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Cold Spring Harb Perspect Med. 2011 Sep; 1(1): a008862.

doi: 10.1101/cshperspect.a008862

PMCID: PMC3234454

PMID: 22229124

The History of Parkinson's Disease: Early Clinical Descriptions and Neurological Therapies

Christopher G. Goetz

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Abstract

Although components of possible Parkinson's disease can be found in very early documents, the first clear medical description was written in 1817 by James Parkinson. In the mid-1800s, Jean-Martin Charcot was particularly influential in refining and expanding this early description and in disseminating information internationally about Parkinson's disease. He separated Parkinson's disease from multiple sclerosis and other disorders characterized by tremor, and he recognized cases that later would likely be classified among the Parkinsonism-plus syndromes. Early treatments of Parkinson's disease were based on empirical observation, and anticholinergic drugs were used as early as the nineteenth century. The discovery of dopaminergic deficits in Parkinson's disease and the synthetic pathway of dopamine led to the first human trials of levodopa. Further historically important anatomical, biochemical, and physiological studies identified additional pharmacological and neurosurgical targets for Parkinson's disease and allow modern clinicians to offer an array of therapies aimed at improving function in this still incurable disease.

Since Parkinson’s disease was first described in 1817, rational treatments have evolved based on anatomical, biochemical, and physiological studies. For example, the discovery of dopaminergic deficits led to the use of levodopa.

Important historical anchors for the study of Parkinson's disease concern the early descriptions of the disorder, its separation from other neurological conditions, and the evolution of therapy from empirical observations to rational treatment designs based on the growing knowledge of anatomy, biochemistry, and physiology of the basal ganglia. Whereas the rest of this collection will focus on the contemporary and future directions of these issues, this article provides the background history of Parkinson's disease, highlighting persons and discoveries primarily from the nineteenth and early twentieth centuries.

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EARLY CLINICAL DESCRIPTIONS

Defining Parkinson's Disease

Parkinson's disease was first medically described as a neurological syndrome by James Parkinson in 1817, though fragments of Parkinsonism can be found in earlier descriptions (Parkinson 1817). As examples, Sylvius de la Boë wrote of rest tremor, and Sauvages described festination (Sylvius de la Boë 1680; Sauvages 1768; Tyler 1992). Much earlier, traditional Indian texts from approximately 1000 BC and ancient Chinese sources also provide descriptions that suggest Parkinson's disease (Manyam 1990; Zhang et al. 2006). In succinct and pithy English, Parkinson captured the clinical picture:

Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forward, and to pass from a walking to a running pace: the senses and intellects being uninjured.

Parkinson reported on six case sketches, three of the patients observed in the streets of London and one only seen from a distance (Fig. 1).

Figure 1.

Essay on the Shaking Palsy. James Parkinson's short monograph is the first clear medical document dealing with Parkinson's disease (Parkinson 1817).

Jean-Martin Charcot, in his teaching at the Salpêtrière over 50 years later, was more thorough in his descriptions and distinguished bradykinesia as a separate cardinal feature of the illness (Charcot 1872):

Long before rigidity actually develops, patients have significant difficulty performing ordinary activities: this problem relates to another cause. In some of the various patients I showed you, you can easily recognize how difficult it is for them to do things even though rigidity or tremor is not the limiting feature. Instead, even a cursory exam demonstrates that their problem relates more to slowness in execution of movement rather than to real weakness. In spite of tremor, a patient is still able to do most things, but he performs them with remarkable slowness. Between the thought and the action there is a considerable time lapse. One would think neural activity can only be effected after remarkable effort.

Charcot and his students described the clinical spectrum of this disease, noting two prototypes, the tremorous and the rigid/akinetic form. They described in full detail the arthritic changes, dysautonomia, and pain that can accompany Parkinson's disease. Charcot was also the first to suggest the use of the term “Parkinson's disease” rejecting the earlier designation of paralysis agitans or shaking palsy, because he recognized that Parkinson's disease patients are not markedly weak and do not necessarily have tremor (Charcot 1872).

William Gowers, working in London, contributed an important study of Parkinson's disease demographics in his “Manual of Diseases of the Nervous System,” describing his personal experience with 80 patients in the 1880s. He correctly identified the slight male predominance of the disorder and studied the joint deformities typical of the disease. Known for his descriptive prose, Gowers offered one of the most memorable similes regarding Parkinsonian tremor (Gowers 1888):

The movement of the fingers at the metacarpal-phalangeal joints is similar to that by which Orientals beat their small drums.

Further clinical descriptions and studies of the pathologic changes related to Parkinson's disease were predominantly reported by the French neurologic school. Richer and Meige (1895) provided clinical and morphologic details of the progressive stages of Parkinsonian disability, and the former provided drawings and statues that remain among the most important pictorial documents related to Parkinson's disease. Babinski commented on the strange motor fluctuations intrinsic to the disease itself (Babinski 1921). Brissaud first proposed damage to the substantia nigra as the anatomical seat of Parkinson's disease, and Trétiakoff and Foix and Nicolesco pursued further pathologic studies of the midbrain in relationship to the disease during the 1920s (Trétiakoff 1921; Brissaud 1925; Foix and Nicolesco 1925).

The most complete pathologic analysis of Parkinson's disease and the clear delineation of the brain stem lesions was performed in 1953 by Greenfield and Bosanquet (Greenfield and Bosanquet 1953). The morbidity and clinical progression of Parkinson's disease was studied in the important article by Hoehn and Yahr in which their internationally recognized staging system was first introduced. This time-honored staging system is anchored in the distinction between unilateral (Stage I) disease and bilateral disease (Stages II–V) and the development of postural reflex impairment (Stage III) as a key turning point in the disease’s clinical significance (Hoehn and Yahr 1967).

Separating Parkinson's Disease from Other Disorders

Prior to Charcot, the classification system, or nosology, of neurological disease was primitive, and disorders were largely grouped by primary symptoms, for instance, tremors or weakness. Charcot’s first important contribution to the study of Parkinson's disease was his differentiation of this disorder from other tremorous disorders, specifically multiple sclerosis (Charcot 1872). Examining large numbers of patients within the vast Salpêtrière Hospital in Paris, he developed a protocol to observe tremor at rest and then during action. He noted that the patients with action tremor had accompanying features of weakness, spasticity, and visual disturbance. In contrast, those with rest tremor differed in having rigidity, slowed movements, a typical hunched posture, and very soft speech. His early tremor studies were highly publicized and helped to establish Parkinson's disease as a distinct neurological entity that could be confidently diagnosed (Fig. 2).

Figure 2.

Charcot and “myographic curves.” (Left) French neurologist Jean-Martin Charcot (1825–1893). (Right) Semi-diagrammatic “myographic curves” published by Charcot in 1887. The top tracing represents an intention tremor in multiple sclerosis. Segment AB indicates “at rest,” and BC indicates increasing oscillations during voluntary movement. The lower tracing represents a Parkinsonian tremor, with segment AB indicating a tremor at rest, which persists in segment BC during voluntary movement. Charcot’s graphical recording method on which these drawings were based is not described, but in other circumstances he relied on various pneumatic tambour-like mechanisms (Charcot 1872; Goetz 1987).

Once the archetype of Parkinson's disease was established, Charcot and his students identified variants with features that were atypical of classical Parkinson's disease. These were termed Parkinson's disease without tremor, Parkinson's disease with extended posture, and Parkinson's disease with hemiplegia. These cases are of historical interest, because they are likely examples of disorders that would later be grouped under the term, Parkinsonism-plus syndromes, including progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy. As one example, Charcot presented a patient named Bachère on several occasions. On June 12, 1888, Charcot emphasized that Bachère did not have marked tremor, and in contrast to the usual arm flexion of typical Parkinson's disease, he had a stiff and extended posture.

Look how he stands. I present him in profile so you can see the inclination of the head and trunk, well described by Parkinson. All this is typical. What is atypical, however, is that Bachère's forearms and legs are extended, making the extremities like rigid bars, whereas in the ordinary case, the same body parts are partly flexed. One can say then that in the typical case of Parkinson's disease, flexion is the predominant feature, whereas here, extension predominates and accounts for this unusual presentation. The difference is even more evident when the patients walk (Fig. 3) (Goetz 1987; Charcot 1888a).

Figure 3.

Atypical Parkinsonism. (A) Drawing from Charcot’s original lesson, given on June 12, 1888, in which he contrasted a typical Parkinson's disease showing a flexed posture (left) with a Parkinsonian variant that included the absence of tremor and extended posture (right). Charcot regularly taught his students by comparing and contrasting cases of patients from the Salpêtrière inpatient and outpatient services. (B) Four drawings by Charcot from his lesson on atypical Parkinson's disease, dated June 12, 1888, showing the distinctive facial features of his patient, Bachère, showing forehead muscles and superior orbicularis in simultaneous contraction, activation of the palpebral portion of the orbicularis and combined activation of the frontalis superior portion of the orbicularis and platysma, giving a frightened expression in contrast to the placid, blank stare of typical Parkinson's disease patients. This case is a compelling case of likely progressive supranuclear palsy (Goetz, 1987; Charcot 1888a).

In addition to extended posture, this patient had particular facial bradykinesia and contracted forehead muscles. Charcot commented that the patient had the perpetual look of surprise, because the eyes remained widely opened and the forehead continually wrinkled (Fig. 3) (Goetz 1987; Charcot 1888a). In a modern setting, Jankovic has detailed similar facial morphology in Parkinsonism-plus patients, specifically those with progressive supranuclear palsy (Jankovic 1984). No specific supranuclear eye movement abnormalities were described. Another Salpêtrière patient with “Parkinson's disease in extension” was described by Dutil in 1889 and eye movement abnormalities are mentioned, although a supranuclear lesion is not documented clinically (Dutil 1889; Goetz 1996). This case also had highly asymmetric rigidity of the extremities, a feature more reminiscent of corticobasal degeneration than progressive supranuclear palsy. In this case, the extended neck posture was graphically emphasized:

The face is masked, the forehead wrinkled, the eyebrows raised, the eyes immobile… . This facies, associated with the extended posture of the head and trunk, gives the patient a singularly majestic air (Dutil 1889; Goetz 1996).

With clinical features reminiscent of both progressive supranuclear palsy and corticobasal degeneration, this patient was mentioned in several articles from the Salpêtrière school, although no autopsy was apparently performed. Collectively, these cases show that even the earliest diagnosticians recognized classic Parkinson's disease and cases that needed to be distinguished from it. Today, these Parkinsonism-plus diagnoses are known to have additional distinctive features, including poor response to dopaminergic therapies and different pathological lesions than seen in Parkinson's disease.

Another important entity to be distinguished from Parkinson's disease was postencephalitic Parkinsonism, today a rare cause of Parkinsonism, but a very frequent disorder in the period after 1916. Following the influenza epidemic of 1916–1917, a neurologic syndrome that included Parkinsonism, along with multiple other signs, occurred in alarming numbers (von Economo 1919). The additional behavioral, ocular, and motor problems of these patients attested to more diffuse neurologic disease than seen typically in Parkinson's disease. This condition has largely disappeared in the twenty-first century, because the survivors have died and no recurrence of an epidemic of this magnitude has recurred. Other important forms of atypical Parkinsonism to be distinguished from Parkinson's disease include a juvenile form of Parkinson's disease, originally described by Willige in 1911 (Willige 1911), with a more full description and its association with atrophy of the globus pallidus provided by Ramsey Hunt and van Bogaert (Ramsey Hunt 1917; van Bogaert 1930).

In the years after these pioneering papers, the concepts of neural circuits evolved with key nuclei of importance to the clinical presentation of Parkinsonism being the substantia nigra, the globus pallidus, and the caudate nucleus and putamen (striatum). Involvement of the striatum resulting in Parkinsonism was documented in a variety of neurological disorders. Striatal-nigral degeneration was described by Adams, van Bogaert, and Vander Eecken, and, though originally classified as a single disease, it has since been merged into the larger diagnosis of multiple system atrophy (Adams et al. 1964). Parkinsonian states related to striatal pathology were later identified in the form of Huntington’s disease, in which a Parkinsonian presentation is referred to as the Westphal variant (Westphal 1883) and in cases of striatal calcification, either on a hereditary basis (Bruyn et al. 1964) or as an acquired metabolic disorder often related to hypoparathyroidism (Muenter and Whisnant 1968).

The historical discussion of Parkinsonian disorders that are frequently confused with Parkinson”s disease includes drug-induced and toxin-induced cases as well. The introduction of the antipsychotic agents, originally termed neuroleptics, led to dramatic improvements in schizophrenic and other psychotic behaviors, but induced Parkinsonism largely indistinguishable from Parkinson's disease itself (Steck 1954). Later understanding that these drugs block dopamine receptors in the striatum explained this clinical presentation and led to the development of antipsychotic drugs with lower proclivity to block striatal receptors and less propensity to induce Parkinsonism. The landmark observation on a cluster of young patients who presented with severe Parkinsonism that appeared to be typical Parkinson's disease except for the young onset and severity of signs led to the discovery that the causative agent was a self-administered narcotic derivative, MPTP, that selectively damages the substantia nigra (Langston et al. 1983). This product has provided a means to induce Parkinsonism in experimental animals and remains the “gold standard” model to study Parkinson's disease in preclinical studies of new treatments for Parkinson's disease.

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THE EVOLUTION OF TREATMENTS

The history of Parkinson's disease is tightly linked to therapeutic interventions, ranging from serendipitous observations to controlled clinical trials of specifically designed agents.

Parkinson devoted a chapter of his monograph to “considerations respecting the means of cure” (Parkinson 1817). In humility and perhaps with a vision toward current concepts of neuroprotection, he hoped for the identification of a treatment by which “the progress of the disease may be stopped” (Parkinson 1817). To this end, he advocated very early therapeutic intervention when signs were largely confined to the arms without balance and gait impairments. Reflecting therapeutic approaches of the early nineteenth century, Parkinson recommended venesection, specifically advocating bloodletting from the neck, followed by vesicatories to induce blistering and inflammation of the skin. Small pieces of cork were purposefully inserted into the blisters to cause a “sufficient quantity” of purulent discharge (Parkinson 1817). All these efforts were designed to divert blood and inflammatory pressure away from the brain and spinal cord, and in this way, decompress the medulla that Parkinson considered the seat of neurological dysfunction.

Pharmacological Advances: Charcot and Gowers

Being the two most celebrated clinical neurologists of the nineteenth century, Jean-Martin Charcot and William Gowers serve as important icons for the study of standard and emerging treatments for Parkinson's disease. Charcot’s intern, Ordenstein, wrote his medical thesis on the treatment of Parkinsonian tremor with belladonna alkaloids, the first well-established treatment of Parkinson's disease (Ordenstein 1972). These agents are centrally active anticholinergic drugs that later would be understood to affect the cholinergic/dopaminergic balance in the striatum and thereby improve Parkinsonism. The credit of the observation of anticholinergic efficacy surely belongs to Charcot himself who managed his Salpêtrière School with strict centralized supervision and oversaw every aspect of the neurological program. As with other young and aspiring students like Gilles de la Tourette and Pierre Marie, Ordenstein profited from publishing the observation with his name as sole author, but contemporaries would not have been deluded into thinking of it as coming from anyone besides Professor Charcot. Of the many centrally active anticholinergic agents of the era, Charcot’s preferred product for Parkinson's disease was hyoscyamine. This plant-based agent was prepared as pills, usually powder rolled into bits of white bread, or as a syrup. As shown in a prescription located in the Philadelphia College of Physicians, Charcot’s anticholinergic treatment was sometimes combined with rye-based ergot products that in fact are the pharmacological basis of some modern dopamine agonists, drugs that directly stimulate striatal dopamine receptors and thereby simulate the activity of dopamine itself (Fig. 4). Although Tyler has aptly documented that Charcot was not the first interventionist to advocate hyoscyamine (Tyler 1992), Charcot’s name became linked to the drug because of the widespread international publication of his lectures and classroom demonstrations.

Figure 4.

Early treatment of Parkinson's disease. Prescription dated 1877 from the College of Physicians of Philadelphia Library. In treating Parkinson's disease, Charcot used belladonna alkaloids (agents with potent anticholinergic properties) as well as rye-based products that had ergot activity, a feature of some currently available dopamine agonists. Charcot’s advice was empiric and preceded the recognition of the well-known dopaminergic/cholinergic balance that is implicit to normal striatal neurochemical activity (Charcot 1872).

A unique historical opportunity to examine the early treatment of Parkinson's disease is provided by a series of 18 unpublished letters in the Charcot collection at the Bibliothèque Charcot in Paris (Portfolio MA VIII: Parkinson's disease). These letters cover a period of at least 15 months from January 1863 through March 1864. Although the collection only contains the patient’s letters and not Charcot’s replies, one can follow the doctor–patient interaction because of Charcot’s technique of closing his letters traditionally with: “I would be most obliged Monsieur, if you would remind me of this prescription the next time you write.” The patient's letters therefore systematically begin with a summary of the prescribed therapy and follow with the patient’s own observations. In addition to hyoscyamine and ergot-based products, Charcot advocated an overall program of rest and reduced stress. This type of therapy was generally advocated for many primary neurological disorders (Mitchell 1908). For this patient, he added camphor, silver nitrate, iron compounds, henbane pills, and zinc oxide. The rationale for using these agents was not explained by Charcot, and their pharmacology does not involve the dopamine system. The use of iron may have been based on Romberg’s earlier observation that carbonate of iron in association with warm baths and cold affusions to the head and back induced “a marked diminution of symptoms.” (Romberg 1846). Whether based on his own experience or Romberg’s warning against trying strychnine, Charcot steered away from this therapy for Parkinson's disease patients. Charcot was highly specific in his instructions, insisting that quinquina, a quinine derivative, must be diluted with syrup made from orange rind and each dose of silver nitrate must be impregnated in 9 g of soft bread to form an ingestible pill. The letters communicate encouragement to the patient, reinforce the need for patience in facing chronic illness, and a willingness to consider new treatment strategies if traditional ones were unsuccessful. However, his enthusiasm to try new interventions never clouded his objective vision of efficacy. In reviewing pharmacologic treatments for Parkinson's disease in 1872, Charcot stated:

Everything, or almost everything, has been tried against this disease. Among the medicinal substances that have been extolled and which I have myself administered to no avail, I need only enumerate a few (Charcot 1872).

