence of predators inducing the young of the water flea to develop defensive armor in adulthood, the trade-off being a decrease in resources for reproduction. In humans, where intrauterine growth restriction may be viewed as an immediate adaptive response of the fetus for surviving maternal ill-health or placental dysfunction, the fetus may also make anticipatory responses to more subtle nutritional or hormonal cues to adapt its developmental trajectory to the type of environment in which, according to its prediction, it will live postnatally. These ideas, and the adaptive nature of developmental plasticity, have been expounded extensively (Gluckman et al. 2005a,b, 2007, 2010).

Anticipation is common across taxa, but becomes more obvious in a long-lived species such as the human. Whereas the strategy of bet-hedging is used by species with very high reproductive outputs (Beaumont et al. 2009), mammals with their relatively low reproductive outputs and high maternal investment rely on predictive adaptation to enhance offspring fitness. Situations when different strategies between mother and offspring will emerge have been modeled (Marshall and Uller 2007). Humans are at one extreme, and the situations in which maternal fitness will dominate as in some other species do not occur in humans. Even in famine, fecundity is maintained to a degree. Prediction need not be accurate to be selected (Lachmann and Jablonka 1996), and biases may exist in prediction. Because the consequences of predicting a high-nutrition environment and ending up in a low-nutrition environment are worse than the converse, there is a bias towards predicting a lower nutrition environment and, consequently, towards human susceptibility to disease in modern obesogenic environments. This argument is supported by the observation that under conditions of severe undernutrition, children of lower birth weight are more likely to develop the more benign syndrome of marasmus than those of higher birth weight, who develop kwashiorkor (Jahoor et al. 2006). We argue that the marasmic children are better adapted to low nutrition by virtue of their lower birth weight and thus tolerate undernutrition better. This hypothesis is supported by the finding that the marasmic children as adults have a bias in their appetite towards carbohydrate and possibly fat consumption (T. Forrester, unpublished data), analogous to the preference observed in rats that have been prenatally undernourished.

In considering life course factors, it is important to recognize that a cue acting in early life may have different effects from cues acting later. For example, in rats, prenatal undernutrition shortens life while postnatal undernutrition prolongs life (Jennings et al. 1999). Similar biphasic effects are seen for the influence of nutrition and possibly stress on the age of puberty (Sloboda et al. 2009).

There is increasing evidence for the role of developmental plasticity in influencing the susceptibility to developing disease in a particular environment. It has been shown that longevity was affected by the season of birth in the Gambia, an environment in which the weight gain of pregnant women drops from 1500 g/month in the harvest season to just 400 g/month in the hungry season (Moore et al. 1999). Offspring born in the hungry season had the same infant and juvenile mortalities as the children born in times of plenty, but after the age of 20 they started to show an increase in mortality such that their average life expectancy was 15 years shorter. David Barker (Hales and Barker 1992) and many others showed that size at birth, which can be taken as a proxy measure of intrauterine conditions, was associated with altered risks of metabolic and cardiovascular disease, mood disorders, and osteoporosis in later life.

