Boys without Fathers

an Endocrine Hypothesis - Rev: 4.3

Internal links are in green in order to distinguish them from links that Google and the web generate, which are blue. This website is an ongoing effort and will gradually change as I continue to research the relevant topics. Please send questions and/or comments to: <hummingbird.lou@gmail.com> . My other websites: Children of the Amphioxus Subcortical Brain Background: I've spent 15 years as a very part-time substitute teacher in the public school system of a moderately large American city. It's been my observation that, using very broad averages, the educational effort is defeated by about 10% of the students whose constant disruptions prevent the other 90% of the students from receiving the quality education which they really want. After I had befriended the disruptors, they explained their situation to me. "We don't have fathers." Once I had been given this key, I was able to confirm it over and over. If a young man was misbehaving, and the disruptors are almost always male, I would ask him: "How would your father feel if he saw you behaving like this?" Their answer was always, always, always the same. "I don't have a father." And it was always said with great sadness. They know something important is missing from their lives. Some time later, I took a class on teaching children who have disabilities. We had to write a term paper, and the instructor was broad-minded enough to allow me to write mine on the disability of not having a father. The result was the first version of "Boys without Fathers, an Endocrine Hypothesis".

Overview: Boys who are forced to try to grow up without a father face many difficulties above and beyond the problems they have and present in school. See: Family Structure . This paper offers an endocrine hypothesis as to why a boy who grows up without a father might end up with the difficulties that seem to come with father-absence. Research into the influence that the endocrine system has on behavior employs two different but mutually reinforcing methodologies. The first methodology is to gather data on the endocrine systems and behavior of a large number of individuals of the same species, either human or non human, and then examine the data for statistically significant correlations between behavior and the levels of the bioactive compounds of interest. The second methodology is to artificially change the levels of the bioactive compounds of interest and then look for changes in behavior. Ethical considerations generally limit this second methodology to experiments with non humans. Both of these methods face practical constraints on the number of parameters that can be measured simultaneously. Because of the enormous complexity of the Human Endocrine System it's never possible to measure all relevant parameters at the same time. So researchers have no choice but to measure some parameters and ignore others, and the decision as to which parameters to measure and which to ignore varies from researcher to researcher. What's more, the various bioactive compounds often have effects on one another, and many of these effects are as yet unresearched. Therefore, we have no choice but to compile the incomplete data that is available and then try to fit it all together into some sort of coherent whole. The Criminal Neuro-Endocrine System: As outlined in Criminal Hormones , socially deviant adults often show abnormalities in their neuro-endocrine systems. The most commonly found abnormalities are: 1. decreased turnover of the Neurotransmitter Serotonin 2. decreased circulating levels of the Hormone Cortisol 3. increased circulating levels of the Hormone Testosterone , and when serotonin, cortisol and testosterone are all measured at the same time, these abnormalities are found together. See: Cortisol & Testosterone & Serotonin .

Statistical analysis of the variations within these abnormalities shows that the increased Testosterone is responsible for the Aggression common to the syndrome, while the reduced Serotonin is responsible for the Impulsivity. See: Criminal Testosterone & Serotonin . Notice that the above abnormalities concern three very different physiological realms: the reproductive hormonal system, the stress response hormonal system and that portion of the nervous system that uses Serotonin as a neurotransmitter. In spite of the great difference between these three systems, all of the abnormalities described above can be traced back to the body's response to Stress . In none of the articles discussing people with the above endocrine profile was there any mention of the Family Structure in which the individuals having the profile had grown up. In particular, there was no way of telling whether or not they had grown up without a father. However, "(R)esults from longitudinal event-history analysis showed that, although a sizable portion of the risk that appeared to be due to father absence could actually be attributed to other factors, such as teen motherhood, low parent education, racial inequalities, and poverty, adolescents in father-absent households still faced elevated incarceration risks." [ Family Structure ]. So there is probably considerable overlap between individuals having the above endocrine profile and men who have grown up without a father. This paper presents an hypothesis as to why a boy who grows up without a father might end up with the above endocrine profile and all of the difficulties that seem to come with it. In particular, we will be discussing how the presence or absence of a father affects the levels and actions of eight bioactive compounds within his son. Four of these are all members of the Corticotropin-releasing factor family . The eight bioactive compounds we will be discussing are The four members of the Corticotropin-releasing factor family , 1. Corticotropin-releasing hormone (CRH) and the three 2. Urocortins - urocortin I (also written urocortin 1 or Ucn1) 3. - urocortin II (also written urocortin 2 or Ucn2) 4. - urocortin III (also written urocortin 3 or Ucn3), all of which seem to be Neuromodulators , 5. the two Steroid Hormones : Cortisol and 6. Testosterone , 7. the Posterior Pituitary Hormone Arginine Vasopressin and 8. Serotonin , which is sometimes called the "happiness hormone" but which is actually a Neurotransmitter.