In rejecting most medicines, Charcot advocated vibratory therapy for the management of Parkinson's disease. Charcot had observed that after long carriage, train, or horseback rides, patients with Parkinson's disease experienced marked symptom amelioration. He therefore developed a replication device to provide rhythmic movement by an electrically powered “shaking chair” (fauteuil trépidant) (Fig. 5) (Charcot 1892a). His student, Gilles de la Tourette, fashioned a helmet that was more easily transported and vibrated the brain rather than the body (Goetz et al. 1995). Other used therapies included hydrotherapy, spa treatments, and light exercise. Electrical stimulation by faradic, galvanic, or direct spark (franklinization) therapy was used to stimulate weakened muscles. Charcot was, however, adamant that patients with Parkinson's disease were not particularly weak, having tested them with dynamometers and finding their strength to be normal for most of the duration of illness. It was partly for this reason that he dismissed the terms, paralysis agitans and shaking palsy, and advocated instead the designation, Parkinson's disease.

Figure 5.

Vibratory therapy. Charcot observed that patients with Parkinson's disease experienced a reduction in their rest tremor after taking a carriage ride or after horseback riding. He developed a therapeutic vibratory chair that simulated the rhythmic shaking of a carriage (Goetz 1996). A vibratory helmet to shake the head and brain was later developed. Such therapies were not used widely but the availability of modern medical vibratory chairs offers an opportunity to confirm or refute Charcot’s observation.

A more unusual and hazardous early treatment of Parkinson's disease involved the use of a suspension apparatus to stretch the spinal cord (Goetz et al. 1995). Developed in 1883 in Russia, the apparatus gained celebrity when Charcot examined its safety and efficacy in a variety of disorders, including Parkinson's disease. Using gravity and the patient’s weight to put excessive vertical traction on the spinal cord and nerves, the therapist hoisted the subject in mid-air with a pulley and a harness that slipped under the chin and occiput. In Parkinson's disease patients, rigidity and some sensory symptoms improved, but tremor was not ameliorated. Edmond de Goncourt described the therapy with allusions to the macabre artwork of Goya, and the serious side effects and stress on patients led Charcot to abandon this strategy shortly after its introduction in France (de Goncourt and de Goncourt 1887–1889).

Charcot’s British contemporary, WR Gowers, followed similar treatment strategies. He stressed the negative effects of mental strain and physical exhaustion, advocating that “life should be quiet and regular, freed, as far as may be, from care and work.” (Gowers 1899). For tremor, he used hyoscyamine and also noted arsenic, morphia, conium (hemlock), and “Indian hemp” (cannabis) as effective agents for temporary tremor abatement. Writing specifically of the power of cannabis and opium in combination, he stated: “I have several times seen a very distinct improvement for a considerable time under their use.” (Gowers 1899). Today, cannabis is known to have some dopaminergic activation properties, but opium affects the motor system in a generalized, sedative manner without direct or primary dopaminergic involvement.

Levodopa and Dopamine-Based Therapies

Through the mid-twentieth century, the treatment of Parkinson's disease remained largely that of the nineteenth century, and though a wide variety of centrally active anticholinergic drugs were developed and used, they all were similar in their efficacy and side effect profiles. In the Handbook of Clinical Neurology, the chapter, “Drug treatment of parkinsonism and its assessment” (published in 1968) discusses ten synthetic anticholinergic compounds and a potpourri of agents under the designation “Other drugs which have been recommended, some of them without any justification.” (Onuaguluchi 1968). The emphasis of this period remained on supportive physical therapy and the management of hypersalivation, seborrhea, decubiti, and infections. In the context of this relative stagnation, the impact of levodopa was magnified.

As summarized by Hornykiewicz, dopamine was first synthesized in 1910 by G. Barger and J. Ewens (Hornykiewicz 2002). In the same year, H. Dale discovered its weak sympathomimetic qualities. These observations were later remembered when P. Holtz discovered the enzyme, dopa decarboxylase and documented that levodopa was synthesized to dopamine through its action. At this time, dopamine was relegated to a simple intermediate compound for the synthesis of noradrenaline and adrenaline. The consistent identification of substantial amounts of dopamine in various tissues, however, prompted the search for a more primary role. Working in Blaschko’s Cambridge University laboratory, Hornykiewicz studied blood pressure control in experimental animals and clearly confirmed that dopamine had distinct effects independent of other catecholamines. Shortly thereafter, in the late 1950s, two seminal discoveries occurred: dopamine localization within the brain, specifically in the striatum; and the development of the reserpine-model, later to be used as the first model of Parkinsonism that was reversed by levodopa treatment. In concert, these discoveries rapidly advanced hypotheses on the role of dopamine loss in the pathogenesis of Parkinson's disease itself (Carlsson et al. 1958; Sano et al. 1959), and led Bertler and Rosengred to conclude that “dopamine is concerned with the function of the striatum and thus with the control of movement.” (Bertler and Rosengred 1959). Ehringer and Hornykiewicz turned to human brain and after examining a series of control specimens, discovered the striatal dopamine depletion in Parkinson's disease and postencephalitic parkinsonism brains (Ehringer and Hornykiewicz 1960). With the knowledge that levodopa was the natural precursor to dopamine, Hornykiewicz was now prepared to suggest human trials in Parkinson's disease patients.

Birkmayer received Hornykiewicz’s supply of laboratory levodopa and injected it intravenously for the first time to Parkinsonian patients in 1961. The antiakinetic effects were quickly published:

Bed-ridden patients who were unable to sit up, patients who could not stand up when seated, and patients who when standing could not start walking performed all these activities with ease after L-dopa [levodopa]. They walked around with normal associated movements and they could even run and jump. The voiceless, aphonic speech, blurred by pallilalia and unclear articulation, became forceful and clear as in a normal person (Birkmayer and Hornykiewicz 1961).

Subsequent open-label levodopa trials with oral preparations confirmed both short and long-term benefits, and a double-blind placebo controlled trial followed (Barbeau 1969; Cotzias et al. 1969; Yahr et al. 1969). These reports launched levodopa’s establishment as the premier agent to treat Parkinson's disease symptoms and signs. Although new formulations and peripherally acting dopa-decarboxylase inhibitors have added new dimensions to the therapy, none of these events rival the first discoveries.

Given that levodopa is a naturally occurring amino acid, researchers have reexamined older therapies to search for possible discoveries of levodopa-containing compounds in early medicine. Of note, cowage or cowitch plant (Mucuna pruriens) is known under the name of Atmagupta in Sanskrit and contains levodopa (Manyam 1990). One of the remedies used to treat the condition thought to be possible Parkinson's disease in traditional Indian medicine is called Masabaldi Pacana, which contains beans of Mucuna pruriens. These observations offer interesting, albeit indirect, evidence that patients with Parkinsonism may have experienced the benefit of levodopa early in the history of medicine.

The more modern discoveries of dopamine agonists and enzyme inhibitors that enhance the bioavailability of dopamine (monoamine oxidase inhibitors and catechol-O-methyl transferase inhibitors) date to the contemporary period and are of less importance to this historical review that emphasizes early discoveries. These developments have been based on the logical understanding of the dopamine system, metabolic pathways, and receptor populations. Further discoveries of modulating influences by serotonin, adenosine, GABA, and glutamate systems have opened horizons for further pharmacological developments. The history of amantadine is of interest because of its serendipitous discovery as an anti-Parkinsonian agent. Developed as an antiviral agent, it was used widely in nursing home populations, and Schwab noted its unexpected benefit on tremor, balance, and akinesia in both Parkinson's disease and postencephalitic parkinsonian patients (Schwab et al. 1969). This agent has mild dopamine effects, likely due to inhibition of striatal synaptic dopamine reuptake so that more dopamine is left within the synapse to activate dopamine receptors. It has effects on the glutaminergic system with likely indirect effects on dopamine function through this mechanism.

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SURGERY

In the early 1900s, surgery for movement disorders was pioneered by V. Horsley and his engineering colleague, R.H. Clarke (Fig. 6). They developed early stereotaxic equipment to target brain nuclei, though their early surgeries dealt with hyperkinetic disorders rather than Parkinson's disease (Horsley and Clarke 1908). Bucy and Case and Klemme excised cerebral cortex to treat Parkinsonian tremor, but this type of ablative surgery induced hemiparesis and was abandoned (Bucy and Case 1939; Klemme 1940). Meyers first focused on the basal ganglia as a lesion target for abating Parkinsonian tremor in the 1940s and noted that rigidity improved as well as tremor. Importantly, spasticity and paresis did not compromise the improvement (Meyers 1940). In 1953, by accident, I. Cooper cut the anterior choroidal artery during surgery on a Parkinsonian patient and was forced to ligate it to prevent a hematoma. The unexpected and remarkable relief of tremor and rigidity on the contralateral side led to more widespread use of this procedure, though mortality was approximately 10% (Cooper 1953). Electrical coagulation procedures involving the globus pallidus, thalamus, and the ansa lenticularis (ansotomy) were performed with early stereotaxic procedures (Spiegel and Wycis 1954). Hassler and Reichert focused more directly on the ventrolateral nucleus of the thalamus, also referred to as the Ventral Oralis Anterior (Voa) nucleus (Hassler 1955; Reichert 1962). All these reports were hampered by the lack of involvement by medical neurologists with resultant concerns of incomplete reporting, lack of long-term follow-up and potential minimalization of morbidity. Further, the role of surgery was eclipsed by the advent of levodopa in the 1960s, so that a long hiatus occurred when surgery was not extensively used in Parkinson's disease. During this time, however, more advanced surgical techniques were developed, and these innovations would be later applied to Parkinson's disease patients near the end of the twentieth century. Such treatments date to the contemporary period and include pallidotomy, subthalamic nucleus ablation, deep brain stimulation to thalamus, pallidum and subthalamic, and various transplantation procedures. Most recent are the developments of gene-based therapies that have entered clinical trials.

Figure 6.

Early surgical interventions. (Left) Victor Horsley (1857–1916) was a celebrated British surgeon who attempted a surgical intervention on a movement disorder patient with athetosis in 1909. He excised motor cortex with substantial improvement in involuntary movements. (Middle) Working in London with his physiologist colleague, Robert Henry Clarke (1850–1926), he developed early stereotaxic equipment, first for animal experiments and then for humans. (Right) This daunting surgical apparatus taken from their reports in Brain in 1908 guided them to deep brain centers including the basal ganglia and the cerebellum (Horsley and Clarke 1908).

Placebo Therapy

The relationships between dopamine release and positive motivation, novelty seeking behaviors, and attention have allowed researchers to understand the long-acknowledged placebo impact on Parkinson's disease. The Charcot letters cited above suggest that Charcot too understood clearly the importance of his presence and command over the patient’s well-being. As anchored as he remained in neuroanatomical concepts through the end of his career, Charcot’s last monograph was titled “Faith Cure” and dealt with the profound improvements that some patients with neurological disease experienced through nontraditional therapies (Charcot 1892b). Placebo-controlled trials have become standard in Parkinson's disease, even in the surgical arena, mainly because a large percentage of patients on placebo treatment experience objective improvement in parkinsonism (Goetz et al. 2008). The facilitation of striatal dopaminergic activity in these settings has been shown by neuroimaging techniques (de la Fuente-Fernandez et al. 2001). The funding of federal grants for the specific study of placebo effects in Parkinson's disease is, in itself, of historical significance (Goetz et al. 2008).

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CONCLUDING REMARKS

Historical documents on Parkinson's disease and descriptions that evoke Parkinsonism from eras prior to the first full medical delineation of the disease provide a continuing source of potential neurological insights. As only one example, summarized in a review of traditional and complementary therapies for Parkinson's disease (Manyam and Sánchez-Ramos 1999), in 1928, Lewin isolated an alkaloid from the Banisteriopsis caapi vine used in ceremonial medicine among Amazonian tribes. He provided purified banisterine to his colleague, Beringer, who tested it on patients with Parkinson's disease with reported marked benefit. The data were presented to the Berlin Medical Association along with a film documenting the changes in rigidity, bradykinesia, and gait impairment. Though this agent was not pursued further, the example underscores the potential lessons from careful reading of traditional medicine sources and the prospects for new discoveries based on older observations. Charcot’s advocacy for vibratory therapy has been tested in a modern setting (Kapur et al. 2011), but Gowers’ encouraged use of Cannabis has yet to be systematically evaluated with strong clinical trial methodology. Numerous other therapies have suggestive roles in Parkinson's disease but have not been rigorously tested, including specific forms of physical exercise, massage therapy, and relaxation techniques. The active participation of the Parkinsonian subject in these treatments complicates a controlled study design, but these interventions scientifically deserve to be tested with the same rigor as new pharmacological or surgical treatments. In the continuing search for therapies to ameliorate current disability and to slow the natural deterioration that is implicit to Parkinson's disease today, the guiding words of Charcot remain modern and applicable: “If you do not have a proven treatment for certain illnesses, bide your time, do what you can, but do not harm your patients” (Charcot 1888b).

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ACKNOWLEDGMENTS

Dr. Goetz acknowledges the Parkinson's Disease Foundation that supports the Rush University Medical Center Parkinson's Disease and Movement Disorder Program with an annual grant.

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Footnotes

Editor: Serge Przedborski

Additional Perspectives on Parkinson's Disease available at www.perspectivesinmedicine.org

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Thats the opener, as a citation as directly understodo to mean quoted article. Lets talk about it as my research now.

Arhcins is a branch of parkers, pews, or alchettimers dissorder known as the parkbench family coined in person quotes via its origiantor and mutated diagnosee veneldel ways. Or vendel walker. I just knew him growing up. Which is a type of source known as bermudas, where its word of mouth that can be verified as second hand knowledge as a criteria source started in victorian england and nazi germany during ww2. Anyways thats just his real name as that doctor. Um. Arhcisins syndrome is aging out of order. Here are my references.

taken in 2019.

taken in 2017.

Taken around the premiere and original christmas month of coffee coke which we herebye coin the name of as cofefe. unique coak falvors in honour of magick or ritual or season or great meaninfulness that becomes that as seasonal coke flavors before or shortly after corona virus.

fat people are steyrypted as older then they are. Anyways. This is in 2022.

https://www.youtube.com/watch?v=r6Wqm-r5w0M&ab_channel=AdamSnowflakearchive with music viral on tick tock at the time that the company and mainstream users of the chinese app could confirm. Its just all emo.

If you dont like girls.

I hear he is a piece of shit hanging above the choro zone.  As a lyric to one.

The greatest showman soundtrack.

Hey ren around release.

Katy perries i kissed a girl nightcore were the main songs featured at the height of popularity which is the eqwuation 6 x 24 as their release date sum magma, which means an equation for their popularity would be the year the song is released like hasbeen hotels angel dust song which had been out for 6 months at the time, over the last song which is epic the musical which was new at the times, athenas song or goodbye song after warrior of the mind in epic the musical by horsehay vantas solve for mind as assigning each song a pridic alement with each letter outside repeating which should be decimals would be a = 1 2 equals b 7 would be g and so on. And you get the year it came out as a sum for totall popularity proved with gasess.

this one is not a repost its this with its real date from 11/14/2023 as standards of youtube. While other videos of this face can and were repsoted around 12 years ago video downloads in that way did not exist and then were quickly monitored after tehy started too.

Its just weight again its not age.

https://www.youtube.com/watch?v=ABgwF2D9Riw&ab_channel=Dionreviewsstuff

He goes by different names per age.

This was high quality home video at the time especially without proper lighting without a rotary when this is written.

This just proves how old he looks here, as ten years ago as a sum estimate from 11/14/2023. Which means how often he looks this age. He went by jaden and was at first a vlogger, then a skit artist, then w awbeshow creator, then a blogger, then an amv artist, then a educational channel on youtube. Proving this man ages out of order as he has claimed by face estimates. You would know because i am him and this prove it. I said i had proof i just get embarrassed about ti so i thought it was magick and made you wait im sorry. For benign 6000 years old.

Lets explain that but finish with the face.

Its a catelog of what was popular at the time. Especially on youtube and phillip defrancos movie club where these videos wer popular but were not often featured if at all.

Otehrkin is a fairly rediscovered contempt so tether this hd video was filmed in 16001 or 1841 or he made a video about it when it came back recently ast htat day. It was.

these were all filmed in real time. So as you can see for 10-15 years he got younger he didnt age older. So what was it. How the hell. These arent archived. The video qualities too good via the history of camera quality especially on teh internet.

https://www.youtube.com/watch?v=y_rILenmgP0, youtubes video quality through the ages, 2kliksphilip, 646K subscribers

History of the internet life noggin. https://www.youtube.com/watch?v=h8K49dD52WA

So heres the theory with numbers and gases to prove it via the help of jc howard snow mary ann oliver and morgan morgan hoffman, and skynewtwork a freindgroup, jason via and venroe the cousins deul hereby after referred to as teh muse network or friends. Um. the thing with age is that is its shapes on the face. This face does have different shapes. But they usually are folds of the cheeks and theres a lot of evidence to suggest instead it just morphs into a different head. If parkes was a face thing rather then a spine it would be a form of scoliosis where the brain and body go younger as you get older. Or stay the same age. Its mental age regression ro acting like a baby and too immature, over and over and over again. Its jus physical its real. He physically doesnt age. The problem is his body type makes him look like a seven year old. Its the reason even though hes tall he gained so much weight to look older. But that would imply hes not fat but bloated which is apart of archins and need liposuction as a non cosmetic surgery which is rare and he will most likely die without it. This is jc writing this part. Its just kind of. He changes ages mentally yeah but he doesnt get older he only gets younger which means in 2 years he wont look 11 anymore he will look 3-6 years old given that time frame. Its also probably hormonal since while people notice each others aging every day age is tied to attention and his family all has add so they think hes older. This is hima t 16, given legal leeway by a lawsuit to get tattoos when he has lived 20 years of life via the oj simpson case as suamtnah ruler, when he was tempaoriyl adopted, its just a closed court case is all city coucnil youll have to contact. Its just kind fo though. Fairly obscure but knwoelgabel thats hes immortal. Theres a snuff film of him online on the dark webshow kiatofromtv as a special with 2 credit films called the rsoebud lips and shiteater, where you see him tortured by this original family treating him like a dog. So for some reason he can probably given those tapes control like what people see him as and what he looks like. Its just given what were about to quote he can change his face, hes the historical figure the doctor form doctor who and claims to be a time traveler.