Elsewhere, we have extensively reviewed this area of research, known as the �velopmental origins of health and disease’, or DOHaD (Gluckman et al. 2010). We view this phenomenon as a classic example of developmental plasticity operating to ensure survival to reproduce but resulting in antagonistic pleiotropic disadvantages in later life. It is argued that constraint of fetal growth, lower maternal nutrition (Gale et al. 2006), or maternal stress (Meaney 2001) signal to the fetus that the postnatal world will be threatening. The developmentally plastic fetus may make responses incurring either immediate or delayed trade-offs and adjust its physiological development accordingly. A threatening world implies less nutritional security, and thus, an appropriate phenotype is based on a nutritional adaptive capacity to a plane that is lower than that of fetuses who anticipate a more benign world. Thus, the fetus exposed to a low-nutrition environment may or may not be smaller (depending on the severity of the limitation), but either way as an adult it may reach the threshold of metabolic load to which it can respond healthily, leading to diabetes and other metabolic conditions at a lower nutritional level than an individual who, early in life, shifted to a developmental trajectory more appropriate for a higher nutrition environment (Gluckman et al. 2010). Evidence to support this hypothesis includes epidemiological studies on humans prenatally exposed to famine, who have a higher risk of coronary heart disease and obesity in adulthood (Painter et al. 2005). Experimental studies have also shown that rats that experienced fetal undernutrition have higher body fat and are more sedentary compared to their counterparts that received adequate fetal nutrition (Vickers et al. 2000, 2003). They subsequently develop a constellation of symptoms similar to the human metabolic syndrome, such as obesity and hypertension, in adulthood, and these effects are exacerbated by a high-fat postnatal diet. However, if leptin, a satiety hormone made by fat, is administered to these rats neonatally thus artificially shifting their perception of their environment from low to high nutrition, neonatal weight gain, caloric intake, locomotor activity, and fat mass in these infant animals are normalized for the rest of their lives despite exposure to a high-fat diet (Vickers et al. 2005).

Pleiotropy describes how a single gene can influence several different physiological and phenotypic characteristics. Antagonistic pleiotropy refers to genes that confer an advantage in early life, but that result in ill effects later in life. We find utility in employing this term to encompass phenotypic traits that involve life course-associated trade-offs for example, because human fitness depends primarily on survival to reproductive age (Jones 2009), a potential adaptive advantage in early life may become disadvantageous later on and manifest as obesity, diabetes, and cardiovascular disease in middle age. High levels of insulin growth factor-1 (IGF-1) promote infant and childhood growth and presumably were selected for their consequent fitness advantage, but in later life are associated with higher rates of prostate and breast cancer.

Importantly, these mechanisms operate in all pregnancies and are a reflection of the role of developmental plasticity in ensuring adaptability to a changing environment on a timescale of change between that of selection (many generations) and homeostasis (minutes�ys). There is a growing body of experimental and clinical data showing that epigenetic processes are involved. Cues that induce plastic responses must be distinguished from those that disrupt the developmental program: clearly teratogens, such as thalidomide or the rubella virus, operate through the latter. For this reason, we would suggest that terms such as metabolic teratogenesis (Freinkel 1980) are not particularly helpful.

The human pregnancy is a co-adaptive compromise. The human fetus is born in a more altricial state than other closely related primates, because the human upright posture determines that the fetus must pass the pelvic canal that is narrower than in other primates (Rosenberg and Trevathan 1995). Brain growth must continue for a long period after birth to reach the disproportionately larger brain size of the hominin clade. Fetal growth in mammals is not solely genetically controlled, otherwise the outcome would be fetal obstruction in every case where pregnancy followed a female mating with a larger male. Indeed, human fetal growth can be shown to be largely determined by the maternal environment (Gluckman and Hanson 2004). In pregnancies where the egg has been donated, birth size is more closely related to the recipient than to the donor size (Brooks et al. 1995). The constraining mechanism on fetal growth is likely primarily a consequence of the utero-placental anatomy of mother and her ability to deliver nutrients to the placental bed. Further, the placenta, at least in sheep, is able to clear excessive concentrations of growth factors such as IGF-1 from the fetal circulation. Other studies, primarily in mice, raise the possibility of a role for parentally imprinted genes in regulating fetal growth. From studies of the IGF-2 system in mice, David Haig has developed the concept of maternal-fetal conflict to explain the evolution of imprinting (Haig 2010). However, imprinting appears in marsupials and possibly monotremes, and Eric Keverne and colleagues have made a good case for considering imprinting in terms of maternal-fetal co-adaptation rather than conflict (Curley et al. 2004).

