the exact opposite, practical application v academic authority.
science is a very subjective concept, people can argue their own philisophical definitions all day long, my point is that practical results are the only objective measure of scientific merit
Yes, like right now how theory of evolution is helping the medical researchers in finding the causes and cures of chronic inflammatory diseases (autoimmune disease, hypertension etc.)..
Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology
Abstract
During the last 10 years, a series of exciting observations has led to a new theory of pathophysiology
using insights from evolutionary biology and neuroendocrine immunology to understand the sequelae of
chronic inflammatory disease. According to this theory, disease sequelae can be explained based on
redirection of energy-rich fuels from storage organs to the activated immune system. These disease sequelae are highly diverse and include the following:
sickness behavior, anorexia, malnutrition, muscle wasting–cachexia, cachectic obesity, insulin resistance with hyperinsulinemia, dyslipidemia, increase of adipose tissue near inflamed tissue, alterations of steroid hormone axes, elevated sympathetic tone and local sympathetic nerve fiber loss, decreased parasympathetic tone, hypertension, inflammation-related anemia, and osteopenia.
Since these d
isease sequelae can be found in many animal models of chronic inflammatory diseases with mammals (e.g., monkeys, mice, rats, rabbits, etc.), the evolutionary time line goes back at least 70 million years. While the initial version of this theory could explain prominent sequelae of chronic inflammatory disease, it did not however address two features important in the pathogenesis of immune-mediated diseases: the time point when an acute inflammatory disease becomes chronic, and the appearance of hypertension in chronic inflammation. To address these aspects more specifically, a new version of the theory has been developed. This version defines more precisely
the moment of transition from acute inflammatory disease to chronic inflammatory disease as a time in which energy stores become empty (complete energy consumption). Depending on the amount of stored energy,
this time point can be calculated to be 19–43 days.
Second,
the revised theory addresses the mechanisms of essential hypertension since, on the basis of water loss, acute inflammatory diseases can stimulate water retention using a positively selected water retention system (identical to the energy provision system). In chronic smoldering inflammation, however, there is no increased water loss. In contrast, there is increased water generation in inflamed tissue and inflammatory cells, and the activation of the water retention system persists. This combination leads to a net increase of the systemic fluid volume, which is hypothesized to be the basis of essential hypertension (prevalence in adults 22–32%).
Excerpts:-
Why do we have chronic diseases?
genes responsible for energy regulation have been positively selected under conditions without chronic inflammation [
8,
10]. Chronic diseases and chronic inflammatory diseases in particular can exert a high negative selection pressure in evolution. Chronic inflammatory diseases can lead to loss of reproduction potential because affected individuals are at strong disadvantage. Such individuals can be excluded or impaired in the competition for food; they can also have low social status in the group and limited choice or availability of sexual partners. In addition, intense, persistent inflammation can inhibit the hypothalamic–pituitary–gonadal axis, leading to impairment of fertility as demonstrated in studies on the effect of chronic inflammatory diseases on fertility despite good medical control.
In some situations, however, the presence of a chronic inflammatory disease may not exert any selective pressure despite its potential severity.
Many chronic inflammatory diseases only become manifested in patients at older ages. Because of the short life expectancy in the past, our ancestors have not suffered from the chronic inflammatory diseases that we know today. Their genes have been positively selected for different aspects such as reproduction, muscular work, defense against infections, metabolism, and similar important activities. .....It has been hypothesized that
the genes relevant to the etiology of today’s chronic inflammatory diseases have been positively selected for their effects on normal host defense as well as the host response to serious, albeit non-life-threatening, inflammatory episodes in contrast to chronic inflammatory diseases (Table
2) [
8]. These issues remain under investigation. Nevertheless, despite uncertainty about their origin, many genes have been linked to an increased risk or more severe forms of chronic inflammatory diseases including polymorphisms for human leukocyte antigens (HLA) and polymorphisms for other elements of the immune system detected by genome-wide association studies. However, these genes were most probably evolutionarily conserved because they supported positive selection at younger ages. T
his concept was developed in the 1950s in the context of aging research and the theory was called “antagonistic pleiotropy” [
7].
An example of antagonistic pleiotropy illustrates these ideas.
HLA DR4 (DRB1*04) is a well-known risk factor for rheumatoid arthritis and other chronic autoimmune diseases,
but HLA DR4 (DRB1*04) also has a strong negative association with dengue hemorrhagic fever [
21].
HLA DR4 (DRB1*04) homozygous individuals are 12 times less likely to develop dengue hemorrhagic fever [
21]. Thus, it seems likely that HLA DR4 (DRB1*04) was positively selected to overcome dengue hemorrhagic fever but not to stimulate rheumatoid arthritis and other autoimmune diseases in later life.
Explaining sickeness and immune response stages in sick individuals using evolution:-
..it can be proposed that
sickness behavior represents an element of an adaptive program that has been positively selected for transient immune and inflammatory reactions to limit energy utilization for such activities as foraging and courtship behavior [
8,
26,
27]. In such a situation, the immune response can not last forever because energy stores run empty.
Furthermore, sickness behavior can restrain activity and, for example, confine the affected individual to a safe place to keep away predators [
8,
26,
27]. In considering energy stores available during these responses, it is important to note that storage occurs primarily in fat tissue (12 kg of triglycerides in the body of a contemporary person, 500,000 kJ), as well as in the liver (150 g glycogen, 2.500 kJ) or muscles (300 g glycogen, 5,000 kJ; 6–7 kg muscle protein, 50,000 kJ) [
11,
12].
Unde
r conditions of sickness behavior and anorexia without uptake of energy-rich substrates but an increased sickness-related metabolic rate (Tables 1 and 6), the total amount of stored energy would only last for 19 to 43 days in females and 28 to 41 days in males (Table
6). The number is relatively similar for domestic fowl which have an evolutionary distance to
Homo sapiens of 300 million years (Table
6). In other words,
an acute consuming infectious disease that uses all energy stores can only last until the stores are empty, say 19 to 43 days. Thus, the evolutionarily positively selected increase and decrease of an adaptive immune response must fit into this prespecified time frame. Due to the physical restrictions of energy storage under natural paleolithic conditions, an acute infectious disease may not last much longer than 3 to 6 weeks. It can be hypothesized that energy considerations can help explain the relatively constant time course of an adaptive immune response in the context of acute infection.
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Just one example among thousands.
What positive contribution has intelligence design theory made to our life?