Its just if a face has those shapes its a scientific theory that x over 9 oplus 22 with carbon being x axis times 11 numerics and 9 being over 52 minus debris solve for x and y as the letterings of axis and rotation and that proves a face like that cant lie and is one a kind. But you can tell how people think based off their faces. Its just usually if its a mutation on teh face, and it looks like its down syndrome faical dymorphsm and retardaiton which means he ages out of order, so kind of, it proves that he ages physically and mentally out of order. But only young with that stetting being 7 but that means via the theory not hypothesis of mutates given its about as faces its now a theory not a hypothesis. It means that he is those ages. Its just cant always tell cus hes tall and they all feel like 16 till a certain point where he has to age again. He always claimed he had this. I jc howard would like to discover it. Please interview me and give me my youtube channel back. It just comes with skisoprhenia which is ages 5 6 and 11 which mirror 21. So he should for lviign for centuries because this is what methodists preach as jesus just as miagkc, be allowed to get adult things because the phyoclogy of this would be torture. For not being the right age. Its just how he comes across in person, and how his traits of autism are shown as very clear in his videos especially how he edits them phychosmyatically which is black and white sahky and incohenrent and splsuhed ors plashe dtogethre and cut as jumpy, so yeah no. its just it means any kids he has would be the carbon copies of him because of how a mouth liike that would work. Mouths are kind of like sex organs and the brain and the heart. Given the similarity of shapes and tooth fungus. So yeah no he probably copies of himself it just means he has to ingest things.

https://www.youtube.com/watch?v=N2IOsCx-JGA

https://www.youtube.com/watch?v=PMGfXSz_JhY

https://www.youtube.com/watch?v=h_2hgYSCCAw

https://www.youtube.com/watch?v=Xe3ABVEbSgw 

So yeah if people can have toe fungus and tooth fungus if he dies and its amputated he woudl probabyl regrow. He probably had a shit ton of parsyse and died and came back. Its that simple for acrians locket whos real name is adam mage snowflake but birth names are tobias cunningham, tobias wintered, jaceson vorhen, jackson vorhees, and danny delval. And ayrain engro gypsy (before those words were bad) and samantha rose cohen. Its just kind of means watson our friend over here its morgan writing this part, probably born in bce died for a second and was adopted by the cohens as apache la shower. Who he was and made native america again over.

While he does mourn his sperate identies its what would happen because each age would a be a symptom of death becomes or because of how coffins work if you were trapped in one that long. I think we found an originator of humanity. But this also means hes probably been animals and can evolve adn can probably go back. Otehrkin is meantla. This is physical.

https://magickforeveryone.itch.io/the-first-and-last-tomb-of-the-original-j-chosen-thorn

“EPISODE 1 Jace Nightengail.  SAVAGE LOVE ( FRENCH VERSION ) JASON DERULO / JAWSH 685 ( SARA'H COVER )

https://www.youtube.com/watch?v=y_uU340Zyls&list=RDzdY1Uhqcfy4&index=27 

Hello yes. My name is ayrian grace. This is my selfish catelog. Selfies whatever. I survived a few bad expeirmeents and a weird case of the mumps with a particle accelerator. I can now control my face shape. It takes a hot second. But it morphs into different settings weird.  These are proofs thst I am a mutant who's face takes different forms over time. Thank-you for reading.

I sculpted it here. I have a weird imprinting feeling. Where I can choose what it looks like and even shift on command. I made this face on the website art breeder.eeder.

Artbreeder.com which is an ai that can create portraits. That means teh tools paints on its own.

わたしわ あゆらん がらす。 はじみました。むうるまぷ わ いお の いしょ と いsつ の sへんた ら いけお の いしぞ。 な おんがく の しす。 の いた の いkた もし に かたら の いしょ の いしさ。 の ひと の か。 いしょ いまと。 の ぱぐ の からが。 の しゃんた。 えと わたしわ。 えこ の ですいまる。でも えと の きと の しんと の かがね でも しんと ひと いもかさのしろ の かおともあくす。 えと 。。。 そ うら だけ の いsつ も。 ぼく づす。 の します。 の あたし の へく きと の します の ぴらたます。 の しなか の げた らかますいますたう （ね ねじんほ ぼく の はみあす た-） た。。。えと よしゅ。 えと むしゅ の いまそか の おぢん の いから が。 の さん の いと の しゅ と いき。 の へた。 そうらだけ。 の いきみおしゅ。 の いしょ の。 そう だ ま かす す。 の えと。 かからがめ。 ：）

clearly a painting given the glowing hair. No i dont choose the coloring. The way i developed this was that i had a case of severe mumps and a heroin injection in me at the time. Under severe stresses and traumas, i pressure pointed my face alot near a particle accelerator. To recreate this at home you’d have to do this while being verbally abused in ritual abuse over trauma, so rape rituals and verbal drill sargent levels of insults and screaming, no physical abuse though, for 2 weeks straight while getting drunk alot pressure pointing your face eating ice cream. Using the metaphor which is a comparison of rain cycles, lets explain via numbers and the periodic table how to do this.

8 = 94.12 over 9 instance sodium phosphite, over glass and carbonic coils which equal each to then over a centered or misplaced by two decimal towards the right. Thats this way einstein san —>.

Then take 4 divide by seven over 12. Minus 42 over 53, = 54.97 = 12.13.456789 -12 = 1.2 turrets thus 7.5 = 12.60 -10 = 84. = 2.

There you go thats how i did it.

Je suis un parta no kil un fil mon strat no at no ikenkah mo 2 weil no f59 bon shon 63 no particle un strat no ilkil no severet. Ayrian GRACE, none un filt no ilt bar no n ish mas un kil ta in fil mas strat. Ill sat no ilil 87. No istrat 6 2  2 non strat no kilil my bank not fil yon it eun shil no infkil fun bielanguala non shatn no fit not il shil ah part frances no shiantmasa.

While my face always does eventually go back to normal via a near death expeirence where i cant ususally die cus of eating toast and honey by the same aprticle accelotra, mixed with bear and a cigerete stolen, my peronality changes with the face everytime so hard that when i go back to normal i just have multiple people i become in my brain as sybol. Ive lived for centureis oops.

un kil t a no history no shan o fil uncantra no history no imosku no bop bop eatary no ishamas honey ga watashi no kilt no fikil no history so maskaa. no n trie. itemeo time travel. mesuka no shonmans no historiy lacka no ta lor no fish haook.baks.

むしゅ の きすつね の しんと の ぱか の へよ の ひと の しょなか いから しょか に すつなみ。だしくえ。 あよん の いんと まか の ほろcあうsつ えxうぺらめんつ の かああもぷ。 えと ない わ えしょ いこあと に にほんご ください。 ごめね。 じゅゐしゅ です。じゃ ん えしょ の いさかたろ いしょ の きき に ほのも そう ら えkしょ。 の へにゃくる。 えと。。。そう か の しん と います の いしょ し の へや の き た る の しへ さ。

Episode 2:

I have a seperate mutation called arhcinsins syndrome. Where you age similarly as a mutation similarly to a spider like arachnid. Which kind of live in their nests and netting mentally as different genders. Its the theory of if you picked off their legs what would happen. So i have a mutation where i age out of order and get stuck at one or two ages. People with archins never grow old. But we do go senile hitting 18. When we age younger we celebrate calling it an unbirthday after alice in wonderland. With achrins your gender chases with your age. Sometimes your sex as well and unless your dumb or numb you usually can tell or atleast others can. Even if it takes some conditioning. I also have venmo venmo which started as a parasyte in the dominican republic. Where a vagina turns into a dick and the chest area is flattened out. I documented developing archins but since its the genitals i have not actually included it in this novel. As of the moment. Maybe later i dont know. Anyways. As Jace i got stuck at 11 and pretended to be older, especially when dating my own age. I was a weird kid.

The theory of archins is the metaphor of sodium representing the age and strawberry syrup representing the process for it. Take a sodium drenched napkin after turning the solid into a liquid or gas. Place the strawberry syrup on a napkin and the process that happens to it is similar to what happens if you have archins aging but on a physical example scale rather then examining blood pours semon and piss alot which can help you carbon date a bodies age like teh clouds in teh sky.

Je su non fit no call THEORY ahcrins syndrome non tun fakarat. Numbness no catelgo no isho. No filtka no kakatam no shiraosqa no fil ish to non inl a tut or isthmus no fle el ele le mush no filt to not icur no ishmuas no n lfa le ela tal un shil mesu. No dosium napet no un filka no shonka no shomas no ilkata no shonta. Urine.

And so, the htoery with those elements are the numbers

500 -200 = emx3 plus 12 over 52 97 over 1 .96 evqals to 24

Shon an imta no ilka.

えむろえ の しゃんた うりか の ぴさ の fいた の えxうcう の しんと の ふいんと の しゅます の きんた の せか つ の と の しんたお の えlから の せんかrど うん か しんと の えむまぱ の しんと の いsこ えと。。。しょのん の きつね の かまぱつ の しんと の きら の かがな のえこ の しんと の えしょ もあす。 えもしょ の ぬむば えしょ えこ か の きつく はい そ か へめさん！ えと ごめえん ろこましゅ。 の しんと の えしょ の さか の ひと の えこしょ の みなか の でものこ と そう ら だか。 に へy あの めんへら あんt の えしょ れあださん の えしょ まかさかうしょ なか つるあ。 ばしょ の し ずfいぜどぽ の と そ せ ち た な はまやら が ざ の きと ど の しもす。

Anyawys on with this chapter.

this one was planned to be the next one. I have many pbrinings and am also a time traveler who can hang out with myself. I sculpt or paint these pictures myself. Then morph into them. I always design what i look like out of order with time travel. The personality imprints like an animal duckling on its mother, based on what the parent is like. It forms the personality and who i am during that time. I dont have photos just yet of me turning into tobias but if i get them here they are.

When my copies die, i get my corpse tucked into bed because of this magick waterfall which was a makeshift particle accelerator a tribe when i was apache la shoe promised me was magick, and i guess in many ways and how i see it it was-! When my copies get tucked back into bed cus of a natural born made accelerator, by wind buffalo i used to frequent, when that hits me, all you have to do is give my corpse after my death do to a weird acid drink i had by that same partcile acceltorato which was apple juice piss, and avocado and brail aile. And basically i come back reset to the time before the adventure and my body as a result of ritual trauma at the time is forced as this expeirement to honour deifciations or divinations and because i kept fucking with a particle accelerator which fabrics time i kind of am time so deficiations via this theory come true. So this was the imprint of my good father paul, occasionally as this one i have a dissorder where everything becomes abusive that i used to enjoy such as bdsm, but while the deaths are honoured i come back from the dead until its time for a reunion cermony in my um haha culture. So yes the particle accesletor effects time and space because it was from teh atom bomb expeirement and made with nuclear atomotoms i helped opeinhemer with his own copy.

Anyways. This is that as a giant theory using how we tuck kids into bed and what happens if you have crabs nad bed bugs in the same bed and dont die from it. Or are a cat with both being tucked into bed.

700 - x-9 = 2030 space theory time truth and justice .5 = 10 

Solve for space then time then truth then justice then theory which equals 10 and 13.7 plus 82 = 5094 - 51.so so desu ne. = 54 over 9200. So 7. Which is 2.

Did you know all theories ever solved can solve for two?

So yeah here are the photos to be, and um, basically. The deaths should still be mourned and maybe dont tell people that i faked it cus given that theory i have to cycle through the copies. Im also a time travler, which is just how clouds make rain applied to human hearts, blood and time as a concept of how it works. It works by shoving through the motions like a current in a pool that gets occasionally foseted. Its not that deep or equsieit. Its just kind of how time works. This experiment made me a time traveler with this throy just keep making positive negative and subtistude 3 for 7 and 6 till it clicks and you have evidence of this. So i like to go back and hang out with myselfs since i am an amensiac.

Bonsho no strottre no paul no tobias no incaratah- no strut no vengences no misaka no illtl desu venra no ray.

And the thing is i plan when i get these guys in order.

So here are the photos wordpress will be updated when i update it with them after this adventure. I just have multiple personalities as that one.

Velkl no strog no ital no filk a no sa day.

ぱうl さん わたし の とそん が の きむかします の いたえろ し ね どえ。 えと の いかます の えこご の いしょか の きろしょ ま すか ね げた る の しんたこ の かんじ てすつも の し。 じゃじ の の む に きたよ いしょ。 まさか の いしょ の へんたい の いしょ ね わひ の いむぷ の しんと の いから。 にほんごん です か も ね。 えしょ の いたる の しんた です か ね かがね の いkます。 でも でも いしょ の ただ。。。わたし わ いしょ ま な。。。そう か ね いしょ べづ の へや の います しきゐし の しゅ しゅ の いと よ えしょ の ん と ん なこも えしょ です ら らゆ。

And yeah um. I tend to imprint on my friends who via this same experiment get the memories of it when they either come back from the grave or go through otherkinship which they all do via this theory and their lifecycles as dreams their whole lifes. Most of my friends are okay with it via this notion or it just um cant be imrpitned. Heres how that occurred.

Vel don no vet no ish a ra kamas no fienta no isho lifuwalt no shentko no esto no hijimasu.

15 over truth = friend as me = 3 2 9.41 12 over 54 - 12 = 556.4 -0198 + -90 over 2 plus 1.

= 10 _3

=2

So yeah tahts tobias since i have very little but some control over my cycle i plan to do him next. I cant control the fact that im doing a cycle i can just include how the range i do it in though.

Velka no insmas no venkal to non t ra s ka n ga ey.d

ぼしゅ の きみまがのねでれう いしょ の かがね と だ わ し の いまか の ひと の ね とまだたち の ちり です よ。

Photos coming soon.

Episode 3 Hatsune Hatunse Jidol star. Izumi with her.

izmui.

miku who is hastune hastune as me. Shes half asian. I dont take race into account cus i dont mind what it looks like or if im stereyptically attatctive i just usually end up being so with whats available to me and what was deified which weve already discussed i had to very instinctively honour.

Episode 4: The pupeteer

I knew i woundt be this ethnicity. I know i keep “accidently doing down syndrome on the faces, let me be clear with you i jst actually have that. Forgive me for not feeling shame for my disability even if i can poke at my brows a certain shape i was taught as that original person, to you know, not appear like i overtly do. I just have it in my brows so a lot of my copies do as well forgive me juliet!

Episode 5 the question

Episode 6: brian.

Episode 7: bradley halo.

Episode 8: Simon says.

Episode 9: Poser.

Episode 10: Aldric

Episode 11: sabrina

Episode 12: Andy Biersack

Episode 13: wallet

“

https://www.youtube.com/watch?v=2lMw1jbl4_k

How time travel is a theory. Not a hypothosis.

time travel is just provable. Plain, and simple...a theory is something we can explain about teh universe with hard cold facts. A hypothosis is the same thing but debatle without much evidance. Wana know the coolest bit? The superest coolest most casual bit? Math can provide hypothosis the magickal girl transformation into theories.

Thats right you guessed it. Not only am I baby, But I can also prove time with math. As always with nuclear phychics we will be establishing, how this is possible through makeup.

x - 7. a slope is  a scale of scoopieness that displays how things are done. A slope is like a slanted hill you can measure things on or a hard cold graph. To put something on a slope is to chart or measure it. I know i know i can hear you booing! But lets play socks.

So the thing about x is that she's a drama queen right? Shes excrecentric. And she can be anything she wants despite when on the clock working at that exact, slope. So here she is used to scale that hot blooded seven.

So we're picking that drama queen seven because their are seven actual provabale ways to date a year. Theirs calenders, lunar cycles, the sky, events, reporting on those events, expeirencing things yourself, and asking another through the moral process of observation.

We have other posts about this process of teh scientific method but as of writing it has yet to be fully written up. Anyways. Those are  a good theory. So lets prove it, and if not, lets hpothetically say we cant prove those dating methods, then we certainly know atleast that there are seven months in a calander, and some calenders use a 7 month dating calender, like some of that of the aztecs, and we also know that, there are seven days in a week by the 21st century american dating calender started in rome that goes month day year, am pm, and monday, tuesday, wedendsay, thursday, friday, saturday, sunday, next week with three weeks in a month.

the reason we use X, is because since 7 is so much of a drama queen, theirs alot we dont know about her. And x is a great journalist. so she'll be a mystery factor. an envangard drag queen. She's our mystery element. Our puzzle to solve.

now just like the numerics we should base this in thought, logic and reason. 2 different ways to time travel. Forwards, and backwards, ways we know for a fact humans feel like or get the vibe or expeireing time. So linear, but time is not though that is not this video.

This clearly means....34! but i know what your thinking. WHAT NO IT DOESNT FUCKASS. it can. karkles. it can it has and it shall. karkaiden. it can. so like heres teh dealio my home scility biscuit. We'll just know this later. To do extra math since this is kinda advanced draw a picture and assign it random numbers. Most humans who do math will just naturally pick things that work in some way or that are easily corected, because humans recognize patterns and I've been -gasp- like that overdramatic fool seven leading you on with this article.

by the american dated calender, tehir were 356 days within a year, and 7 days within a week. Got it? Got it. this calender was used for centuuries thus has basis on the foundings of american and several other western civilizations. SO WE KNOW we can use it as a base here. Its measurable. Also for note their are 24 hours in a day and 30 seconds in a minute, and 60 minutes in an hour by this dating system.

To do equals is very very simple. blank number equals to blank number. just means that its the same in some way of metephor. five pens equals one tray of markers, that has lots of pens on it. So on and so forth. A decimal is a fragemnt of that. For exmaple each marker in that tray of art suppleis or droor or case or bag of it, would be .2 if theirs to markers out of 5 and more, and so on.

So now we have to pick a variable from something in the equation. so lets picked 34 because like that hot blooded seven it is yet something unsolved. So we subsitute it and we do the numbres, and that clearly indicates if you divide it and everything that we have 24. Thus there are 24-/..... -drum roll please-

the history of chance provides that there are 24 whole ideas we can deduce about teh probability of time travel. Unique means there are one of a kind versions of something, or it stands out because its just so much unlike otehr things. Probability is how likley something is. So we just deduced the universe. Deduction is peicing something to gether to figure it out.