Given the long life course of our species, this emergent field of developmental plasticity will become a major part of clinical medicine. As our understanding of epigenetic mechanisms including DNA methylation, histone modifications, and small noncoding RNAs grows, this area is likely to play a major role in clarifying disease causation and treatment. A major challenge for studies in contemporary evolution is the role of epigenetic inheritance. While epigenetic marks have long been established to transfer across mitosis, there is increasing evidence that some epigenetic marks transfer across meiosis. The most well-demonstrated mechanisms are via small RNAs in sperm that can transfer between generations inducing phenotypic effects on pigmentation and heart development in mammals (reviewed in Nadeau 2009). Transgenerational genetic effects on body weight and food intake have also been shown to be passed through the mouse paternal germline for at least two generations (Yazbek et al. in press), again implying the involvement of sperm in the molecular basis for such effects. There is inferential evidence of environmentally induced epigenetic inheritance in experimental animals. For example, the effects of glucocorticoid exposure in pregnant rats on their offspring's metabolic control extend to the F2 generation even when the intermediate F1-exposed fetus is male (Drake et al. 2005). Similarly, there is some inferential evidence in humans of male line-mediated environmental influences (Hitchins et al. 2007).

In addition to direct epigenetic inheritance, epigenetic marks may be induced in the F1 generation as a result of maternal effects as discussed in the DOHaD example earlier, or via grand-parental effects where the F1 generation is female. This is because the oocyte that will contribute genetic material to the F2 offspring is formed by the F1 female fetus while in the uterus of the F0 generation and is therefore exposed indirectly to the F0 environment. Similarly, male-line germ cells that will form spermatogonia are sequestered in the testis when the male is itself a fetus. Indeed, in the grandchildren of women who became pregnant in the severe Dutch famine of 1944�, where the exposed fetus was female, their children are more likely to be obese (Painter et al. 2005). A further form of indirect epigenetic inheritance may be seen in those cases where the environmental niche inducing the epigenetic change leading to the phenotype is recreated in each generation. The best demonstration is in rodents, where altered maternal care has been shown to induce epigenetic changes in the brain, resulting in behavioral changes and, in the next generation, the same pattern of maternal care (Weaver et al. 2004). Cross-fostering and pharmacological agents both reverse the epigenetic change and associated phenotype. The potential implications of direct and epigenetic inheritance, as well as maternal and grand-parental effects, are likely to be particularly important in human medicine, where we must focus on a single generation. This has theoretical implications for the use of traditional genotype–phenotype interactive models. Contemporary evolutionary studies need to develop models that focus on phenotype𠄾nvironment interaction. In these models, the phenotype at any point in time should be seen as a consequence of the cumulative effects of early environmental influences inducing epigenetic change, extending back to conception where the phenotype is determined by inherited genetic and epigenetic information.

Demographic change, acting through these developmental processes, may also play a role in the changing patterns of disease. First-born children are smaller because of the processes of maternal constraint (Gluckman and Hanson 2004), and they have higher risk of obesity (Reynolds et al. in press). Their smaller size reflects greater maternal constraint and has also been interpreted in life history terms (Metcalfe and Monaghan 2001). We have shown that they have a very different pattern of DNA methylation at birth (McLean et al. 2009), and falling family size may be a factor in changing patterns of chronic disease.

There are other dimensions to life course pathways to disease. The progressive loss of oocytes from the ovary is an inherent property and explains the decline in fertility in women from the beginning of the fourth decade of life. However, cultural changes mean that women can and do delay their pregnancies, and then, because of lower fertility in their later reproductive years, have a much greater requirement for medical intervention to treat infertility. Here is another example of how cultural developments have impacted on human biology this phenomenon has arisen because of the interaction between prolongation of life course resulting from technological developments in medicine and public health, and shifting of reproductive timing caused by the social changes associated with the development of contraceptive technologies.