Although, the boys who cause problems in the classroom seem more Impulsive than violent, the endocrinology of Impulsivity is much more complex and, therefore, less well understood than the endocrinology of Aggression. So I originally intended to begin this paper by focusing on Aggression. However, I've changed my mind. As discussed in Amphioxus Stress Hormones , the Amphioxus does not have any of the elements of the Direct Cortisol Pathway , which in humans is associated with Aggression . In contrast, as discussed in Amphioxus Serotonin System , the amphioxus does have many elements of the Direct Serotonin Pathway , which in humans is associated with Impulsivity . This provides strong evidence that the much more complex Direct Serotonin Pathway evolved before the much less complex Direct Cortisol Pathway . I was thinking that I would deal with the Direct Cortisol Pathway first, because of its greater simplicity. But, whenever possible, I prefer to take things in their evolutionary order. So I'll consider the Direct Serotonin Pathway first. This will not be an easy task. The Human Endocrine System is extremely complex, and, even when we limit our inquiry to just the eight bioactive compounds listed above, we will find that there is still much that is not yet fully understood. Endocrine Data: The Corticotropin-releasing factor family seems to be the key. It has direct influence on the levels of both Serotonin and Cortisol , and indirect influence on the levels of both Arginine Vasopressin (AVP) and Testosterone . At this point we encounter two complications. Corticotropin-releasing hormone (CRH) was the first member of the Corticotropin-releasing factor family to be discovered. The earliest reference to it in PubMed is dated 1955. Most of the research on the Corticotropin-releasing factor family has actually been on the two CRH Receptors , CRHR1 and CRHR2. Not surprisingly, the two receptors received their names because they accept Corticotropin-releasing hormone (CRH) as a Ligand. However, as is the case with most receptors, CRHR1 and CRHR2 also accept other ligands in addition to CRH. More recent research has suggested that the endogenous ligand for one or both these receptors is actually not CRH but rather one of the much more newly discovered Urocortins , which were first mentioned in PubMed in 1995.

The first complication is that if additional research continues to point to one or more of the urocortins as the endogenous ligand(s) for what are now called the CRH receptors, one or both of these receptors will probably be renamed to reflect the fact that their primary ligand is one of the urocortins. Since this renaming has not yet occurred, I will continue to refer to the receptors as CRH Receptors even though the operant ligand for one or both of them may actually be one of the Urocortins . The second complication is that we've had an extra 40 years to study Corticotropin-releasing hormone (CRH) , so we know much more about it than we know about the Urocortins . This research is ongoing. What we think we know today may change tomorrow. If I understand correctly, members of the Corticotropin-releasing factor family influence Serotonin and Cortisol through two different pathways which may turn out to be completely separate. The uncertainty about how completely separate these pathways are will be explained below. Additionally, the end products of both of these two, possibly separate, pathways can influence the other pathway. So Serotonin , the product of the Direct Serotonin Pathway, is able to influence the Direct Cortisol Pathway and Cortisol , the product of the Direct Cortisol Pathway , is able to influence the Direct Serotonin Pathway . First I'll discuss the direct pathway by which members of the Corticotropinreleasing factor family influence Serotonin. Second I'll discuss the direct pathway by which members of the Corticotropin-releasing factor family influence Cortisol. Third I'll consider the indirect pathway by which members of the Corticotropin-releasing factor family influence Arginine Vasopressin , and fourth, I'll consider the indirect pathway by which members of the Corticotropin-releasing factor family influence Testosterone. After analyzing the papers which consider members of the Corticotropinreleasing factor family and only one other parameter, I'll look at the papers which measured multiple parameters. Direct Serotonin Pathway The Dorsal Raphe Nucleus (DRN) is, if not the only, at least one of the sites at which Serotonin turnover is modulated. Members of the Corticotropinreleasing factor family influence the level of Serotonin in the brain by modulating the activity of serotonergic neurons in the caudal portion of the DRN . CRH & Serotonin gives a meta analysis of some of the references on the relationship between Corticotropin-releasing hormone (CRH) and Serotonin.