So we got theory = 34, and 34 = known equations. What reprsents what in our heads here my homeie, my pal.

so theory is equivelent. and over ideas. so ideas in comparison to how they work which is what heory is, plus all this chance and shit we dvided by equals ourselves too- with enough addition and rounding we can guess that each day of the yeaer means! 2

[rounding: making a fraction whole] so basically we did all that work and all we got was what we wanted to know w -__-; their are two possible ways atleast rounded or sumed up and simplfied to time travel. forwads and backgwards by most peoples defintions. given hwo the years work.

basic maths. If you want to see this much more formal and BROING snooze for old people watch the video rather then using text to speech or theory on it. :p

Thanks so much.

Now lets get fun with it. our reward: makeup metephor or a makeup pallete if your parent is cool sheesh.

a makeup pallate, is usually- in american society powder you smeer or apply artistically or creativly to your face to make it prettier or more handsome or just transform it objectivly. It looks good, a face before contour and after eyeshadow. What we learned with the makeup pallete is that it moves forward and backwards. The way people think about time. We feel like something happeend in teh past, and something happened in the moment or future. The third would be considered present which is always forwards in time because of that 34.

SO because of our GLORIAS BASTARD 7, we know that there are multiple ways to think about time. And thus there are because we are going forward, eventually to be thus already, current ways to go into and out of its movement via probability. Kind of liek applying makeup to your face.

Different methods to look like a hotshot astronautght or a pretty princess or an agender mermaid or a centaur that just lacks everything and is still somethign though or not at all! bascially yeah.

NUclear physhics.

“

So yeah clearly he picks out his faces, chooses what they will look like, artbreeder cant make real faces but is hypothosised to one day. As chance theory. And so yeah all these will come to be or have. Its just he can probably hang out with hismelf as at ime travleer. I have proof here.

Dolls are alive and clouds tell time, heres why. TIME TRAVEL LAND. -samantha and john pond

the sun sets and the clouds eveperate. No two clouds look the same even if they all have individual formations. Similarly to a snowflake their are repeating pattenrs but they each indivually stand out. Water everpatees in rain cycles. Thus. The thing to note about all of this. Is that, the sun sets on a cycle similarly in the sky to a moon. So its safe to say that throughout the day that time and the star in the sky the moon or the sun indicate and showcase, a unique cloud and sky setting, perfectly for the wrath of a unique day. Thus, every single day has a unique outlook. because of the nature of how clouds everpate at different levels of height and water everpateion in the atmosphere.

Now everything has a life and a spirit and a name. The rason this is is because most matter goes through evolutinary formats of gas and ebhliteration like that of rain cycles. Matter cannot be created or destroyed only transformed.

every atom has a serires of makeup. I call these things lovlingly mitochandria because mitochandria is the power house of the cell, which is very similar to the vibrating layers of the atom. Everything has a vibe of energy right? And these little orbs have their own matter we'd call dark matter or less then zero right? When they vibe together they form a sort of brain like structure that works to oeprate the cell as you can see in teh graph of the atom. Which resmebles a power house like mitochandria.

The reason we say everythign has a life and a spirit and a name, is one, because we're quoting disney's pochantus. ANd native american relgiions. And two, because this is sort of a brain like structure. Despite how far science has come we still dont know alot about brains. But judging by the tank top video we've deduced that alot of it corelates within each other and can talk and speak.

In that video we talked about how, math works. We talked about how, virbations pull. We talked about how you can get an equation out of a drwaing. And by corelating it to the numbers so we just know our metephor of our nuclear phychisc we were able to deduce that atoms themselves are alive and thus everything has thought. But it is a mandatory watch that video. Pleaes mirror it even with comentary on your youtube channels, cus that channel might be going' down soon.

-Adam Snowflake

Hydnellum peckii Banker - Devil's Tooth

Phylum: Basidiomycota - Class: Agaricomycetes - Order: Thelephorales - Family: Bankeraceae

Distribution - Taxonomic History - Etymology - Identification - Culinary Notes - Reference Sources

At its best, this is a very beautiful fungus... but unfortunately it is rarely seen at its best and often grows embedded with plant stems and debris. Although variable in shape and colour, fruitbodies of Hydnellum peckii invariably have pinkish tones. Young caps are often (but not always) decorated with bright red liquid droplets that exude from the upper surface. Particularly attractive when solitary, the fruitbodies more often occur in small groups that merge and become fused at the caps and sometimes also along their stems.

Droplets can also exude from the fertile undersurface, and the effect is sometimes quite stunningly beautiful:

Distribution

The Devil's Tooth is a woodland mushroom rarely if ever found in Britain except in Scotland and then most often in the Caledonian Forest, where in some years it is abundant but still fairly localised. The beautiful specimens shown on this page were seen in Scotland's Abernethy Forest. All official records for this species on the Fungal Records Database of Britain and Ireland (FRDBI) are from Scotland. This hydnoid fungus occurs also in parts of northern mainland Europe and in North America.

Taxonomic history

Tooth fungi of various kinds can be found in many taxonomic orders, and over the years their classification has changed considerably. This particular fungus was first described in 1912 by American mycologist Howard James Banker (1866-1940), who gave this species its present name Hydnellum peckii.

Synonyms of Hydnellum peckii include Hydnum diabolus, reflecting the common name Devil's Tooth, Calodon peckii, and Hydnum peckii. This rare (in Britain and Europe; less so in the USA) fungus has been referred to by several other common names including Strawberries and Cream, Bleeding Tooth Fungus, and Bile Tooth.

Etymology

Hydnellum, the generic name, is derived from the ancient Greek word hudnon, meaning an edible mushroom; this term was applied particularly to edible truffles. (See, for example, Tuber melanosporum, the Perigord Truffle.)

The specific epithet peckii honours American mycologist Charles Horton Peck (1833-1917) who described nearly 3000 fungi species of North America. The standard abbreviation Peck is used to identify Charles Horton Peck as the author when citing a botanical/mycological name.

Identification Guide

	Cap 3 to 8cm across when fully developed, sometimes round but often oval or multi-lobed; initially shallowly domed or flat topped but with a bumpy surface, becoming slightly funnel-shaped with a thin margin; white or very pale pink, palest near the margin, becoming deeper pink or buff and eventually turning brown from the centre before blackening and decaying. Young caps often exude red liquid droplets; cap flesh is tough and fibrous. Above-ground height 3 to 10cm.
	Spines 1 to 5mm long (shortest near to the cap margin) and less than 1mm in diameter; crowded, decurrent; pinkish, becoming buff later as the spores mature.
	Stem The stem of the Devil's Tooth fungus is very variable in size, sometimes as squat as just 0.5cm in height; occasionally as tall as 5 or 6cm but with most of the stem below ground; diameter ranges from 0.5 to 2cm; usually more or less cylindrical but sometimes tapering in towards the base. Pinkish buff like the outer region of a mature cap; coarsely velvety in texture.
	Spores Almost spheroidal but with a sharp point at one end; 5-5.5 x 4-4.5µm; tuberculate (covered with small, wart-like nodules); inamyloid. Spore print Dull brown.
Odour/taste	No significant odour; taste very hot indeed.
Habitat & Ecological role	On soil in coniferous woodland; nearly always with pine trees, with which it is ectomycorrhizal.
Season	Late summer and autumn.
Similar species	Hydnum ferrugineum is very similar in appearance but its flesh is reported to be mild tasting rather than hot. There are significant hyphal structure differences that are visible only with a high-powered microscope: Hydnellum peckii has clamps on the septa, whereas Hydnellum ferrugineum does not. Hydnum rufescens is tan coloured without concentric zones; its spines are adnate to the stem rather than decurrent.

Culinary Notes

In common with the other members of the genus Hydnellum, Devil's Tooth is a tough and insubstantial fungus. Needless to say we have no recipe information for this species.

Reference Sources

Fascinated by Fungi, 2nd Edition, Pat O'Reilly 2016, reprinted by Coch-y-bonddu Books in 2022.

British Mycological Society (2010). English Names for Fungi

Dictionary of the Fungi; Paul M. Kirk, Paul F. Cannon, David W. Minter and J. A. Stalpers; CABI, 2008

Taxonomic history and synonym information on these pages is drawn from many sources but in particular from the British Mycological Society's GB Checklist of Fungi.

Acknowledgements

This page includes pictures kindly contributed by Stevie Smith.

https://sci.muni.cz/botany/mycology/hydna.htm

Evolution and development of shape: Integrating quantitative approaches

• September 2010

• Nature Reviews Genetics 11(9):623-35

DOI:10.1038/nrg2829

• Source

• PubMed

ArticlePDF AvailableLiterature Review

Evolution and development of shape: Integrating quantitative approaches

• September 2010

• Nature Reviews Genetics 11(9):623-35

DOI:10.1038/nrg2829

• Source

• PubMed

Authors:

Chris Klingenberg

• The University of Manchester

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Citations (596)

References (135)

Figures (1)

Abstract and Figures

Morphological traits have long been a focus of evolutionary developmental biology ('evo-devo'), but new methods for quantifying shape variation are opening unprecedented possibilities for investigating the developmental basis of evolutionary change. Morphometric analyses are revealing that development mediates complex interactions between genetic and environmental factors affecting shape. Evolution results from changes in those interactions, as natural selection favours shapes that more effectively perform some fitness-related functions. Quantitative studies of shape can characterize developmental and genetic effects and discover their relative importance. They integrate evo-devo and related disciplines into a coherent understanding of evolutionary processes from populations to large-scale evolutionary radiations.

Relative and absolute constraints.a | Absence of constraints. Variation is equally abundant in all directions of the phenotypic space (circle), so selection in any direction will produce an equally strong evolutionary response (arrows). Empirical studies suggest that this situation is very rare. b | Relative constraints. Variation is concentrated mainly in one direction, but there is some variation in all directions — and thus there is an evolutionary response to selection in all directions — although some directions produce bigger responses (black arrows) than others (grey arrows)68. This situation is common for shape and other morphological traits. c | Absolute constraints. Variation is so concentrated that one or more dimensions of the phenotypic space are entirely devoid of variation, meaning that evolution cannot proceed in those directions (crossed-out arrows)68. Absolute constraints seem to be rare in extant populations. d | Example of a relative constraint: the relative sizes of the dorsal eyespots on the wings of Bicyclus butterflies. Artificial selection for small (S) or large (L) anterior and posterior eyespots in different combinations yielded an evolutionary response in all experiments7, 78. e | A possible example of an absolute constraint (or a very strong relative constraint): the colour composition of ventral eyespots on the wings of Bicyclus butterflies. Artificial selection seems to be successful only if the more extensive gold or black colour is favoured in both anterior and posterior eyespots (GG and BB). By contrast, selection for gold in one and bl in the other eyespot (GB and BG) seems to produce no or only a very small evolutionary response78. Parts b and c are modified, with permission, from Ref. 68 © (2005) Elsevier. Parts d and e are modified from Ref. 78.

… 

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Evolutionary developmental biology, or ‘evo-devo’, has

grown rapidly over the past two decades as a synthesis of

evolutionary and developmental biology1,2. The key ques-

tions in evo-devo studies are how development affects

the evolution of morphological traits and, in turn, how

developmental processes evolve. In particular, consider-

ing development in conjunction with evolutionary pro-

cesses can shed light on the origin of new variation that

serves as raw material for natural selection. Evo-devo

therefore contributes an aspect to evolutionary biology

that complements population biology and the evolution-

ary synthesis2. Similarly, the focus on the evolution of

developmental processes provides a crucial perspective

that permits developmental biologists to relate findings

from different model organisms to evolving lineages.

Evo-devo has long emphasized morphological traits1,3.

Decisive advances in recent years have been achieved by

using quantitative approaches to characterize shapes4 and 

by integrating them with methods from evolutionary

biology, genetics and developmental biology. As a result,

investigators have a powerful and flexible set of analytical

tools for answering specific questions, and new ones are

added regularly. Moreover, a wide range of study designs

can be used in evo-devo studies, from experiments in

the classical model species to broad comparative analyses

across major taxonomic groups (BOX 1).

Following the tradition of developmental genetics,

evo-devo has predominantly focused on drastic morpho-

logical changes: clear-cut ‘phenotypes’ that can easily be

scored without measurement, such as flowers that have

different types of symmetry5. If shape variation is quanti-

fied, however, a more subtle picture emerges. For instance,

a population may contain a continuum of flower shapes,

of which the different symmetry types are the extremes,

and quantifying shapes may reveal the adaptive value of

shape through its effect on pollination success6. Whereas

the drastic phenotype simplifies the experiments in the

laboratory, quantitative information permits a more

detailed picture of evolutionary processes4.

In recent years, more and more studies have quan-

tified shape to address evo-devo questions. These stud-

ies use shape variation as a ‘common currency’ to link

experimental or comparative approaches from different

biological disciplines. In the first two sections of this

Review, I briefly survey the approaches for quantifying

morphological variation and its genetic components,

which are important preliminary steps that provide the

basis for further analyses. I then present an overview of

morphological integration and modularity, which have been

a particular focus of attention for research into the evo-

devo of shape. I also introduce allometry and functional

aspects, which have not been as widely discussed in evo-

devo as modularity but are both important topics. Finally,

I review studies on the macroevolution of shape and

discuss what direction future analyses might take.

Quantifying shape variation

Many morphological traits can be quantified effec-

tively by single measurements of the size of a part — for

example, the diameters of eyespots on butterfly wings7

Faculty of Life Sciences,

University of Manchester,

Michael Smith Building,

Oxford Road, Manchester

M13 9PT, UK.

e-mail: cpk@manchester.ac.uk

doi:10.1038/nrg2829

Published online

10 August 2010

Shape

The shape of an object

encompasses all of its

geometric properties except its

size, position and orientation.

Morphological integration

The covariation of

morphological structures in an

organism or of parts in a

structure, which may reflect

developmental or functional

interactions among traits.

Allometry

The dependence of shape on

size, often characterized by a

regression of shape on size.

Evolution and development of shape:

integrating quantitative approaches

Christian Peter Klingenberg

Abstract | Morphological traits have long been a focus of evolutionary developmental

biology (‘evo-devo’), but new methods for quantifying shape variation are opening

unprecedented possibilities for investigating the developmental basis of evolutionary

change. Morphometric analyses are revealing that development mediates complex

interactions between genetic and environmental factors affecting shape. Evolution

results from changes in those interactions, as natural selection favours shapes that more

effectively perform some fitness-related functions. Quantitative studies of shape can

characterize developmental and genetic effects and discover their relative importance.

They integrate evo-devo and related disciplines into a coherent understanding of

evolutionary processes from populations to large-scale evolutionary radiations.

REVIEWS

NATURE R EVIEWS

|

GENETICS VOLUME 11

|

SEPTEMBER 2010

|

623

© 20 Macmillan Publishers Limited. All rights reserved10

Box 1 | Study organisms and study designs

A key factor in evolutionary

developmental biology

(‘evo-devo’) has been the

search for new model

species in addition to those

traditionally used in genetics

and developmental biology99.

As a result, a wide variety of

experimental, observational

and comparative study

designs is now available

for studying the evo-devo

of shape. These include

experiments using classical

model organisms that are

fully controlled for genetic

and environmental

factors41,42,44,83, studies

of variation in natural

populations in the field6,25,

analyses of shape variation in

domesticated species17,100 and

broad comparative studies in

large groups of extant or

fossil organisms76,87. Each of

these approaches has its own

strengths and weaknesses.

The primary advantage of

classical model organisms is

the ease of experimental

manipulation and the degree

of control over factors that

are not of specific interest.

Inbred lines provide genetically identical individuals, and laboratory culture under standardized conditions provides

full control over environmental conditions. Consequently, it is easy to separate shape variation that is due to specific

genetic factors or to spontaneous variation in the developmental system44. Likewise, in experimental settings,

developmental changes can be visualized and quantified precisely with tools such as vital staining and strains of

organisms carrying mutations of interest or marker transgenes10,41,42,83.

Studies of natural populations cannot use these specialized tools, but instead they can directly examine actual

evolutionary processes. For example, Gómez and colleagues studied natural selection6,94 and quantitative genetic

variation25 of flower shape in Erysimum mediohispanicum, which is an excellent ‘population model’ for floral evolution

because its populations contain considerable variation in flower shape, including differences in floral symmetry

(see the figure; part a shows an actinomorphic flower and part b shows a zygomorphic flower).

Even greater morphological variation can be found in domesticated species, such as pigeons100 or dogs17,20. In dogs,

the amount of cranial shape variation has been shown to be comparable to that across the entire order Carnivora, and

many dogs have entirely novel shapes outside the range of wild species17 (see the figure; part c shows the skull of a pug

and part d shows the skull of a bull terrier). In some cases, it is possible to follow changes over time and relate them to

artificial selection by breeders20.

The results of natural evolution over long timescales can be studied by comparative studies of diversification in groups

of related organisms. Various comparative methods are available to extract information on evolutionary changes of shape.

Sidlauskas76 reconstructed the evolution of head shape in a group of characid fishes to identify factors involved in their

diversification (see the figure; part e shows Synaptolaemus cingulatus and part f shows Hypomasticus julii).

By combining study designs and databases, investigators can set up approaches for addressing a wide range of

evo-devo questions.

Images in parts a and b courtesy of J. M. Gómez, Universidad de Granada, Spain. Images in parts c and d courtesy of

A. G. Drake, College of the Holy Cross, USA. Images in parts e and f courtesy of M. Sabaj Pérez, Academy of Natural

Sciences of Philadelphia, USA.

c

e

d

f

Nature Reviews | Genetics

ab

Vital staining

Staining of live organisms

to follow developmental

processes (for example,

calcium-binding stains, such 

as Alizarin Red and Calcein,

label bone tissue and, if

administered at different times,

can indicate bone growth).

or the lengths of primate limb elements8. Other traits are

inherently more complex and cannot be characterized

sufficiently by their size alone. For these traits, analyses

also should consider information about shape, which

concerns the proportions and relative positions of parts.

Extracting shape information. Shape is mathematically

defined as all of the geometric features of an object

except its size, position and orientation9. This definition

may sound somewhat abstract, but it is the same defini-

tion that we intuitively use when we view a photograph:

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Shape space

A special type of morphospace

in which each point represents

a shape and the distances

between points correspond to

the amount of shape change

between the respective shapes.