Adolescence is an illustrative example of the changing nature of the human life course and the interaction with a changing social context. The age at menarche, the best documented sign of reproductive maturation, in Paleolithic times was probably around the ages of seven to 13 (Gluckman and Hanson 2006) full reproductive competence would have been achieved in concert with the psychosocial maturation required for function as an adult within society. The subsequent occurrence of agriculture and settlement, and the attendant negative outcomes of childhood disease and postnatal undernutrition, resulted in the delay of puberty onset, but again this would have been matched to the increased complexity of society. However, the age at menarche has fallen in Europe from a mean of 17 years around 1800 to about 12 years now (Gluckman and Hanson 2006). This decline can be attributed to better maternal and child health subsequent to the enlightenment support for population growth, improved sanitation and access to food in the postindustrial era, as well as public health and medicine from the late nineteenth century on. But whereas the age of puberty has fallen, the age at which an individual is treated as an adult appears to have risen dramatically in modern Western society. While in the nineteenth century individuals in their late teens were accepted as adults, this is now less likely. If the term adolescence is restricted to the period between the completion of biological maturation and acceptance as an adult in society, then adolescence has probably extended from one to 3 years in the nineteenth century to over a decade in the twenty-first century. Indeed, modern neuro-imaging techniques demonstrate that the brain shows ongoing maturation until well into the third decade, with the pathways influencing impulse control and higher levels of executive function being the last to mature (Lebel et al. 2008). There is, thus, a mismatch between biological and psychosocial maturation, reflected in a far greater morbidity in children who undergo earlier biological maturation, because of acting out behaviors and emotional disorders, including suicidal attempts (Michaud et al. 2006).

These observations raise several hypotheses. Is the delayed maturation of the brain evolutionarily old but has it only recently become of significance, because the higher functions are only needed for coping with the complexities of modern society? Have the complexities of modern society induced a longer period for skills to be learnt and the brain to mature, as has been suggested in the arguments related to the origins of the juvenile period in children? These two hypotheses could be tested by studies of brain maturation across different cultures. Or does the way in which we now rear children change the pattern of brain maturation? In most Western societies, we now control the children's environment much more rigorously than ever before, and the effect of this can be assessed by comparisons between different educational systems.

Excessive defence mechanisms

Many symptoms can be explained as demonstrations of evolved defence processes that have become inappropriate or excessive, and thus potentially harmful to the individual. For example, fever is an appropriate anti-bacterial response that activates some components of the immune system, but, if excessive, can harm the individual. Similarly, a depressed mood might be the appropriate response in some situations, but inappropriate depression of mood or excessive anxiety leads to dysfunction. Fear is an appropriate response to many situations, but if the level of fear induced is excessive or if it is inappropriately triggered, then a phobia may be manifest. Nesse has expanded on this class of mechanism extensively (Nesse 2005).

The long historical exposure of humans to microorganisms such as helminthic worms is the basis of the ‘hygiene hypothesis’, which argues that since humans have begun to be reared in more hygienic circumstances, the incidence of certain diseases has risen (Bresciani et al. 2005). While the hygiene hypothesis has generally been applied to asthma, it may also apply more broadly. Crohn's disease is an inflammatory disease of the bowel, which can be very debilitating. Recent evidence suggests its incidence has risen as gastrointestinal worm infection has fallen. Thus the disease might be caused by the defence mechanisms against gut parasites now targeting the gut wall. Indeed, there are promising clinical trials in which patients suffering from Crohn's disease are treated with either pig hookworms or their extracts (Croese et al. 2006). Another study of patients with multiple sclerosis found that those with worm infections developed symptoms significantly more slowly than those without (Correale and Farez 2007), and clinical trials are presently underway to determine whether treatment with worms has therapeutic value.

Co-evolutionary considerations and the evolutionary arms race

Humans live in symbiotic relationships with a large population of bacteria, particularly in their gastrointestinal tract. Increasingly, it is recognized that this extended symbiome needs to be considered in understanding human health. Alterations in the gut flora are associated not only with acute gastroenteritis but also with chronic disease. For example, there is growing evidence that the gut microbiome plays a role in determining metabolic homeostasis and the risk of diabetes mellitus type 2 and obesity (Tschöp et al. 2009). It is not clear whether the significance of the gut microbiome arises simply from its role in predigestion, from the potential it has to release inflammatory cytokines, or whether it might induce epigenetic changes in the human host.