CRH Receptors discusses the difference between the two receptors: CRHR1 and CRHR2. Although this area is still an active field of research and many questions are still unanswered, much has been learned. In particular, even though CRHR1 and CRHR2 are both stimulatory, they have opposite affects on the transmission of Serotonin to other parts of the nervous system. Activation of CRHR1 reduces the transmission of serotonin while activation of CRHR2 increases the transmission. At the moment, the most likely explanation for this seems to be that the CRHR1 are located on and activate GABAergic interneurons which inhibit the serotonergic neurons with which they Synapse while the CRHR2 are located directly on serotonergic neurons, which they stimulate. For reasons which are still unclear, CRHR1 activation and subsequent inhibition of serotonergic neurons occurs at low levels of Corticotropin-releasing hormone (CRH) while CRHR2 activation and subsequent excitation of serotonergic neurons occurs at high levels of CRH. Therefore, at low levels of CRH, the transmission of serotonin is reduced, and at high levels of CRH, the transmission of serotonin is increased. Urocortins provides at least two suggestions as to how members of the Corticotropin-releasing factor family regulate the the transmission of Serotonin from the Dorsal Raphe Nucleus to the Nucleus Accumbens Septi . At the moment, the hypothesis that I find the most appealing is that the CRHR1 receptor is activated by CRH and the CRHR2 receptor is activated by Ucn2. However, this is still very much a matter of continuing research, and there is only a very tentative suggestion that initial and/or mild stress produces CRH which activates the CRHR1 receptor while prolonged and/or sustained or repeated stress produces Ucn2 which activates CRHR2 receptor. The origin of the CRH-type ligand which modulates the serotonergic neurons in the DRN is uncertain. Early research suggested that it is extrahypothalmic. That is that it does not come from the Paraventricular nucleus (PVN) of the Hypothalamus. Rather it seemed more likely to originate in the Amygdala and/or Bed Nucleus of the Stria Terminalis and/or Hippocampus and/or Edinger-Westphal nucleus and/or Locus Ceruleus (LC). Now, more recent research opens the possibility that it may originate in the PVN after all. As discussed in: Serotonin & Impulsivity , Criminal Serotonin, Serotonin & Dominance decreased Serotonin turnover seems to be the chief endocrine correlate of impulsivity.

However, I have, as yet, no idea how Serotonin modulates the level of Dopamine at the Dopamine Receptors in the Nucleus Accumbens Septi, and this seems to be the critical factor determining the level of Impulsivity. Direct Cortisol Pathway The first function of Corticotropin-releasing hormone (CRH) to be discovered was its role in releasing ACTH (originally known as 'corticotropin') from the anterior portion of the Pituitary Gland . From the anterior portion of the pituitary, the corticotropin (latin for 'that which goes to the cortex') is carried by the blood to the Adrenal Cortex. The adrenal cortex responds to the ACTH by releasing Cortisol back into the blood stream. This is known as the HPA Axis . It's very important to recognize that this pathway by which members of the Corticotropin-releasing factor family influence the level of Cortisol in the blood stream is completely distinct and independent of the pathway by which members of the Corticotropin-releasing factor family influence the amount of Serotonin supplied by serotonergic neurons in the caudal Dorsal Raphe Nucleus (DRN) to other parts of the nervous system, particularly the brain, as described in the previous section. For more detailed discussion, see: Stress Cortisol & Behavior Cortisol & Dominance Criminal Cortisol Indirect CRH Influence on Arginine Vassopressin According to the articles reported in the sections below, Corticotropinreleasing hormone (CRH) influences Arginine Vasopressin (AVP) only through the HPA Axis (the Direct Cortisol Pathway). I found no evidence that CRH or the Urocortins influence AVP through the Dorsal Raphe Nucleus (the Direct Serotonin Pathway). references: Arginine Vasopressin Criminal Vasopressin CRH & Vasopressin Criminal CRH & Vasopressin Indirect CRH Influence on Testosterone