Principal component

analysis

A multivariate analysis that

provides a new coordinate

system whose axes, the

principal components,

successively account for the

maximum amount of variance

and are uncorrelated with 

each other.

Canonical variate analysis

A multivariate analysis that

finds new shape variables

that maximize the separation

between groups (such as

species or genotypes) relative

to the variation within groups.

Multivariate regression

A type of analysis in

which variation in one set 

of variables, the dependent

variables, is predicted or

explained by variation in 

one or more other variables,

the independent variables.

Partial least squares

analysis

A multivariate analysis that

aims to find the optimal

variables for showing patterns

of covariation (for example, 

in studies of integration).

The analysis looks for new

variables that maximize

covariation between two sets

of variables (for example,

between the shapes of two

anatomical structures).

Constraint

The tendency for evolutionary

change to occur in some

directions of a morphospace

more than in other directions.

we routinely ignore information about size, position and

orientation (we can easily recognize the Eiffel Tower on a

small picture, even if we are far from Paris when looking

at it or we are holding the picture upside down).

To apply this definition, investigators collect data that

represent biological forms as length measurements, the

arrangement of morphological landmarks9 or the entire

outlines10,11 or surfaces12 of the specimens. The most

widely used approach in current morphometrics is to rep-

resent organismal forms by landmarks, and this Review

will therefore focus mostly on methods related to them.

Landmarks are points that can be located precisely on all

forms and establish a clear one-to-one correspondence

between all specimens included in a study. For example,

in the human face, the tip of the nose or the corners of

the mouth are possible landmarks. Landmarks are cho-

sen to cover the entire structure under study in suffi-

cient anatomical detail, but the number and distribution

of landmarks are often limited in practice.

For some structures, landmarks are sparse or una-

vailable over extensive regions because there are few

anatomical features that can be used for defining land-

marks (for example, the surface of the cranial vault in

humans). In such situations, many studies have added

semi-landmarks: points on an outline or surface that

can be slid along the outline or surface to correspond-

ing locations according to some criterion (for example,

the semi-landmarks could be regularly spaced points11

or be distributed to minimize localized deformations13).

Different criteria for sliding semi-landmarks make

different implicit assumptions about the changes in

the tissue between landmarks. Using different criteria

can influence the results of morphometric studies14

and therefore the results of such analyses need to be

interpreted with some caution15.

To extract the shape information from the positions

of landmarks, the extraneous variation of size, position

and orientation is removed in a procedure called the

Procrustes superimposition9 (BOX 2). The coordinates of

landmarks aligned by this procedure exclusively contain

shape variation. All possible shapes for any given number

of landmarks define a shape space: a multidimensional,

nonlinear space in which each point represents a differ-

ent shape, and of which the Procrustes-aligned shapes

in a sample provide a local approximation9 (BOX 2).

Morphometric studies address specific biological ques-

tions by examining the variation in this shape space with

the methods of multivariate statistical analysis.

Multivariate analysis. Shape variation is inherently mul-

tidimensional because even simple shapes can vary in

many different ways. Accordingly, analyses should use

multivariate methods that simultaneously consider the

covariation of all landmark coordinates16.

A variety of multivariate methods are available for

answering specific questions9. Most of them find new

variables, corresponding to directions in shape space,

which optimize criteria related to the question of inter-

est. For instance, principal component analysis can be

used for examining the main patterns of variation in

the data11,17, canonical variate analysis provides the best

separation of known groups18, multivariate regression can

be used for analysing allometry or evolutionary change

in shape over time19,20 and partial least squares analysis

can be used to examine covariation of shapes21,22. A wide

range of additional multivariate methods exist, some of

which have been specifically devised for morphometric

applications.

Visualization. Geometric morphometrics differs from

other applications of multivariate statistics in that most

results from the analyses can be visualized as shape

changes and interpreted anatomically. Every possible

shape corresponds to a point in the shape space and,

conversely, every direction in shape space corresponds

to a specific shape change, which can be shown graphi-

cally by relative shifts of landmarks or by deforma-

tions of outline diagrams (BOX 2) or three-dimensional

surface models12,17.

Interpretations of shape changes need to take into

account that the displacements of landmarks are inher-

ently relative to each other. It is important to realize

that landmarks are not ‘moving’ independently but are

‘pushed’ or ‘pulled’ around by changes in the tissues in

which they are embedded.

Morphometric analyses tend to answer biological

questions by going back and forth between abstract

representations of variation as a scatter of data points

in the shape space and the concrete anatomical changes

associated with specific directions.

Genetic and epigenetic control of shape

The degree to which genetic and environmental factors

influence the development of morphological traits is the

subject of a long-standing debate in biology. In particu-

lar, a central question for evo-devo is how development

translates genomic variation into the shape variation that

is available for evolution by selection or drift.

Quantifying total genetic variation. To assess how

much of shape variation has a genetic basis, a range of

approaches from quantitative genetics can be used23. If

breeding experiments can be performed or pedigree

information is available, genetic variances and cov-

ariances among shape variables can be estimated and

assembled in a matrix, called the G matrix. This matrix

characterizes the genetic component of shape variation

in the population, integrating effects of loci throughout

the entire genome. This has been done for a wide range

of organisms, including laboratory mice24 and samples

from natural populations of plants25, insects26,27, turtles28

and even humans29.

Using estimated G matrices, it is possible to predict

the response to selection for specific shape features —

that is, the shape change between the generations before

and after selection. For most examples, the directions of

predicted responses are deflected substantially from the

direction of the original selection24,27,29. In other words,

for selection on some particular feature of shape, there

is also a response in other aspects of shape that were not

originally selected for. These results indicate that genetic

constraints on evolution of shape may be widespread30.

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Quantitative trait loci

Genes or small genomic

regions that affect a

phenotypic trait of interest.

Specific loci affecting shape. A different strategy is to esti-

mate the effects of individual genes or specific genomic

regions on shape. For example, genetic marker informa-

tion can be used for mapping quantitative trait loci (QTLs)

that affect shape in experimental populations derived

from interspecific or interpopulation crosses11,31–34, from

crosses of laboratory strains after artificial selection35–37 or 

from variation in natural populations38. An alternative is to

use panels of controlled genotypes carrying mutations39–43

or chromosomal deficiencies44 to pinpoint effects on

shape. Analyses identifying gene effects on shape require

specific multivariate methods, but in return they provide

unique information about the developmental basis and

evolutionary implications of genetic variation (BOX 3).

Nature Reviews | Genetics

Original configurations

Scaling to the same size

Translation to the same location

Rotation to optimal fit

Box 2 | Extracting shape information: the core of geometric morphometrics

Most morphometric analyses in evolutionary

developmental biology (‘evo-devo’)4 and other areas of

biology use information from configurations of landmarks.

Because shape is defined as the geometric attributes of

an object except for size, position and orientation,

information about shape variation can be obtained by

removing this extra information in a procedure called the

Procrustes superimposition9.

The Procrustes superimposition starts with the

configurations of landmark coordinates, as they were

measured, and successively removes variation in size,

position and orientation (see the figure). The procedure

starts by scaling configurations to a standard size and

moving them to a standard position. Size is quantified as

centroid size, which is computed as the square root of

the sum of squared distances of the landmarks from the

centre of gravity of a configuration. To remove variation

in position, all configurations are translated so that their

centres of gravity are at the origin of the coordinate

system. Finally, configurations are rotated about this

common centre of gravity to bring all configurations into an

optimal orientation in which the sum of squared deviations

between corresponding landmarks is minimal.

The variation in the landmark coordinates after the

Procrustes superimposition (for example, the bottom

diagram in the figure) is the variation in shape. These

coordinates can therefore be used in subsequent analyses.

Because this variation concerns the relative displacements of

landmarks to each other in many directions, it is important to

use multivariate methods16 (analyses of individual landmarks

or even coordinates ignore the correlations between them).

Shape variation can be characterized in shape spaces.

A shape space represents all possible shapes for a given

number of landmarks by points, so the distances between

points represent the similarities between the

corresponding shapes. Accordingly, shape changes are

associated with distances and directions in the shape space16.

Shape spaces are complex, non-Euclidean spaces: for instance,

for the simplest shapes, triangles, the shape space is the surface

of a sphere9. For a limited range of shapes, the Procrustes

superimposition provides a local approximation of the

positions in shape space9. This approximation is satisfactory

even for large scales of biological variation95, as it might be

encountered in studies of large-scale evolutionary

diversification17,76 or through development41,83. The

resulting shape data can be used for analyses with

the usual tools of multivariate statistics.

Shape changes can be visualized so that the results

of statistical analyses can be interpreted anatomically.

For instance, morphing techniques such as the thin-plate

spline9 can interpolate shape changes from the landmarks to

rectangular grids or entire outline drawings representing the

specimens (see the figure). The deformations of the grids or

drawings then show the shape changes from comparisons between

species or from the results of statistical analyses.

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AA

BB

AB

d

a

a

Direction of selection

Box 3 | Quantifying gene effects on shape

Because shape variation is inherently multidimensional, gene effects have not

just magnitudes but also directions. Unless most of the shape variation is

concentrated in a single dimension of the shape space31, it is likely that focusing

on individual principal components34,38 or landmark coordinates33 for genetic

analysis will miss interesting information. Therefore, fully multivariate

methods are required for estimating genetic

parameters11,24,32,35,36. These analyses provide a wealth

of information about patterns of genetic effects.

Integration of genetic effects

Because multivariate estimates describe genetic effects

as the joint effect on multiple aspects of shape, they are

suitable for the study of pleiotropy as a genetic basis for

integration. Several studies have shown the integration of

quantitative trait locus (QTL) effects within structures32,36,37 

and joint effects of QTLs on different anatomical structures34.

Patterns of total genetic integration, as they are seen in genetic covariance

matrices (G matrices), are the composite of the effects of all QTLs that influence

shape variation. Although many studies have examined the genetic architecture of shape in various organisms11,31–44,

limitations of statistical power and genetic resolution have so far prevented a comprehensive analysis how individual

QTLs contribute to the overall patterns of shape variation in the G matrix.

QTL effects and dominance

Multivariate QTL studies have found that the vectors of additive and dominance effects tend not to be colinear but

point in different directions of shape space35,37,101 (vectors a and d in the figure). This means that the phenotype of a

heterozygous individual tends not to be on the midpoint between the two homozygotes, but is different from both of

them in some aspect of shape: the average shapes for the three genotypes form a triangle in shape space (AA, AB and

BB in the figure).

This means that the combination of two different alleles has a developmental effect that is distinct from both

homozygous genotypes for the corresponding alleles. Therefore, the combination of alleles at a locus does not just

determine whether there is more or less of the same developmental activity; there also seems to be an interaction

among alleles that alters the developmental outcome qualitatively. This type of interaction may provide useful

information about the regulation of developmentally relevant genes.

That the two homozygotes and the heterozygote form a triangle in shape space also has an evolutionary

consequence. It implies overdominance of shape for a range of directions in shape space (blue sector in the figure,

limited by directions perpendicular to the lines connecting AB to AA and BB). If directional selection acts in these

directions (heavy arrow in the figure), the fitness of AB is higher than that of both homozygotes and balanced

polymorphism may result35,101,102. This multivariate view of genetic effects provides a new perspective on the

maintenance of variation under selection that is applicable not just to shape but to multidimensional traits in general.

Such studies, despite limitations of statistical power,

consistently reveal multiple loci that affect shape, suggest-

ing that shape is influenced by many genes distributed

throughout the genome. Likewise, the genetic control of

variability around the average shape of a genotype seems

to be influenced by many genes39,44. These results are

consistent with theoretical studies that have modelled

phenotypic variation as an outcome of nonlinear dynam-

ics of developmental processes45 or, more specifically, the

processes of regulation of developmental genes46.

Genetic and epigenetic effects. Shape variation may

originate directly from genetic changes in developmental

processes that build morphological structures, or it

may be mediated by epigenetic effects47–49. Epigenetic

effects are defined as the developmental interactions

among cells, tissues and their environments47,49. This

definition follows Waddington’s original concept of epi-

genetics49 and includes a wide range of developmental

mechanisms (it thus differs from the more recent redefi-

nition of the term that focuses on chromatin modifica-

tion). Epigenetic interactions can translate a localized

developmental change into integrated and widespread

morphological variation50. Because of their role in trans-

mitting genetic effects, epigenetic interactions are crucial

for understanding how genetic variation is expressed and

integrated among traits50,51 (BOX 4).

For instance, the shape of bones is influenced by the

mechanical forces they experience during development48.

The mandible shape of mice was significantly affected

both by hard or soft food and by a mutation causing

muscular dystrophy10. Both treatments reduced epi-

genetic effects on mandible growth under mechanical

loading, one by environmental manipulation and the

other by genetic means. Similarly, the discovery that

localized defects in human craniofacial development are

associated with widespread changes in skull and brain

shape18,52 suggests a developmental association.

The key importance of epigenetic effects in evo-devo

is in shaping the patterns of integration in morphological

structures via interactions among developmental

processes50,51. Epigenetic effects are also of key impor-

tance in that they provide flexibility in developmental

programmes, such as in phenotypic plasticity.

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Box 4 | Inferring developmental interactions from morphological data

Morphological integration between traits can originate in different ways68.

Covariation between traits can result from a direct interaction between the

developmental pathways (for example, signalling between tissues) that generate the

traits50; this can be regarded as an epigenetic interaction. Alternatively there can be

parallel variation in separate developmental pathways without an actual interaction

between them — for example, two separate developmental processes could be

affected by the same environmental stimulus or allelic variation for a gene could be

involved in both processes68. In addition to the developmental differences, the two

modes of integration may also differ in their evolutionary implications68.

A useful and practical way to distinguish the two origins of integration is to

examine the covariation between the fluctuating asymmetries of the two traits.

Because the deviations between the left and right sides, which are the focus of

fluctuating asymmetry, are produced by random perturbations in the development

of the traits103, there will be no covariation between the asymmetries of two traits

unless the developmental perturbations are transmitted between traits by epigenetic

interactions. Moreover, because the left and right sides of an individual share the

same genome and very nearly the same environmental conditions, there is no basis

for covariation of traits by parallel variation (note that this latter condition does not

apply to plants and sessile animals). The covariation of the asymmetries of different

traits is therefore due to direct interactions of the respective developmental

pathways, and not parallel variation68.

This reasoning has been applied to a wide range of traits and organisms, including

the wings of flies44,62 and crickets27, the mandibles of rodents62,63,71 and shrews70, vole

teeth21, and the skulls of newts65 and of various mammals17,72. In many of these studies,

the patterns of fluctuating asymmetry and of variation among individuals are similar,

so it is plausible that direct interactions of developmental pathways also mediate the

expression of variation from environmental or genetic sources. In other examples,

however, marked discrepancies in the patterns of integration were found69,72.

A different approach to uncovering developmental interactions is to use organisms

with alterations of specific developmental processes caused by, for example,

mutations of developmental genes, and to record the effects on shape41,50. If localized

developmental changes result in widespread morphological changes, they are

interpreted as consequences of developmental interactions. The crux of this

approach is to assure that the initial developmental effect of the mutant is indeed

localized to exclude the possibility that the gene of interest has parallel effects on

multiple developmental pathways that do not interact. Genetic mosaic analysis may

be a promising approach to address this issue.

Fluctuating asymmetry

Subtle deviations between

paired structures on the left

and right body sides due to

random perturbations of

developmental processes.

Modules

Parts of biological systems

tend to be organized into

clusters, or modules, which

consist of parts that are

integrated tightly by many or

strong interactions and which

are relatively independent

from other modules because

there are fewer or weaker

interactions between them.

Phenotypic plasticity and developmental instability.

The non-genetic component of variation is not just a

‘residual’ but is itself of interest in evo-devo. Phenotypic

plasticity, the component of variation induced by

environmental effects, can be of key evolutionary

importance53,54 and even the random component of

developmental instability can provide information

on developmental interactions among parts (BOX 4).

Plasticity is based on epigenetic effects; an environmen-

tal stimulus can alter developmental processes so that a

difference in the adult shape arises48,53. Environmental

stimuli can be physical factors, such as temperature39, or

complex stimuli, such as diet55.

Another non-genetic component of variation is

developmental instability — that is, the morphological

variation arising from random fluctuations in the devel-

opmental system. Its link to plasticity is controversial and

empirical studies have produced mixed results27,39,44,56–58.

It has been used to infer the developmental basis of

morphological covariation (BOX 4).

Sensitivity to environmental stimuli or random fluc-

tuations can be influenced by genetic variation in a wide

range of genes39,44. It is unclear whether specific pathways

involved in buffering of variation (such as chaperone

proteins59) have stronger effects on buffering of shape

than other genes57,58, or whether buffering and plasticity

are generic outcomes of the functioning of developmen-

tal systems45,46. Because these mechanisms regulate the

expression of new phenotypic variation, understanding

them is an important challenge for evo-devo.

Morphological integration and modularity

Whether genetic or non-genetic variation is the main

focus of interest, a central question in evo-devo is how

this variation is organized. Traits of organisms do not

vary independently but are integrated with each other,

reflecting coordination in development, function and

evolution51. This integration is usually not homogene-

ous, but there are complexes of more tightly integrated

traits, called modules, that are relatively independent of

one another1,51. Integration and modularity are there-

fore closely linked concepts in evo-devo that have been

studied in a wide variety of different systems, from

intraspecific studies to macroevolutionary analyses across

large clades21,22,37,41,51,60–65.

Modularity is found in the organization of biological

networks in various different contexts, from gene regu-

lation to food webs in ecosystems. Studies of morpho-

logical integration and modularity differ from analyses

of networks in other contexts because the interactions

responsible for integration are not directly observable

and instead need to be inferred from the patterns of cov-

ariation among traits51. Accordingly, delimiting modules

from data on patterns of covariation is a key concern for

the evo-devo of shape62.

Defining and delimiting modules. Modules are defined

as complexes that are highly integrated internally but

are relatively independent of each other. Therefore,

the covariation among groups of traits corresponding

to modules is expected to be weaker than the covaria-

tion among groups made by partitioning traits differ-

ently37,62,63. This means that systematic comparison of

a partition of traits made according to a hypothesis

of modularity to other partitions of traits can be used

to test the hypothesis of modularity62. This approach

has been used with landmark data in a range of organ-

isms17,22,27,41,62,65. As a rule, these studies have found that

the strength of covariation varies within a fairly limited

range — that is, even if the covariation among mod-

ules is weaker than the covariation among arbitrary

subsets of landmarks, this difference is not very big.