A key to understanding the consequences of our relationships with the microbial world is in their fast generation times, leading to an evolution much more rapid than that of humans. This is best illustrated by antibiotic resistance. The interval between the commercial introduction of antibiotics and the appearance of resistance in human commensals and pathogens is often frighteningly short, on the order of 1𠄲 years. Broad use of antibiotics leads to rapid spread and high frequency of resistant strains, particularly in hospital and long-term care settings where rates of antibiotic use are the highest. Moreover, it can be difficult to get rid of resistance once it evolves. Compensatory mutations ameliorate the costs of resistance for bacteria (Schrag and Perrot 1996) and can create fitness valleys that prevent reversion to drug-sensitivity even after drug use is discontinued (Levin et al. 2000). The challenge for medicine is similar to that faced in agriculture, where insecticide use leads to insecticide resistance and herbicide use leads to herbicide resistance. Evolutionary theory has proven useful for suggesting approaches for more effectively deploying our antibiotic resources in ways that will minimize resistance evolution (Lipsitch et al. 2000). For example, despite early enthusiasm, results from trials of antibiotic cycling have been somewhat disappointing (Brown and Nathwani 2005). Evolutionary theory explains why (Bergstrom et al. 2004) and suggests alternative approaches that may be more effective.

Similarly, evolutionary models allow us to understand the process by which viral threats emerge. Phylogenetic analysis has helped us reconstruct the early spread of the human immunodeficiency virus around the globe (Korber et al. 2000), and the genetic origins of the H1N1 influenza pandemic (Smith et al. 2009). Models of sequence evolution can inform the process of designing each year's influenza vaccine (Russell et al. 2008). Mathematical models of disease emergence have likewise been useful in developing mitigation plans for potential pandemic strains of influenza (Ferguson et al. 2005).

Infections can also shape human evolution. While much in the historical record remains speculative and inferential, there are some contemporary, well-recorded examples. For example, kuru is a prion-caused neurodegenerative disease transmitted by cannibalistic funeral rites in New Guinea. Some mutations in the prion protein gene confer partial or even strong resistance to the disease. There is now evidence that these resistance genes only emerged in recent generations from a common ancestor some 10 generations ago and that that resistance gene is now well spread throughout the population at risk. This may in part explain the recent reduction in the incidence of kuru (Mead et al. 2009).

Evolutionary constraint and history

Many features of human anatomy associated with potential pathology represent the consequences of our evolutionary history. A well-known example is the appendix: while it evolved to improve digestion for the vegetarian diet of earlier members of our clade, it has no function in human digestion and infection in the appendiceal lumen leads to appendicitis. The appendix cannot become lost over evolutionary time, because it will first need to decrease in size and this inherently promotes the development of appendicitis (Nesse and Williams 1995). Other examples include the risk of detached retina, which arises because the mammalian lineage evolved with the vascular layer in front of the neural layer, in contrast to the cephalopod eye (Fernald 2000), and the risks of obstruction at birth resulting from the conflict between the shape of the female pelvis in a bipedal ape and the large human fetal brain size (Rosenberg and Trevathan 1995). In comparison with the chimpanzee, the human infant encounters a much narrower pelvis and must go through a series of rotations during delivery. Therefore, if the fetus is large and/or the mother is small, dystocia may result. Back pain and spinal problems can be understood in terms of the compromises made some 6 million years ago, when human ancestors adopted an upright posture (Anderson 1999), and our large head and truncal weight serve as risk factors for spinal disk injury. Scurvy, as discussed earlier, represents the result of a mutation that was presumably neutral when it first arose in a frugivorous ancestor.