As was the case for Arginine Vasopressin, above, Corticotropin-releasing hormone (CRH) influences Testosterone only through the HPA Axis (the Direct Cortisol Pathway). I found no evidence that CRH or the Urocortins influence Testosterone through the Dorsal Raphe Nucleus (the Direct Serotonin Pathway). Cortisol directly inhibits testicular Luteinizing Hormone (LH) receptor function without decreasing the level of circulating LH. Therefore, increased levels of circulating cortisol cause decreased levels of circulating testosterone. Since increased levels of CRH cause increased levels of cortisol via the Direct Cortisol Pathway , increased levels of CRH cause decreased levels of testosterone. sections to be reviewed: Testosterone CRH & Testosterone Criminal Testosterone Simultaneous Pairwise Data As mentioned, above, researchers have no choice but to measure some parameters and ignore others, and the decision as to which parameters to measure and which to ignore varies from researcher to researcher. This poses a dilemma for those of us who try to index their results. If a researcher measures more than one parameter, under which parameter do we file their research? In the list of pairwise data below, I've placed papers concerning serotonin at the top of the list, followed by those concerning cortisol and finally by those concerning testosterone and vasopressin. Cortisol & Serotonin So far, I've found only one paper which measured both cortisol and serotonin and nothing else. I didn't find its interpretation of its results convincing. Vasopressin & Serotonin Criminal Vasopressin & Serotonin Criminal Testosterone & Serotonin Cortisol & Testosterone Cortisol, Testosterone & Dominance Criminal Cortisol & Testosterone Testosterone & AVP Criminal Testosterone & Vasopressin

Simultaneous Three-way Data Cortisol & Testosterone & Serotonin Criminal Testosterone, Serotonin & ACTH Although I haven't yet provided comments on the sets of pairwise and three-way data listed above, I'm going to go on and attempt a first statement of an endocrine hypothesis which emphasizes Serotonin. I'll come back and add comments on the list of data sets, above, after I've made a first statement of the endocrine hypothesis. The Male Dominance Hierarchy: There is a phenomenon, usually referred to as the " Male Dominance Hierarchy " , which seems to be universal among all vertebrates, including humans. This paper will offer an endocrine explanation for the male dominance hierarchy and then suggest how its disruption might help to explain the many difficulties faced by boys who try to grow up without a father [ Family Structure ]. In particular, fathers train their sons' endocrine systems as the boys grow into manhood. The endocrine systems of boys who grow up without the influence of an older, dominant male, such as a father, never receive this training, and their untrained endocrine systems prevent them from ever fitting comfortably into society. The Endocrine Hypothesis: As explained in the Direct Serotonin Pathway, the Dorsal Raphe Nucleus (DRN) may be, if not the only, at least one of the sites at which Serotonin turnover is modulated. Low levels of Corticotropin-releasing hormone (CRH) and/or the Urocortins inhibit the serotonergic neurons and reduce transmission of Serotonin to other parts of the brain. Higher levels of CRH stimulate the serotonergic neurons and increase transmission of serotonin to other parts of the brain. Increased serotonin increases self-control by decreasing Impulsivity . Very high levels of serotonin result in Learned Helplessness . A dominant father controls his son's Serotonin level through Stress . He uses stress to adjust the amount of serotonin transmitted from the Dorsal Raphe Nucleus (DRN) to the remainder of his son's brain. He adjusts the amount of serotonin transmitted from his son's DRN so that his son's Impulsivity remains within acceptable limits without lapsing into Learned Helplessness . As a son matures into manhood, his father will allow his son's serotonin to decline during approved activities such as competition in sports, academics or business, but will maintain his son's elevated serotonin level relative to unapproved activities