This indicates that morphological modularity is not an

all-or-nothing phenomenon but tends to be a matter

of degrees63. In other words, modules are not totally

independent of each other and they are not completely

integrated internally.

Several other approaches for identifying mod-

ules from patterns of covariation have also been

proposed64,66,67. These include clustering methods64 and

various statistical models66,67 that address the relative

strengths of integration within and between modules.

Because of the discrepancies in methods, the results

from different analyses can be difficult to compare51.

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Box 5 | Modularity in different contexts

Modularity is a general property of biological systems from molecular interactions to

ecosystem function; even if we limit the discussion to morphological traits, modularity

occurs in a series of distinct but interrelated contexts51.

Developmental modularity

Developmental interactions, such as inductive signalling, are not homogeneously

distributed but tend to be localized within specific regions (morphogenetic fields; for

example, imaginal discs, limb buds or tooth germs). These interactions provide strong

integration in these regions, which therefore form modules.

Developmental modularity can be studied in morphological data by examining

covariation of fluctuating asymmetry (BOX 4). Because the developmental system

expresses variation from other sources (such as genetic or environmental sources),

developmental modularity is fundamentally important for these other levels as well.

Genetic modularity

Genetic modules are established by genetic covariation among traits. This can be by

pleiotropic effects of single loci or by genetic linkage between loci with effects on

different parts.

Genetic modularity can be analysed in G matrices or quantitative trait locus (QTL)

effects (BOX 3). Covariation by pleiotropy can be due to direct developmental

interaction and is therefore related to developmental modularity. In turn, changes in

the genetic basis of development can affect developmental modularity.

Functional modularity

Interactions among parts that carry out organismal functions produce integration at

the functional level. For example, masticatory forces apply to broad regions of the

skull and mandible and can influence their growth93. These interactions relate to the

biomechanical role of parts — for example, as lever mechanisms or resonators — so

parts that contribute to the same functions form functional modules.

Biomechanical studies are needed to identify the interactions of the parts involved

in functional modularity. Functional modularity is related to developmental

modularity because development affects function through morphological variation,

and function in turn can influence development via processes such as bone

remodelling in response to mechanical load. There is a connection between functional

and genetic modularity through natural selection on functional performance, which

moulds genetic variation within populations79.

Evolutionary modularity

Evolutionary modularity is the result of integrated evolution in distinct complexes of

traits. This integration of evolutionary changes may result from coordinated selection

or from drift of genetically correlated traits73.

Evolutionary modularity can be inferred from comparative analysis of data from

multiple taxa in an evolutionary lineage. It relates to genetic modularity through the

effects of genetic constraints on evolutionary change (for example, under random drift,

evolutionary modularity is expected to match genetic modularity). It is also linked to

functional modularity by the effects of selection on functional performance, which is

expected to produce evolutionary change structured according to functional modules.

To establish the relationships among these levels of modularity, more studies will be

needed that systematically collect data across multiple levels. Such comparisons have

only just begun to be made17,27,60,70.

Modularity has been found in many, but not all,

structures that have been studied. In particular, studies

of wings in flies62 and crickets27 found strong inte-

gration throughout the wing rather than a modular

structure. Studies of mammalian mandibles60,62,63,66

and skulls17,64 have tended to show some degree of mod-

ularity. Comparative analyses have shown that modu-

larity can evolve among related species60,64,66, but there

are also features of modularity that are conserved on

macroevolutionary timescales17,64.

As a further development of the modularity perspec-

tive, Hallgrímsson et al.41 proposed the metaphor of the

palimpsest. Like reused parchment, on which older writ-

ing may not have been erased completely and therefore

might be partly visible under a newer text, several suc-

cessive developmental processes can all leave traces in

the pattern of covariation among traits. If the patterns

of modularity and integration produced by these proc-

esses are incongruent, each of the superimposed patterns

will obscure other patterns. As a result, even if distinct

modularity exists in the developmental processes, it may

not be decipherable in the cumulative pattern accrued

throughout development and no clear modular structure

may emerge in the covariation among traits.

Sources of integration and modularity. Morphological

integration can originate from any process that produces

joint variation in multiple traits, from within-individual

variation to long-term evolution (BOX 5). It is therefore

possible to compare patterns of integration and modu-

larity at different levels, which can provide insights into

evolutionary processes51.

Because all genetic or environmental effects on mor-

phometric traits are expressed through the develop-

mental system that produces the structure under study,

the developmental origin of integration and modular-

ity is of crucial importance for the evolution of shape68.

Accordingly, comparing developmental integration

(inferred from integration of asymmetry; BOX 4) to pat-

terns of genetic or phenotypic integration is important

for assessing the role of developmental processes in

determining shape variation. Comparisons have pro-

vided mixed results17,27,39,44,56,58,63,69–72 and thus suggest

that developmental interactions are major contributors

to the total genetic and phenotypic shape variation in

populations, but other factors may also contribute to a

greater or lesser extent.

The fact that the G matrix characterizes the genetic

variation available for evolution by natural selection

or neutral drift provides a link from these levels of

intra-population variation to the patterns of evolution-

ary diversification73. Evolutionary integration can be

analysed with comparative methods73,74, which can

be applied to shape data in combination with information

on the phylogeny of the study group12,17,74–76. Whether the

patterns of evolutionary integration agree with those of

G matrices in populations provides information about

the possible roles of selection and constraints in the

evolution of the group.

Constraints. Integration among traits can act as a con-

straint on evolution by concentrating variation in some

specific directions of the shape space and limiting varia-

tion in other directions (FIG. 1). This may be easiest to see

for examples that are simple measurements, such as the

diameters of eyespots on butterfly wings7 or the lengths

of limb bones in primates8. If there is a very strong cor-

relation between two measurements, a scatter plot of two

such traits will show that most data points fall along a

single line. There is much more variation in the direction

along the line than perpendicular to it. The stronger the

correlation is — that is, the more integrated the traits are

— the more extreme is the discrepancy in the amounts

of variation in different directions. If genetic variation

is concentrated in such a manner, there is a genetic

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ed

bca

Relative size of anterior eyespot

Relative size of posterior eyespot

6

4

2

0

–2

–4

–6

20–2 6–4 4–6

Colour composition of eyespot 4

Colour composition of eyespot 6

3

2

1

0

–1

–2

–3

10–1 3–2 2–3

BG BB

GG GB

LS LL

SS SL

Figure 1 | Relative and absolute constraints. a | Absence of constraints. Variation is equally abundant in all directions

of the phenotypic space (circle), so selection in any direction will produce an equally strong evolutionary response

(arrows). Empirical studies suggest that this situation is very rare. b | Relative constraints. Variation is concentrated

mainly in one direction, but there is some variation in all directions — and thus there is an evolutionary response to

selection in all directions — although some directions produce bigger responses (black arrows) than others (grey

arrows)68. This situation is common for shape and other morphological traits. c | Absolute constraints. Variation is so

concentrated that one or more dimensions of the phenotypic space are entirely devoid of variation, meaning that

evolution cannot proceed in those directions (crossed-out arrows)68. Absolute constraints seem to be rare in extant

populations. d | Example of a relative constraint: the relative sizes of the dorsal eyespots on the wings of Bicyclus

butterflies. Artificial selection for small (S) or large (L) anterior and posterior eyespots in different combinations

yielded an evolutionary response in all experiments7,78. e | A possible example of an absolute constraint (or a very

strong relative constraint): the colour composition of ventral eyespots on the wings of Bicyclus butterflies. Artificial

selection seems to be successful only if the more extensive gold or black colour is favoured in both anterior and

posterior eyespots (GG and BB). By contrast, selection for gold in one and black in the other eyespot (GB and BG)

seems to produce no or only a very small evolutionary response78. Parts b and c are modified, with permission, from

REF. 68 © (2005) Elsevier. Parts d and e are modified from REF. 78.

constraint — that is, evolutionary change is more likely

to be in some particular directions than in others68. In

other words, such constraints can channel evolutionary

change along ‘lines of least resistance’77.

Experiments with artificial selection on different

butterfly eyespots showed that evolutionary change is

much faster along the line of least resistance than per-

pendicular to it7,78 (FIG. 1d,e). For geometric shape data,

constraints are manifest in the deflections of the evolu-

tionary response from the direction of selection in shape

space24,27,29, which suggests that constraints may have a

major role in the evolution of shape.

It is important to distinguish between relative and

absolute constraints68 (FIG. 1). Relative constraints deflect

evolutionary change away from the direction of selec-

tion and towards lines of least resistance, but they cannot

completely prevent evolution in any direction (although

intense selection may be required). This is the type of

constraint that is usually found in experimental studies7

(FIG. 1d) or in phenotypic8 or genetic24,27,29 studies of mor-

phological variation in populations. By contrast, abso-

lute constraints completely prevent any evolution in one

or more dimensions of the shape space because those

dimensions are totally devoid of any genetic variation.

There is a continuing debate on how to demonstrate

absolute genetic constraints26,27,30, but no clear example

of an absolute constraint for shape characters has been

published. The best example of an absolute constraint,

to my knowledge, concerns the colour composition of

butterfly eyespots78 (FIG. 1e).

Constraints themselves can potentially evolve as the

patterns of integration among traits change. Therefore,

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constraints that affect particular populations or evolu-

tionary lineages, even if they are absolute constraints, may

be overcome at larger phylogenetic scales. Weakening or

loss of a constraint can facilitate evolutionary change.

For example, intraspecific integration between fore- and

hindlimb elements is weaker in great apes than it is in

Old or New World monkeys; the fact that great apes

show a much greater variation of relative limb lengths

than other apes has been interpreted as resulting from

the relaxation of an evolutionary constraint8. The ease

with which such uncoupling of traits can be achieved

by selection depends on the developmental-genetic

architecture of the traits68,78.

Much of the discussion on evolutionary constraints

in the context of evo-devo has centred on modularity

as a way to break constraints1,78,79. If traits under diver-

gent selection are organized into different modules,

they will be able to evolve towards their respective optima

with minimal interference with each other. Accordingly,

modularity should increase the potential for evolution-

ary change79. Some evidence for this hypothesis has been

found80, but there is much scope for further studies.

Allometry

Allometry is the dependence of shape on size and tends

to be one of the dominant factors of morphological

variation, reflecting the abundant variation of size81.

As organisms grow, their size and shape change jointly

— this is the reason why allometry is tightly linked to

development. Even if only adults are considered, there

is a link to ontogeny because the size differences among

adults reflect variation in the extent of growth they

have undergone82.

Because size variation affects the entire organism, it

is often a strong integrating factor and thus allometry is

potentially a strong constraint. Although exceptions

exist83, allometries are often nearly straight lines in shape

space. Accordingly, allometry can channel evolutionary

changes along the corresponding directions. For exam-

ple, sex dimorphism has long been related to allometry

because the larger sex may be an allometrically scaled-up

version of the smaller sex22,84,85.

In geometric morphometrics, allometry is usu-

ally analysed by a multivariate regression of shape on

size19. Regression fits a straight line to the data points

that represent the expected shape for each value of

size. The deviations of individual data points from this

line — the residuals — represent shape variation that

is not explained by size. A correction for the effects of

allometry can be done simply by using these residuals

from the regression of shape on size in further analyses.

Because allometry is an integrating factor, other pat-

terns, such as modularity, tend to be more apparent after

size correction62.

Allometry is not constant but can differ among

closely related species84–86. The evolution of allometry

can be studied by constructing ‘allometric spaces’ in

which taxa are arranged according to the similarity of

their allometric patterns86,87. The importance of these

analyses for evo-devo is that they reflect evolution-

ary change in growth patterns, which in turn may be

related to ecological factors. For example, a comparison

of allometries in rodents found that there are distinct

groupings according to diet86.

Evo-devo and function

Research in evo-devo has tended not to emphasize

functional aspects of evolution, and has mostly focused

on the origin of new variation1,3. But function and

adaptive value are essential for fully understanding the

evolution of morphological features. Therefore, a ‘func-

tional evo-devo’ is needed to bring these considerations

into evo-devo88.

Function has been an important aspect in discus-

sions of modularity88. Because divergent adaptation of

traits involved in different functions may be impeded

by integration among parts, modularity offers a possible

escape from such evolutionary constraints. Accordingly,

one might expect developmental systems to evolve so

that the patterns of genetic integration and modularity

match the patterns of functional interactions among

traits79,89. This hypothesis can be tested in systems in

which developmental units are not congruent with func-

tional units, either because multiple parts of different

developmental origins are jointly involved in a single

function or because different parts of a developmental

unit perform different functions88. There have been few

rigorous tests of this hypothesis; of the studies performed

so far, some provide support (for example, some stud-

ies show that flowers and inflorescences are integrated

for accurate pollination90), whereas others are inconsist-

ent with the hypothesis (for example, the cricket wing

consists of functionally differentiated parts that are not

separate modules27).

Many other evo-devo studies have shown clear impli-

cations for function. In teeth, for example, development

provides great flexibility for shape changes with clear

functional implications91. Moreover, if multiple molar

teeth are to form an effective grinding surface, their

shapes, sizes and positions need to be coordinated by

the development of the teeth and the growth processes

of the jaws, so the developmental and genetic integra-

tion in the molar tooth rows is an important aspect of

their function21,36.

Some studies have explicitly included biomechanical

aspects to identify morphological features that are

relevant for function. For example, the lower jaw of

cichlid fish can be viewed as a lever system for open-

ing and closing, and simple genetic changes have been

shown to produce functionally relevant changes in its

development89. Moreover, biomechanical methods

can estimate the mechanical strains that result from

the use of structures92. Such methods could be used

to examine the effects of masticatory forces on facial

growth patterns93.

For a full understanding of function, it is neces-

sary to know the selection regime for the structure of

interest. An excellent example is the plant Erysimum

mediohispanicum (BOX 1), in which detailed studies of

selection on flower shape were conducted6,94. Plants with

more zygomorphic flowers attracted more pollinators6.

Experiments with artificial flowers of different shapes

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Box 6 | Mapping shape data onto phylogenies

To understand the

evolution of shape, it is

useful to reconstruct the

history of shape changes

explicitly. Starting from

the shape data obtained

from extant species

and information on the

phylogeny of the study

group, the primary task is

to estimate the shapes at

the internal nodes of the

phylogeny — that is, the

shapes of the hypothetical

ancestors in the lineage.

A range of methods exist

for this purpose, but

the method in most

widespread use is

squared-change

parsimony73–75.

Squared-change

parsimony minimizes the

sum of squared distances

in shape space between

each node and the nodes

to which it is connected

by the branches of the

phylogenetic tree. This

method has a number of

properties that makes it

useful as an estimate of

the ancestral shapes in the

phylogeny and is readily

integrated in the multivariate

context of shape spaces74,75.

Inferred ancestral shapes can

be visualized directly12,104 or

the information on shape

changes can be used in further

analyses75,76. The method

also can be used to study the

evolution of shape differences,

such as the male–female

differences for studies of

sexual shape dimorphism85.

An example of this approach is shown in the figure. The coloured dots represent the species averages in the space

spanned by the first two principal components of head shape in a group of fishes consisting of two main clades and

two outgroup taxa. The black lines represent the branches of the phylogeny based on reconstructions of ancestral

shapes by squared-change parsimony. It is evident that clade C has diversified relatively little (red and orange dots),

whereas clade A has continually expanded into new regions of morphospace (blue dots).

Squared-change parsimony is also the basis for other analyses concerning the phylogeny of shape, such as testing

whether there is a phylogenetic signal in shape data75. If such a signal is present, comparative methods, such as the

method of independent contrasts73,74, should be used that take into account the phylogenetic relationship among species.

Comparative methods provide estimates of the patterns of evolutionary changes across the phylogeny of the group

under study. For example, these patterns provide information about evolutionary integration and the patterns of

covariation of phylogenetic shape changes17. Comparing these patterns of evolutionary integration to patterns

of intraspecific variation can provide insights into the mechanisms that produce evolutionary change17,60,61, 

including the role of genetic constraints that may force evolutionary change to follow ‘lines of least resistance’77.

Systematic and large-scale studies have only just begun but are a promising approach for gaining insights into the

developmental and genetic basis of morphological change at large phylogenetic scales, which is a central task for

studying the evolutionary developmental biology of shape.

Figure is modified, with permission, from REF. 76 © (2008) John Wiley & Sons, Inc.

Nature Reviews | Genetics

Principal component 2

Principal component 1

–0.1 0.2–0.2 00.1–0.3

0.1

0

0.2

–0.1

–0.2

Clade A

Anostomidae

Chilodontidae

Clade C

Curimatidae

Prochilodontidae

Outgroups

Hemiodus and Parodon

Squared-change parsimony

A method for inferring

ancestral phenotypic values in

a phylogeny by minimizing the

sum of squared phenotypic

changes over all branches of

the phylogeny.

Independent contrasts

A method that addresses

the interdependence in

comparative data due to

shared ancestry among species

by focusing on differences

between contrasts of

phenotypic values between

sister nodes in a phylogeny.

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showed that different pollinators prefer specific shapes

and therefore may impose variable selection dep-

ending on the composition of pollinator communities94.

Together with information on quantitative genetic

variation25 and the developmental basis of flower

symmetry5, such studies can establish a strong functional

context in evo-devo.

Macroevolution

Evo-devo studies have mostly focused on large-scale

evolutionary phenomena, such as the conservation of

Hox gene clusters or the origin of body plans in animals,

whereas morphometric studies have mostly focused on

evolution at much smaller scales. An increasing number

of studies have investigated shape variation at large

scales17,64,76,80,95,96. As phylogenetic trees and comparative

methods for shape data74–76 become more widespread, it

is becoming more feasible to conduct detailed analyses of

morphological diversification based on a reconstructed

history of shape change60,75,76.

Filling morphospaces. If shapes are represented as points

in a morphospace, evolutionary change is visualized as

paths from ancestors to descendants through the mor-

phospace. The evolution of a group of organisms appears

as a branching tree expanding from the location of the

common ancestor in various directions of the space. This

information can be obtained by mapping shape data onto

a phylogeny (BOX 6).