Sexual selection and its consequences

Many anatomical features of humans, such as the loss of most of their body hair, may have their origin in sexual selection. Men at all ages have a higher mortality than women (Office for National Statistics 2006), and the life history explanation for this phenomenon has been extensively discussed (Kruger and Nesse 2006). Male mortality is particularly high in the early reproductive years and is associated with violence and other acting out behaviors. Such differences might be best understood in terms of mate-seeking behaviors, where the investment in competition for a mate leads to comparatively greater fitness pay-offs for men. Some sexually dimorphic characteristics also impose a burden on men: higher testosterone favors higher body mass and aggressive behavior, but is also thought to be an immunosuppressant, therefore increasing susceptibility to infectious disease (Muehlenbein and Bribiescas 2005). Other factors like higher somatic maintenance and faster aging in males are also thought to play a role.

There is an extensive evolutionary psychology literature that aims to explain much of human behavior in terms of mate-seeking behavior and sexual competition. Unfortunately, there has been much over-statement and popularization in this domain that has harmed the overall incorporation of evolutionary thought into medicine. However, while evolutionary psychology has its limitations, the role of sexual selection in the origin of both physical and behavioral traits should not be ignored.

Balancing selection

In population genetics, the examples of sickle cell anemia, the thalassemias, and glucose-6-phosphate dehydrogenase deficiency have all been explained in terms of the heterozygote advantage providing resistance against malaria, whereas the homozygous form is associated with more severe disease (Luzzatto 2004). Recently, the possession of two variants in the APOL1 gene𠅊 characteristic common in Africans but absent in Europeans—was shown to be associated with an increased risk of renal disease (Genovese et al. 2010). The protein produced by these variants showed lytic activity against the trypanosome parasite that causes sleeping sickness, suggesting that the risk alleles were maintained to help confer a protective effect. The association of the variants with protection was dominant, while that with renal disease was recessive, pointing towards a heterozygous advantage model.

Speculation persists about other common alleles that are in apparent equilibrium within populations. For example, in European populations, the most common recessive disease is cystic fibrosis, a disorder of the chloride-secreting channel in epithelia such as the lung associated with excessively viscous secretions and subsequent wheezing and infections a carrier frequency of one in 25 has been seen in some populations (Massie et al. 2005). It has been suggested this frequency could not persist unless there was an advantage to being a heterozygote. Possible past selective pressures include typhoid, cholera and other diarrheal diseases, or perhaps tuberculosis, but no firm data exist. A recent study analyzing the genome in two human populations was able to identify genes associated with various functions, such as immunity and keratin production, that strongly demonstrated long-term balancing selection (Andres et al. 2009) such studies provide a step towards finding functional variants that may be of phenotypic and medical relevance.

Balancing selection has also been used to explain differences between allelic forms that confer different behaviors. For example, there are alternate alleles of the promoter for the vasopressin receptor that is associated with pair bonding, with one form being more common in individuals who have less stable relationships (Walum et al. 2008). While at the moment such observations are speculative and premature, as human genomic information becomes more widely incorporated into the understanding of human biology and behavior, such inferences and associations will become more frequent they raise ethical issues that will need to be confronted.

Demographic history

There are many examples of founder effects and population effects affecting disease distribution. For example, blood group distribution in American-Indians is dominated by the O blood type, possibly reflecting a founder effect when humans crossed the Bering strait (Halverson and Bolnick 2008). The contemporary Finnish population also descended from a founder population that underwent a tight bottleneck during migration northwards across the Gulf of Finland. It is a highly homogeneous population that displays a distinct pattern of disease compared to the rest of Europe, such as being prone to multiple rare genetic diseases but also being much less likely to develop some other diseases like cystic fibrosis (Peltonen et al. 1999). A similar situation is seen in the French Canadians, whose ancestors underwent a series of regional founder effects, leading to a characteristic geographical distribution of genetic diseases (Laberge et al. 2005). There are clusters of individuals with rare diseases of genetic origin found in different locales: for example, Huntington's disease has a large Venezuelan cluster, while Laron dwarfism, caused by a mutation in the growth hormone receptor, is largely clustered in southern Ecuador. The distribution of leprosy strains maps to human migration (Monot et al. 2009).