such as disrupting class in school, selling drugs or other forms of crime. When a boy doesn't have a father to keep his serotonin level up, he experiences an inappropriate decrease in serotonin leading to poor impulse control. As explained in Direct Cortisol Pathway, the stress imposed by a father on his son also controls the his son's level of circulating Cortisol, and this in turn controls the level of his son's circulating Testosterone which, in turn, controls his son's Aggression. When a boy doesn't have a father to keep his Serotonin level up and his Testosterone level down, he experiences an inappropriate decrease in serotonin leading to poor impulse control (Impulsivity), and an inappropriate increase in testosterone, leading to Aggression. From the point of view of the Male Dominance Hierarchy, a boy without a father is making a premature attempt to assert himself as dominant. All boys struggle to ascend the male dominance hierarchy, but we live in a complex world. Males who achieve endocrine dominance before mastering civilization's complexity can do society more harm than good. References: All references now and have at least some links, whether included in the original copy or provided by me. Children of the Amphioxus Subcortical Brain Family Structure Human Endocrine System Hormone Criminal Hormones Corticotropin-releasing factor family Corticotropin-releasing hormone (CRH) Criminal Corticotropin-Releasing Hormone ACTH Corticosteroids Cortisol Criminal Cortisol Corticosterone Glucocorticoids Glucocorticoid Receptor Glucose Androgens

Testosterone Criminal Testosterone Gonadotropins Gonadotropin-Releasing Hormone (GnRH) Luteinizing Hormone Nonapeptides Arginine Vasopressin Oxytocin Cytokines Melatonin

Neurotransmitter Synapse Serotonin Criminal Serotonin 5-HIAA Serotonin Receptors GABA Acetylcholine Urocortins Biogenic Amines Monoamine Catecholamine Dopamine Dopamine Receptors Norepinephrine MHPG HVA Neuropeptides Neuromodulators Neuromodulator Receptors Fos Immunohistochemistry Dorsal Raphe Nucleus Edinger-Westphal nucleus Paraventricular nucleus (PVN) Amygdala Bed Nucleus of the Stria Terminalis Hippocampus Nucleus Accumbens Septi Ventral Tegmental Area Limbic System Hypophyseal Portal System

Pituitary Gland Anterior Pituitary Posterior Pituitary Adrenal Gland Adrenal Cortex Adrenal Medulla HPA Axis Thalamus Hypothalamus Reticular Activating Sytem Cerebral Cortex Prefrontal Cortex Periaquiductal Gray Cingulate Cortex Ventricular System Cerebrospinal Fluid Locus Ceruleus (LC) Brainstem Medulla Oblongata Central Nervous System (CNS) Autonomic Nervous System Sympathetic Nervous System Parasympathetic Nervous System Receptors CRH Receptors G-Protein Coupled Receptors Ligands Agonist Pheromones Stress Stress Evolution Pain Fear Agonistic Behavior Aggression Impulsivity Learned Helplessness CRH & Serotonin Serotonin & Impulsivity Serotonin & Dominance Criminal Corticotropin-Releasing Hormone Testosterone & Serotonin

Cortisol & Behavior Cortisol & Dominance CRH & Vasopressin Criminal CRH & Vasopressin CRH & Testosterone Cortisol & Serotonin Cortisol & Testosterone Vasopressin & Serotonin Testosterone & AVP Criminal Testosterone & Serotonin Criminal Vasopressin & Serotonin Criminal Cortisol & Testosterone Criminal Testosterone & Vasopressin Cortisol, Testosterone & Dominance Cortisol & Testosterone & Serotonin Criminal Testosterone, Serotonin & ACTH Direct Cortisol Pathway Direct Serotonin Pathway Male Dominance Hierarchy Lamprey Dominance Hierarchies Shark Dominence Hierarchies Teleost Dominance Hierarchies Lungfish Dominance Hierarchies Salamander Dominance Hierarchies Monotreme Dominance Hierarchies Marsupial Dominance Hierarchies Rodent Dominance Hierarchies Primate Dominance Hierarchies Human Dominance Hierarchies Endocrinology of Dominance

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Perserverence furthers. (The I Ching)