The patterns of changes in the morphospace can then

be interpreted to reconstruct the dynamics of the evo-

lutionary process. Major shifts manifest themselves as

‘jumps’ that are candidates for the search for key develop-

mental and adaptive changes. Evolutionary trends appear

as strings of changes along a particular direction.

Sidlauskas76 reconstructed the evolution of head shape

in two lineages of characiform fishes (BOX 1; BOX 6). One

of the lineages occupies a compact area of the morphos-

pace, whereas the sister lineage diversified substantially

along one direction in morphospace that corresponds

to a trend associated with the elongation of the quadrate

bone and new variation in the orientation of the snout

that can be directed up or down. The elongation of the

quadrate changed the position of the jaw joint and thus

seems to have provided an opportunity for continued

morphological diversification into new regions of shape

space, resulting in more and more extreme head shapes

and adaptation to various new feeding modes76.

Patterns in morphospaces can be informative even

when no phylogeny is available (meaning that direc-

tions of evolutionary changes cannot be inferred). For

example, parallel scatters of skull shapes in placental

and marsupial groups in morphospace suggest cor-

responding evolutionary processes in both groups of

mammals97. Such parallelisms of variation may be due

to selection and adaptation to corresponding niches (for

example, for the mammalian skulls there is an associa-

tion with diet97) or a shared constraint, such as allometry.

Similarly, analysis of head shape in cichlid fish showed

that radiations in different lakes produced parallel

adaptations to diet96.

Evolution of developmental systems. The question of

how developmental systems evolve is at the core of evo-

devo and is a key factor for understanding the evolution

of shape. If the developmental system is altered, the con-

straints it imposes on the production of new variation

may also change, which in turn will modify the dynamics

of evolution68. Such a change may well be involved in the

diversification of head shape in characiform fishes76.

Some results indicate that the nature of developmental

processes is crucial for the evolutionary flexibility of

traits. In butterflies, artificial selection can more readily

break the size association among the serially homolo-

gous eyespots than the association of colour composi-

tion among the eyespots78 (FIG. 1d,e), and among related

species the relative sizes of eyespots differ more than does

the colour composition78. This finding is consistent with a

morphogen gradient model78 in which local regulation is

more easily achieved for the amount of the signal rather

than for the specific nature of the response in the target

tissue. Accordingly, changes to developmental processes

can overcome some constraints more easily than others.

Laboratory studies indicate that mutations in many

genes can produce changes in the patterns of shape

variation39,41, and QTL studies suggest that many loci

affect average shape37,38. These observations imply that

there are many targets for evolutionary change that affect

shape. It may therefore be somewhat surprising that some

key genes have important roles in changes in widely sepa-

rate groups of animals. For example, bone morphoge-

netic protein 4 and calmodulin have been shown to have

important roles in the differentiation of shapes of fish jaws

and bird beaks98. The role of key developmental genes, a

long-term focus of evo-devo, in the context of polygenic

inheritance of shape remains to be fully explored.

Conclusions

The study of shape has many aspects to offer to the field

of evo-devo. Analysis of shape requires an explicitly

quantitative approach and therefore provides the power

to identify a multitude of subtle effects. Such analyses

show that development mediates interactions between

many genetic and environmental factors and affects

evolution in a dynamic manner.

Modularity and integrating factors, such as allometry,

have been identified as important determinants of con-

straints on the evolution of shape. But they have also

been shown to evolve. Hence the constraints themselves

are not constant but can change over evolutionary time:

most microevolutionary constraints are dynamic and

not static on macroevolutionary timescales. Accordingly,

a task for future analyses will be to identify the factors

involved in their evolution: is the evolution of allometries

and modularity a result of selection on those constraints

themselves or is it a by-product of the evolution of the

average shapes of taxa?

Functional and ecological considerations are highly

relevant to the evolution of shape, and quantitative analy-

ses can make these aspects more prominent in evo-devo.

As a result, evo-devo will provide a richer picture of the

interactions of development with external factors in

the process of evolution.

Morphospace

A multidimensional space

in which forms of organisms 

are represented by points,

and distances between

points correspond to the

morphological similarity

between forms.

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Acknowledgements

I thank J. M. Gómez, A. Drake, B. Sidlauskas and M. Sabaj

Perez for providing the images in Box 1, and C. Allen and

B. Sidlauskas for providing the graphs in Figure 1 and Box 6,

respectively. I greatly appreciate the thoughtful comments of

three anonymous referees on earlier versions of this article.

Competing interests statement

The author declares no competing financial interests.

FURTHER INFORMATION

Christian Peter Klingenberg’s homepage: 

http://www.flywings.org.uk

Morphometrics at SUNY Stony Brook (includes

announcements of meetings and courses, software, a

bibliography and a list of researchers):

http://life.bio.sunysb.edu/morph

Morphometrics.org (includes access to the MORPHMET

community mailing list): http://www.morphometrics.org

ALL LINKS ARE ACTIVE IN THE ONLINE PDF

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Citations (596)

References (135)

... The developmental origins of cranial parts are mainly from two embryological primordial structures that later become the definitive postnatal structure composed of anatomically related by proximity but not embryologically related entities; the zygomatic, maxillary and temporal bones of the skull develop from neural crest of the first pharyngeal arch (Elliot 2010) whereas more posterior portions of the cranium develop from differently derived mesenchymal cells (Le Lievre 1980;Le Douarin and Kalcheim 1999). Embryological and morphological modularity (Olson and Miller 1958;Klingenberg 2010) forms the basis of the current investigation in assessing the accuracy of integration of skull development since anatomically related parts do not necessarily translate to developmental relationships, this produces phenotypes. Evolutionary modularity relates to comparing minute modularity changes in skull structural components over time; such data on species progression of change identify probable taxon radiations in time space and to relocate phylogenetic asynchrony intra and interspecifically (Klingenberg 2010). ...

... Embryological and morphological modularity (Olson and Miller 1958;Klingenberg 2010) forms the basis of the current investigation in assessing the accuracy of integration of skull development since anatomically related parts do not necessarily translate to developmental relationships, this produces phenotypes. Evolutionary modularity relates to comparing minute modularity changes in skull structural components over time; such data on species progression of change identify probable taxon radiations in time space and to relocate phylogenetic asynchrony intra and interspecifically (Klingenberg 2010). Modularity hypotheses of development will be tested using landmark partitions to verify whether co-variations among embryologically-related landmarks are lower in comparison to partitions based on anatomical proximities. ...

... DA and asymmetry studies are relatively scarce or nonexistent in the literature for small African pangolins, while FA is the bilateral asymmetry that represents minute random developmental differences between the right and left sides (Benitez et al. 2020). Klingenberg (2010) showed that within the concept of geometric morphometrics studies of asymmetry can be combined with other morphological issues -modularity and integration. While modularity refers to the covariance among morphological structures that originates in independent developmental processes (socalled modules), integration, a counterpart to modularity is a measure of the interconnection among parts to function as a whole unit (Klingenberg 2010). ...

Three areas of cranial evolution in the white-bellied pangolin (Phataginus tricuspis): An initial report on asymmetry, ontogeny and modularity

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... Solid tissues, such as bones, are composed of topological configurations that do not follow any classical geometric shapes, while soft tissues are subjected to dynamic shape changes due to biomechanical force exertions. These biological dynamics result in osteological reconfiguration influenced by tendinous mechanical stress, which has shaped bones to adapt overly irregular margins and projections [1]. Characterizing these complex morphologies of bones in correlation to their soft tissue surroundings, as well as post-injury remodeling, is of importance in medical practice [2−6]. ...

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• David Kachlík

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... In addition to body size, another easily measurable morphological parameter affected by heat stress is symmetry, which might offer insights into an individual's fitness (Klingenberg 2010). High temperatures during the larval stage can impact the stability in an insect's development, and the extent of thermal stress can be reflected in the symmetry and shape of the resulting adult individual (Hoffmann et al. 2002). ...

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... The first is traditional or linear morphometry, based on the analysis of linear measurements, such as the length, width, and height of the body, and other morphological traits [8]. The second, more recent, is geometric morphometry, which aims to analyze and quantify the differences between complex morphological shapes, through multivariate analysis and the visualization of variation in a morphospace [8,9]. Based on these morphometric tools, it is possible to explore several biological factors, ranging from the recognition and delimitation of possible cryptic or morphologically related species [10,11] to the exploration of patterns of ecogeographic variation [12][13][14]. ...

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[tooth fungus]

[shape theories]

[roach theory]

https://fau.digital.flvc.org/islandora/object/fau%3A39473#:~:text=According%20to%20Roach%2C%20caring%20is,conscience%2C%20commitment%2C%20and%20comportment.

Date Issued:

2014

Summary:

The use of the telephone to speak to study participants about health-related issues is useful when logistics make it difficult for participant and researcher to meet in person. However, gaining the trust of the participant can be a challenge, partly due to fears of fraud and identity theft. A spirit of openness and caring must come across the telephone lines between interviewer and interviewee. Roach’s six C’s can be applied to convey a sense of caring, thereby relaxing the participant and increasing their sense of safety to enhance the quantity and quality of health data being collected. According to Roach, caring is manifested through six C’s – compassion, competence, confidence, conscience, commitment, and comportment. Interviewers can be trained through role playing and scripting using Roach’s caring model. Compassion is expressed by being sensitive to the anxiety and apprehension they may feel toward receiving a call from a stranger, who is asking about health-related issues. Competence is expressed by being able to give the participant the information they need to have an understanding as to what they are consenting. Confidence is achieved by ensuring the participant that the information they share will be used appropriately and for the greater-good. Conscience is expressed by following ethical research protocols, adhering to confidentiality, and respecting the relationship with the research participant. Finally, interviewers manifest caring through comportment by identifying themselves with their name, credentials, and institution; addressing the participant formally; using language the participant can understand; and projecting caring through tone of voice.

[pregancy and still births]

[aturois mushrooms]

[age regression]

Understanding Age Regression

• What it is

• Types

• Recreational

• Is it safe?

• Takeaway

Age regression occurs when someone reverts to a younger state of mind. This retreat may be only a few years younger than the person’s physical age. It could also be much younger, into early childhood or even infancy.

People who practice age regression may begin showing juvenile behaviors like thumb-sucking or whining. Others may refuse to engage in adult conversations and handle issues they’re facing.

Age regression is sometimes used in psychology and hypnotherapy. It can also be used as a self-help tool, or something someone does to reduce stress.

Keep reading to find out when age regression might be used and what it might achieve.

What is age regression?

Sigmund Freud believed age regression was an unconscious defense mechanism. It was a way the ego could protect itself from trauma, stress, or anger.

Still, other psychologists think of age regression as a way for people to achieve a therapeutic goal. It might be used to help a patient recall memories of trauma or painful events. The therapist can then help their patient heal properly from those experiences.

Psychiatrist Carl Jung believed age regression wasn’t a means to escape anything. He believed age regression could be a positive experience. It could be used to help people feel younger, less stressed, and more open.

With all these different theories for age regression, several types exist.

Types of age regression

Each of these age regression types share two common elements:

• People who regress revert to a younger state of mind than their physical age. The length of years varies from type to type and person to person.

• Age regression is in no way sexual.

As a symptom

Age regression may be the result of a medical or psychiatric issue. For example, some individuals experiencing significant distress or pain may revert to childlike behavior as a means to cope with anxiety or fear.

Certain mental health issues make age regression more likely. Age regression could be a symptom of one of these conditions:

• schizophrenia

• dissociative identity disorder

• schizoaffective disorder

• post-traumatic stress disorder (PTSD)

• major depressive disorder

• dementia

• borderline personality disorder

Age regression may occur in personality disorders when people come face to face with distressing memories or triggers. In this case, the age regression may be spontaneous.

What’s more, some individuals may begin to revert to a younger age as they grow older. This can be a sign of dementia. It might also be a coping mechanism for worries about the impact of aging.

Clinical

Age regression can be used as a therapeutic technique. Some mental health professionals use hypnotherapy and age regression to help patients return to painful periods in their lives. Once there, they can help them overcome the trauma and find healing.

However, this practice is controversial. Some experts suggest it could be possible to “uncover” false memories. Plus, it’s unclear how reliable these “recovered” memories are.

Trauma recovery

People with a history of trauma may be more likely to regress. In fact, age regression may be common in people who have been diagnosed with dissociative identity disorder (DID), a disorder formerly known as multiple personality disorder.

People with this disorder frequently have a younger personality among their distinctive personalities. However, it’s believed that the “little” may not be a separate personality. Instead, it may be a regressed version of the original personality.

In other words, the person with DID may be aware of everything, but they feel like they’re a different age. They may talk like a child or begin behaving like one. In other instances, the “little” is entirely separate.

In this case, age regression is a form of security against fear or insecurity. This type of age regression may be triggered by particular events or stressors.

Self-help

For others, age regression may be intentional. Some individuals may select reverting to a younger state as a means to block out stress and worry. They can also revert to a younger age so they can avoid tough issues or personal problems.

As a form of self-help, age regression may help you revert to a time in your life when you felt loved, cared for, and secure. In that sense, this can be a positive experience.

However, age regression may be a sign of a larger mental health issue. You should speak with a mental health care provider about this practice. They can help you learn how to use it safely. They can also evaluate your experiences to determine if a different type of treatment is needed.

Recreational age regression

Age regression is never considered sexual. It’s a type of defense mechanism that allows you to mentally escape to a different time in your life.

This is different from pretending to be younger. Indeed, some individuals portray themselves many years younger than they are as part of a hobby, sexual fetish, or kink.

For example, some members of fandom communities may use costumes and portrayals to “pretend” to be younger and more naïve. This is not real age regression.

Is age regression safe?

There’s no inherent risk in age regression. If you practice it as a form of self-help or relaxation, you may want to make sure you’re in a safe place and around people who understand this technique.

If, however, you find yourself reverting to a younger age without your control, you should seek help from a mental health professional. You may be showing symptoms of an underlying issue that needs to be addressed differently.

The takeaway

Age regression occurs when you mentally retreat to an earlier age. In all ways, you believe you’re back at that point in your life, and you may exhibit childish behaviors, too.

Some people choose to revert to a younger age. In this case, it can be a coping mechanism to help them relax and eliminate stress. Age regression may be a symptom of a mental health condition, such as dissociative identity disorder or PTSD.

Age regression can also be used a therapeutic technique, though it’s a controversial practice. A mental health professional can help you return to a time in your life when you were abused or experienced trauma. From there, you can work together to heal.

Speak to your healthcare provider if you notice symptoms of age regression or you’re interested in learning more.

Last medically reviewed on August 30, 2019

How we reviewed this article:

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Medically reviewed by Timothy J. Legg, PhD, PsyD — By Kimberly Holland on August 30, 2019

What Are the Short- and Long-Term Effects of Emotional Abuse?

• Short-term effects

• Long-term effects

• Effects on children

• PTSD

• Ways to begin recovery

• Seeking help

• Find a professional

Emotional abuse can cause physical and mental issues, ranging from muscle tension and feelings of shame to insomnia and post-traumatic stress disorder.

When thinking about abuse, physical abuse may come to mind first. But abuse can come in many forms. Emotional abuse is just as serious as physical abuse and often

Trusted Source

 precedes it. Sometimes they happen together.

If you’re wondering whether it’s happening to you, here are some of the signs:

• yelling

• name-calling

• spewing insults or otherwise ridiculing you

• attempting to make you question your own sanity (gaslighting)

• invading your privacy

• punishing you for not going along with what they want

• trying to control your life

• isolating you from family and friends

• making subtle or overt threats

If you’ve been emotionally abused, know that it’s not your fault. There’s also not a “correct” way to feel about it.

Emotional abuse isn’t normal, but your feelings are.

Continue reading to learn about the effects of emotional abuse and how to get help.

Short-term effects

You might be in denial at first. It can be shocking to find yourself in such a situation. It’s natural to hope you’re wrong.

You may also have feelings of:

• confusion

• fear

• hopelessness

• shame

This emotional toll can also result in behavioral and physical side effects. You may experience:

• difficulty concentrating

• moodiness

• muscle tension

• nightmares

• racing heartbeat

• various aches and pains

Long-term effects

Studies

Trusted Source

 show that severe emotional abuse can be as powerful as physical abuse. Over time, both can contribute to low self-esteem and depression.

You may also develop:

• anxiety

• chronic pain

• guilt

• insomnia

• social withdrawal or loneliness

Some researchers theorize

Trusted Source

 that emotional abuse may contribute to the development of conditions such as chronic fatigue syndrome and fibromyalgia.

Does it affect children differently?

As with adults, emotional abuse of children can go unrecognized.

If a child is experiencing emotional abuse, they may develop:

• social withdrawal

• regression

• sleep disorders

If left unresolved, these conditions can continue into adulthood and leave you vulnerable to more mistreatment.

Most children who are abused don’t grow up to abuse others. But some research suggests that they may be more likely than adults who weren’t abused during childhood to engage in toxic behaviors.

Adults who were abused or neglected as children may also be more likely to develop chronic health problems, including:

• eating disorders

• headaches

• heart disease

• mental health issues

• obesity

• substance use disorders

Does emotional abuse lead to post-traumatic stress disorder (PTSD)?

Emotional abuse doesn’t always lead to PTSD, but it can.

PTSD can develop after a frightening or shocking event. Your doctor may make a PTSD diagnosis if you experience high levels of stress or fear over a long period of time. These feelings are usually so severe that they interfere with your daily functioning.

Other symptoms of PTSD include:

• angry outbursts

• being easily startled

• negative thoughts

• insomnia

• nightmares

• reliving the trauma (flashbacks) and experiencing physical symptoms such as rapid heartbeat

PTSD in children might also cause:

• bed-wetting

• clinginess

• regression

You may be more likely

Trusted Source

 to develop PTSD if you have:

• been through traumatic events before, especially in childhood

• a history of mental illness or substance use

• no support system

PTSD is often treated with therapy and antidepressants.

When you’re ready to begin recovery

Emotional abuse can lead to mental and physical symptoms that shouldn’t be ignored. But what works for one person may not work for another. And not everyone is ready to begin recovery right away.

When you’re ready to take the next step, you may find it helpful to start with any of the following tips.

Reach out for support

You don’t have to go through this alone. Talk to a trusted friend or family member who will listen without judgment. If that’s not an option, consider joining a support group for people who have experienced abuse or trauma.

