How Do Trematodes Induce Cancer? A Possible Evolutionary Adaptation of an Oncogenic Agent Transmitted by Flukes.

There is strong epidemiological evidence that development of various cancer types is linked to infection with flukes (Platyhelminthes: Trematoda) in Africa, Asia and the Middle East. The exact nature of the mechanism by which cancer is induced by these parasites is unknown. Here, we provide a new hypothesis suggesting that flukes are not the primary cause of cancer but act as vectors of cancer-inducing microbial pathogens.

Domestication and microbiome succession may drive pathogen spillover.

Emerging infectious diseases have posed growing medical, social and economic threats to humanity. The biological background of pathogen spillover or host switch, however, still has to be clarified. Disease ecology finds pathogen spillovers frequently but struggles to explain at the molecular level.

Tick bite induced α-gal syndrome highlights anticancer effect of allergy.

Tick bite induced α-gal syndrome (AGS) following consumption of mammalian meat is a recently described intriguing disease occurring worldwide. Here we argue that AGS and delayed allergy in general is an adaptive defence method against cancer. Our hypothesis synthesizes two lines of supporting evidence.

Harm or protection? The adaptive function of tick toxins.

The existence of tick toxins is an old enigma that has intrigued scientists for a long time. The adaptive value of using deadly toxins for predatory animals is obvious: they try to kill the prey in the most effective way or protect themselves from their natural enemies. Ticks, however, are blood-sucking parasites, and it seems paradoxical that they have toxins similar to spiders, scorpions and snakes.

Paradoxes of tumour complexity: somatic selection, vulnerability by design, or infectious aetiology?

The aetiology of cancer involves intricate cellular and molecular mechanisms that apparently emerge on the short timescale of a single lifetime. Some of these traits are remarkable not only for their complexity, but also because it is hard to conceive selection pressures that would favour their evolution within the local competitive microenvironment of the tumour. Examples include 'niche construction' (re-programming of tumour-specific target sites) to create permissive conditions for distant metastases; long-range feedback loops of tumour growth; and remarkably 'plastic' phenotypes (e.

The evolutionary logic of sepsis.

The recently proposed Microbiome Mutiny Hypothesis posits that members of the human microbiome obtain information about the host individuals' health status and, when host survival is compromised, switch to an intensive exploitation strategy to maximize residual transmission. In animals and humans, sepsis is an acute systemic reaction to microbes invading the normally sterile body compartments. When induced by formerly mutualistic or neutral microbes, possibly in response to declining host health, sepsis appears to fit the 'microbiome mutiny' scenario except for its apparent failure to enhance transmission of the causative organisms.

The microbiome mutiny hypothesis: can our microbiome turn against us when we are old or seriously ill?

Background: The symbiotic organisms of the healthy microbiome tend to be harmless or even beneficial for the host; however, some symbionts are able to adjust their virulence in response to external stimuli. Evolutionary theory suggests that optimal virulence might increase if the mortality of the host (from unrelated causes) increases.

Presentation Of The Hypothesis: We hypothesize that microorganisms of the human microbiome may be capable of a coordinated phenotypic switch to higher virulence ("microbiome mutiny") in old or seriously ill people, to optimize their transmission under the conditions of increased background mortality.

Why infest the loved ones--inherent human behaviour indicates former mutualism with head lice.

Head lice transmit to new hosts when people lean their heads together. Humans frequently touch their heads to express friendship or love, while this behaviour is absent in apes. We hypothesize that this behaviour was adaptive because it enabled people to acquire head lice infestations as early as possible to provoke an immune response effective against both head lice and body lice throughout the subsequent periods of their life.

Sociosexually unrestricted parents have more sons: a further application of the generalized Trivers-Willard hypothesis (gTWH).

Background: The generalized Trivers-Willard hypothesis (gTWH) proposes that parents who possess any heritable trait which increases male reproductive success at a greater rate than female reproductive success in a given environment will have a higher-than-expected offspring sex ratio, and parents who possess any heritable trait which increases the female reproductive success at a greater rate than male reproductive success in a given environment will have a lower-than-expected offspring sex ratio.

Aim: One heritable trait which increases the reproductive success of sons much more than that of daughters is unrestricted sociosexual orientation. We therefore predict that parents with unrestricted sociosexual orientation (measured by the number of sexual partners, frequency of sex, and attitudes toward relationship commitment and sexual exclusivity) have a higher-than-expected offspring sex ratio (more sons).

The tripartite immune conflict in placentals and a hypothesis on fetal-->maternal microchimerism.

There is a two-way traffic of immune cells through the placenta; and fetal immune cells are often present in the maternal body even long after giving birth. We present an adaptationist theory to interpret fetal-->maternal microchimerism and the diverse set of concomitant medical phenomena. We handle fetal, maternal, and paternal adaptive interests separately and in interaction with one another.

Deal in the womb: fetal opiates, parent-offspring conflict, and the future of midwifery.

This paper argues that parent-offspring conflict is mediated by placental beta-endorphins in placental mammals, i.e., foetuses make their mothers endorphin-dependent then manipulate them to increase nutrient allocation to the placenta.