Five to 14% of European Caucasians possess a deletion in the CCR5 gene, a mutation that is not found among Africans, American-Indians, and East Asians, indicating that the mutation probably arose after the ancestral founders of these populations had separated. The mutation results in a defective chemokine receptor, and its high frequency in Europeans appears to have been attributed to selective pressure caused by infectious disease (Duncan et al. 2005). While this mutation has been well established to confer a high level of resistance to infection by the human immunodeficiency virus, it also increases the risk of succumbing to encephalitogenic West Nile virus infections (Glass et al. 2006).


Research for Your Health

The NHLBI is part of the U.S. Department of Health and Human Services’ National Institutes of Health (NIH)—the Nation’s biomedical research agency that makes important scientific discovery to improve health and save lives. We are committed to advancing science and translating discoveries into clinical practice to promote the prevention and treatment of heart, lung, blood, and sleep disorders including hemolytic anemia. Learn about the current and future NHLBI efforts to improve health through research and scientific discovery.

Learn about the following ways the NHLBI continues to translate current research into improved health for people who have hemolytic anemia. Research on this topic is part of the NHLBI’s broader commitment to advancing blood disorders and blood safety through scientific discovery.

  • Program Helps Protect Blood Transfusion Recipients. The NHLBI’s Recipient Epidemiology and Donor Evaluation Study (REDS) program began in 1989 to protect the Nation’s blood supply and improve the benefits and reduce the risks of transfusions. Now in its third phase, called REDS-III, the program supports research in the United States and around the world.
  • Providing Access to NHLBI Biologic Specimens and Data. The Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC) centralizes and integrates biospecimens and clinical data that were once stored in separate repositories. Researchers can find and request available resources on BioLINCC’s secure website, which maximizes the value of these resources and advances heart, lung, blood, and sleep research.
  • New Treatments for Hemolytic Anemia. NHLBI-sponsored clinical trials showed that eculizumab is an effective treatment for a rare and life-threatening type of hemolytic anemia called paroxysmal nocturnal hemoglobinuria (PNH). Eculizumab can reduce or stop the need for blood transfusions. NHLBI research helped eculizumab become the standard treatment for PNH.
  • Supporting Safe Manufacturing of Cell-Based Therapies. The NHLBI’s Production Assistance for Cellular Therapies (PACT) program supports translational research on cellular and genetic therapies by increasing the capacity to manufacture cell products that follow current Good Manufacturing Practices (cGMP) regulations. The PACT program aims to increase the supply and safety of genetically modified cells available for people who have blood disorders such as hemolytic anemia.
  • Accelerating Cures for All People Who Have Sickle Cell Disease. Our Cure Sickle Cell Initiative is a NHLBI-led collaborative research effort to develop genetic therapies for patients who have sickle cell disease. The goal is to have these genetic therapies ready to safely use in clinical research within 5 to 10 years. This patient-focused Initiative will bring together researchers, private sector researchers, patients, providers, advocacy groups, and others as it supports research, education, and community engagement activities.
  • Improving Care for Adolescents and Adults Who Have Sickle Cell Disease. While most U.S. children who have sickle cell disease survive to adulthood, the transition from pediatric to adult care is often challenging. By funding the Sickle Cell Disease Implementation Consortium, we are working to understand current barriers to care, test interventions to overcome those barriers, and develop a new sickle cell disease registry.
  • Network Accelerates Research on Blood and Bone Marrow Transplants. The NHLBI and NCI launched the Blood and Marrow Transplant Clinical Trials Network (BMT CTN) in 2001 to promote large multi-institutional clinical trials that seek to understand the best possible treatment approaches in blood and marrow transplantation. In the United States, about 20,000 patients receive blood or marrow transplants annually.

In support of our mission, we are committed to advancing hemolytic anemia research in part through the following ways.

  • We perform research. The NHLBI Division of Intramural Research and its Hematology Branch are actively engaged in research on conditions related to hemolytic anemia. Research in the Hematopoiesis and Bone Marrow Failure Laboratory spans the basic sciences, clinical trials, and epidemiology, focusing on blood cell production in healthy individuals and patients who have bone marrow failure.
  • We fund research. The research we fund today will help improve our future health. Our Division of Blood Diseases and Resources is a leader in research on the causes, prevention, and treatment of blood diseases, including hemolytic anemia and sickle cell disease. Search the NIH RePORTer to learn about research the NHLBI is funding on hemolytic anemia.
  • We stimulate high-impact research.The NHLBI Strategic Vision highlights ways we may support research on hemolytic anemia over the next decade.

Learn about exciting research areas the NHLBI is exploring about hemolytic anemia.

  • Preventing complications from hemolytic anemia. During hemolytic anemia, red blood cells release heme molecules into the blood. These heme molecules may become toxic because they are no longer bound by protective proteins. They may also collect in organs, such as the kidneys, and cause damage. NHLBI-supported researchers are looking into treatments that may be able to prevent this damage.
  • Supporting research on rare types of hemolytic anemia. We support research on new treatments for a rare type of autoimmune hemolytic anemia called cold agglutinin disease.
  • Understanding rare but life-threatening reactions to blood transfusions. Some people are more at risk of developing hemolytic reactions to a blood transfusion even when the blood type is matched. The NHLBI supports research to identify the cause, predict people who have a greater risk, and find treatments that prevent hemolytic anemia.

Biology Final

Ferns have well-developed vascular tissue, roots, and stems.

experience a drop in its body temperature

wait to see if it goes lower

increase muscle activity to generate heat

too much heat produced by the body

upward adjustment of the body temperature set point

inadequate cooling mechanisms in the body

Essential nutrients can be synthesized by the body.

Vitamins are required in small quantities for bodily function.

Some amino acids can be synthesized by the body, while others need to be obtained from diet.

When we breathe in, air travels from the pharynx to the trachea.

The bronchioles branch into bronchi.

Alveolar ducts connect to alveolar sacs.

Blood in the pulmonary vein is deoxygenated.

Blood in the inferior vena cava is deoxygenated.

Blood in the pulmonary artery is deoxygenated.

provides body tissues with oxygen

provides body tissues with oxygen and carbon dioxide

establishes how many breaths are taken per minute

nasal cavity, trachea, larynx, bronchi,
bronchioles, alveoli

nasal cavity, larynx, trachea, bronchi, bronchioles, alveoli

nasal cavity, larynx, trachea, bronchioles, bronchi, alveoli

Arteries have thicker wall layers to accommodate the changes in pressure from the heart.

Arteries have thinner wall layers and valves and move blood by the action of skeletal muscle.

Hypothyroidism, resulting in weight gain, cold sensitivity, and reduced mental activity.

Hyperthyroidism, resulting in weight loss, profuse sweating and increased heart rate.

Hyperthyroidism, resulting in weight gain, cold sensitivity, and reduced mental activity.

regulate production of other hormones

stimulates production of red blood cells

causes the fight-or-flight response

thoracic cage and vertebral column

thoracic cage and pectoral girdle

All viruses are encased in a viral membrane.

The capsomere is made up of small protein subunits called capsids.

DNA is the genetic material in all viruses.

A virion contains DNA and RNA.

Viruses replicate
outside of the cell.

In the process of apoptosis, the cell survives.

During attachment, the virus attaches at specific sites on the cell surface.

The viral capsid helps the host cell produce more copies of the viral genome.

secondary immune response

systemic lupus erythematosus

The vas deferens carries sperm from the testes to the seminal vesicles.

The ejaculatory duct joins the urethra.

Both the prostate and the bulbourethral glands produce components of the semen.

LH and FSH are produced in the pituitary, and estrogen and progesterone are produced in the ovaries.

Estradiol and progesterone secreted from the corpus luteum cause the endometrium to thicken.

Both progesterone and estrogen are produced by the follicles.

The carrying capacity of seals would decrease, as would
the seal population.

The carrying capacity of seals would decrease, but the seal population would remain the same.

The number of seal deaths would increase, but the number of births would also increase, so the population size would remain the same.



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