Get physically active

Exercise can do more than just keep you more physically fit.

Research shows

Trusted Source

 that doing moderate-intensity aerobics or a mix of moderate aerobic and muscle-strengthening activity for at least 90 minutes a week can:

• help you sleep better

• keep you sharp

• reduce your risk of depression

Even less intense physical activity, such as a daily walk, can be beneficial.

If you’re not interested in home workouts, consider joining a class. That could mean swimming, martial arts, or even dance — whatever gets you moving.

Get social

Social isolation can happen so slowly that you don’t even notice, and that’s no good. Friends can help you heal. That doesn’t mean you have to talk to them about your problems (unless you want to). Simply enjoying the company of others and feeling accepted may be enough to boost your spirits.

Consider doing the following:

• Call an old friend you haven’t spoken to in a long time just to chat.

• Invite a friend to the movies or out for a bite to eat.

• Accept an invitation even when your instinct is to stay home alone.

• Join a class or club to meet new people.

Mind your diet

Emotional abuse can wreak havoc with your diet. It can lead you to eat too little, too much, or all the wrong things.

Here are some tips that can help keep your energy level up and minimize mood swings:

• Eat a variety of fruits, vegetables, and lean protein.

• Eat several well-balanced meals throughout the day.

• Avoid bingeing or skipping meals.

• Avoid alcohol and drugs.

• Avoid sugary, fried, and highly processed foods.

Make rest a priority

Fatigue can rob you of energy and clear thinking.

Here are some ways to promote a good night’s sleep:

• Go to bed at the same time each night and get up at the same time each morning. Make it your goal to sleep at least seven hours a night.

• Do something relaxing in the hour before bedtime.

• Remove electronic gadgets from your bedroom.

• Get room-darkening window shades.

You can also help ease stress by practicing relaxation techniques, such as:

• listening to soothing music

• aromatherapy

• deep breathing exercises

• yoga

• meditation

• tai chi

Volunteer

It may seem counterintuitive, but volunteering your time can help ease stress, anger, and depression. Find a local cause you care about and give it a try.

When to seek professional help

Although lifestyle changes may be all it takes for some people, you may find that you need something more. This is totally OK and normal.

You may find professional counseling helpful if you’re:

• avoiding all social situations

• depressed

• frequently fearful or anxious

• having frequent nightmares or flashbacks

• unable to carry out your responsibilities

• unable to sleep

• using alcohol or drugs to cope

Talk therapy, support groups, and cognitive behavioral therapy are just a few ways to address the effects of emotional abuse.

How to find a professional

If you decide to seek out professional help, look for someone with experience in emotional abuse or trauma. You can:

• Ask your primary care physician or other doctor for a referral.

• Ask friends and family for recommendations.

• Call your local hospital and ask if they have mental health professionals on staff.

• Search the American Psychological Association database.

• Search the database at FindAPsychologist.org.

Then, call a few and schedule a Q&A session over the phone. Ask them:

• What are your credentials, and are you properly licensed?

• What experience do you have with emotional abuse?

• How will you approach my therapy? (Note: This may not be decided until the therapist conducts their initial assessment of your issues.)

• How much do you charge?

• Do you accept my health insurance? If not, can you arrange a payment plan or sliding scale?

Keep in mind that finding the right therapist can take time. Here are a few questions to ponder after your first visit:

• Did you feel safe enough to open up to the therapist?

• Did the therapist appear to understand and treat you with respect?

• Do you feel good about having another session?

Meeting with a therapist once doesn’t mean that you have to stick with them. You’re perfectly within your rights to try someone else. Keep going until you find the right fit for you. You’re worth it.

Last medically reviewed on May 16, 2018

How we reviewed this article:

SOURCES

HISTORY

Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.

Current Version

Apr 3, 2023

Written By

Ann Pietrangelo

Edited By

Heather Hobbs

May 16, 2018

Medically Reviewed By

Timothy J. Legg, PhD, PsyD

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Medically reviewed by Timothy J. Legg, PhD, PsyD — By Ann Pietrangelo — Updated on April 3, 2023

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Dissociative Identity Disorder

• Symptoms

• Causes

• Treatment

• When to see a doctor

• Takeaway

Overview

Dissociative identity disorder, previously known as multiple personality disorder, is a type of dissociative disorder. Along with dissociative amnesia and depersonalization-derealization disorder, it’s one of the three major dissociative disorders.

Dissociative disorders can be found in people of all ages, races, ethnicities, and backgrounds. The National Alliance on Mental Illness (NAMI) estimates that about 2 percent of people experience dissociative disorders.

What are the symptoms of dissociative identity disorder?

The most recognizable symptom of dissociative identity disorder (DID) is a person’s identity being involuntarily split between at least two distinct identities (personality states). Other symptoms might include:

• Dissociative amnesia. This is a type of memory loss — beyond forgetfulness — that’s not associated with a medical condition.

• Dissociative fugue. A dissociative fugue is an episode of amnesia that involves not having memory of certain personal information. It may include wandering off or a detachment from emotion.

• Blurred identity. This occurs when you feel like there are two or more people talking or living in your head. You might even feel like you’re possessed by one of several other identities.

It’s important to note that according to the Diagnostic and Statistical Manual of Mental Disorders, many cultures around the globe include possession as part of a normal spiritual ritual or practice. This isn’t considered a dissociative disorder.

Interacting with someone with dissociative identity disorder

If you believe someone you know has DID, you may get the impression that you’re communicating with not one, but several different people, as the person switches between personalities.

Often, each identity will have their own name and characteristics. They’ll each commonly have an unrelated detailed background with obvious differences in age, gender, voice, and mannerisms. Some might even have individual physical characteristics such as a limp or poor vision that requires glasses.

There are often differences in each identity’s awareness and relationship — or lack thereof — to the other identities.

Causes of dissociative personality disorder

Dissociative identity disorder — along with other dissociative disorders — usually develop as a way to deal with some type of trauma they’ve experienced.

According to the American Psychiatric Association, 90 percent of people with dissociative identity disorder in the United States, Canada, and Europe have experienced childhood neglect or abuse.

What types of treatment are there for DID?

The primary treatment for DID is psychotherapy. Also known as talk therapy or psychosocial therapy, psychotherapy is focused on talking with a mental health professional about your mental health.

The goal of psychotherapy is to learn how to cope with your disorder and to understand the cause of it.

Hypnosis is also considered by some to be a useful tool for DID treatment.

Medication is sometimes used in the treatment of DID, as well. Although there are no medications specifically recommended for the treatment of dissociative disorders, your doctor might use them for associated mental health symptoms.

Some commonly used medications are:

• anti-anxiety medications

• antipsychotic drugs

• antidepressants

Online therapy options

Read our review of the best online therapy options to find the right fit for you.

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LEARN ABOUT PERSONALITY DISORDERS

---

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When to see a doctor

If you can identify with any of the following, you should make an appointment to see your doctor:

• You are aware — or others observe — that you involuntarily and unwillingly have two or more personalities or identities that have a distinctly different way of relating to you and the world around you.

• You experience beyond ordinary forgetfulness, like extensive gaps in your memory for important personal information, skills, and events.

• Your symptoms aren’t caused by a medical condition or from the use of alcohol or drugs.

• Your symptoms are causing you problems or stress in important areas such as your personal life and at work.

Takeaway

If you identify with the symptoms of dissociative identity disorder, you should make an appointment to see your doctor.

If your friend or a loved one is displaying the common symptoms, you should encourage them to seek help. You can also contact the NAMI HelpLine at 1-800-950-6264 or email info@nami.org for support.

Last medically reviewed on June 28, 2018

How we reviewed this article:

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HISTORY

Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.

Current Version

Jun 29, 2018

Written By

Scott Frothingham

Edited By

Frank Crooks

Jun 28, 2018

Medically Reviewed By

Timothy J. Legg, PhD, PsyD

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Medically reviewed by Timothy J. Legg, PhD, PsyD — By Scott Frothingham — Updated on June 29, 2018

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What to Know About People with Borderline Personality Disorder

Borderline personality disorder is often misunderstood. It’s time to change that.

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Borderline personality disorder — sometimes known as emotionally unstable personality disorder — is a personality disorder which affects how you think and feel about yourself and others.

People with borderline personality disorder (BPD) often have a strong fear of abandonment, struggle to maintain healthy relationships, have very intense emotions, act impulsively, and may even experience paranoia and dissociation.

LEARN ABOUT PERSONALITY DISORDERS

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It can be a scary illness to live with, which is why it’s so important that people with BPD are surrounded by people who can understand and support them. But it’s also an incredibly stigmatized illness.

Due to an abundant of misconceptions around it, many people with the disorder feel scared to speak out about living with it.

But we want to change that.

That’s why I reached out and asked people with BPD to tell us what they want other people to know about living with the condition. Here are seven of their powerful responses.

1. ‘We’re scared you’re going to leave, even when things are good. And we hate it too.’

One of the biggest symptoms of BPD is fear of abandonment and this can occur even when things in the relationship seem to be going well.

There’s this pervasive fear that people will leave us, or that we aren’t good enough for that person — and even if it seems irrational to others, it can feel very real to the person who’s struggling.

Someone with BPD would do anything to stop that from happening, which is why they may come across as being “clingy” or “needy.” Though it can be difficult to empathize with, remember that it stems from a place of fear, which can be incredibly hard to live with.

2. ‘It feels like going through life with third-degree emotional burns; everything is hot and painful to touch.’

This person says it exactly right — people with BPD have very intense emotions that can last from a few hours to even a few days, and can change very quickly.

For example, we can go from feeling very happy to suddenly feeling very low and sad. Sometimes having BPD is like walking on eggshells around yourself — we never know which way our mood is going to go, and sometimes it’s hard to control.

Even if we seem “overly-sensitive,” remember that it’s not always within our control.

3. ‘Everything is felt more intensely: good, bad, or otherwise. Our reaction to such feelings may seem out of proportion, but it’s appropriate in our minds.’

Having BPD can be very intense, as though we’re vacillating between extremes. This can be exhausting for both us and for the people around us.

But it’s important to remember that everything the person with BPD is thinking is more than appropriate in their mind at that time. So please don’t tell us we’re being silly or make us feel as though our feelings aren’t valid.

It may take them time to reflect on our thoughts — but in the moment things can feel scary as hell. This means not judging and giving space and time where it’s warranted.

4. ‘I don’t have multiple personalities.’

Due to it being a personality disorder, BPD is often confused with someone having dissociative identity disorder, where people develop multiple personalities.

But this isn’t the case at all. People with BPD don’t have more than one personality. BPD is a personality disorder in which you have difficulties with how you think and feel about yourself and other people, and are having problems in your life as a result of this.

That doesn’t mean that dissociative identity disorder should be stigmatized, either, but it certainly shouldn’t be confused with another disorder.

5. ‘We aren’t dangerous or manipulative… [we] just need a little bit of extra love.’

There’s still a huge stigma surrounding BPD. Many people still believe that those living with it can be manipulative or dangerous due to their symptoms.

While this can be the case in a very small minority of people, most people with BPD are just struggling with their sense of self and their relationships.

It’s important to note that we’re not dangerous people. In fact, people with mental illness are more likely to harm themselves than they are others.

6. ‘It’s exhausting and frustrating. And it’s really hard to find quality, affordable treatment.’

Many people with BPD are untreated, but not because they’re unwilling. It’s because this mental illness isn’t treated like many others.

For one, BPD isn’t treated with medication. It can only be treated with therapy, such as dialectical behavioral therapy (DBT) and cognitive behavioral therapy (CBT). There are no drugs known to be effective for treating BPD (though sometimes medications are used off-label to relieve symptoms).

It’s also true that due to stigma, some clinicians assume people with BPD will be difficult patients, and as such, it can be difficult to find effective treatment.

Many people with BPD can benefit from intensive DBT programs, but these aren’t the easiest to access. Which is to say, if someone with BPD isn’t “getting better,” don’t be quick to blame them — getting help is hard enough on its own.

7. ‘We aren’t unlovable and we love big.’

People with BPD have a lot of love to give, so much that it can be overwhelming.

Relationships can feel like a whirlwind at times, because when someone with BPD — especially those grappling with chronic feelings of emptiness or loneliness — makes a real connection, the rush can be just as intense as any other emotion they experience.

This can make being in a relationship with someone with BPD difficult, but it also means that this is a person that has so much love to offer. They just want to know that their feelings are returned, and may need a little more reassurance to ensure that the relationship is still fulfilling for you both.

If you’re in a relationship or have a loved one with BPD, it’s important to do your research into the condition, and be wary of the stereotypes you may come across

Chances are, if you read something about borderline personality disorder that you wouldn’t want said about you, a person with BPD won’t benefit from having that assumed about them, either.

Working to gain a compassionate understanding of what they’re going through, and how you can help both your loved one and yourself cope, can make or break a relationship.

If you feel like you need some extra support, open up to someone about how you’re feeling — bonus points if it’s a therapist or clinician! — so they can offer you some support and tips on how to improve your own mental well-being.

Remember, the best support for your loved one comes from taking the best possibltiies.

Etiology          In 1889 Pierre Janet, a French psychiatrist, wrote that “certain happenings would leave indelible and distressing memories – memories to which the sufferer was continually returning and by which he was tormented by day and by night.”  (Van der Kolk, 1989) Janet understood over 100 years ago what lay at the very core of dissociation.  Dissociation is defined as a disturbance or alteration in the normally integrative functions of identity, memory, or consciousness.  Freud felt that dissociation was a process of defense which would remove threatening or overwhelming thoughts from a person’s awareness.          This same idea is supported by today’s professionals.  Dissociation is seen as a coping mechanism and develops when normal coping mechanisms are depleted or over-taxed.  In this weakened state the individual withdraws consciousness, or dissociates from the event, while the brain then encodes the event in a different fashion so that the intense shock can be split off and thereby not completely experienced by the individual.          The most extreme level of dissociation is called Multiple Personality Disorder, or MPD.  Multiple Personality Disorder is described as chronic dissociative posttraumatic stress psychopathology (Braun, 1990).  It is the result of trauma which is far greater than normal stress and surpasses the individual’s ability to cope.  In these cases the individual is so traumatized that the young developing mind fragments, or splits off, into different selves.  The psyche creates a separate consciousness, or personality, in which it absorbs the overwhelming trauma and stores the information.  Often there are several of these other personalities.  Each of the personalities then responds to the traumatic information in a different way.  With the information about the trauma split up, the child is then better able to cope with it.  It is the same idea as sharing a problem with friends.  Once the burden is shared, it becomes easier to bear.          MPD begins in childhood, between the ages of two and eight.  Because the very nature of children’s dependence upon adults renders these incapable of “fight or flight” they will instead flee inward, thereby abandoning the sense of involvement or responsibility for the situation.  Otherwise, the feelings of guilt and terror would be overwhelming.  Without this coping mechanism, the child might perish under the pressure, either through suicide or psychotic break.          Childhood physical or sexual abuse is commonly found in the history of someone with MPD.  It has been found that 97-98% of MPD’s have experienced child abuse in some form – physical, sexual, or psychological mistreatment and neglect.  (Talbott, 1988).          Approximately two percent of MPD’s report no incidence of child abuse, but have experienced a trauma often perceived as life-threatening, such as near drowning or witnessing the violent death of another person.  (Steele, 1989). The traumas could be a single event, such as a case of rape, although the chronic dissociation seen in MPPD patients is, in most cases, the result of repeated severe or inhuman abuse, rather than an isolated experience (Steele, 1989).          The child is usually from an environment where not only has trauma occurred, but also where the necessary protection to prevent the trauma re-occurring, or the nurturing to enable the child to resolve the trauma is nonexistent.          Though the disorder begins in childhood it may remain undiagnosed for many years.  Not all individuals with MPS are as obvious as Hollywood would have us believe.  Sometimes the switching, or changing to other personalities, is very subtle and can only be detected by those who know the person very well.  Because of amnestic barriers the individual may be unaware of the presence of other personalities.  It may only come to the person’s attention after others have remarked about unusual behavior.  Often people with MPD will find articles among their personal belongings that seem to belong to someone else.  This may lead them to think they are going crazy.          The person with MPD may feel that something is terribly wrong, but have no idea about the multiplicity.  This is a condition which can be hidden for long periods of time and only show itself during stressful situations, such as problems with work or relationships.          Females represent 75 – 90% of reported cases.  This is most likely due to the different manner in which men and women respond to emotional trauma.  Women tend to act out in harmful ways against themselves and find their way into treatment after self-mutilation or suicide attempts.  Self-mutilation includes such behavior as cutting superficially without suicide intent, burning the skin with a cigarette, and banging the head against a wall.  Men, on the other hand, have been found more likely to respond to psychic paid by committing violent crimes against others and ending up in the criminal justice system.  (Talbott, 1988) FIGURE 2 The 3-P model of multiple personality disorder (Braun & Saches, 1985) SDL = state dependent learning.  Note.  From Treatment of Multiple Personality Disorder (p.6) by B.G. Braun (Ed.) 1986, Washington, DC: American Psychiatric Press.  Copyright 1986 by American Psychiatric Press.  Printed by permission. Etiological Models          Kluft offers the following etiological model.  He suggests that these four factors must be present in order for an individual to develop MPD:   Factor 1:   The individual possesses a predisposition for dissociation, seen by a high degree of hypnotizability.   Factor 11:   Normally adaptive capacities are overwhelmed by traumatic events, such as severe child abuse,  so that the organism dissociates as a defense mechanism.   Factor III:   The unique combination of psychological substrates occurring in each individual provides the building materials for specific alternate personality formations.  These shaping influences include self=object constancy, cognitive structures of separateness, developmental lines, and normal dissociative phenomena.   Factor IV:   An absence of nurturing, soothing, and restorative experiences which might enable the child to recover from the trauma.  Also, the failure of significant others to protect the child from further trauma.  The trauma is repeated over and over again.  (Steele, 1989) Braun and Sachs suggest the 3-P model as an explanation of the development of MPD.  It is a similar model to Kluft’s in etiological framework.  (See Figure 1)  This model consists of predisposition, precipitation, and perpetuation: Predisposition – The biopsychological capacity to disassociate and the child’s exposure to an environment in which server abuse was meted out unpredictably by parents and other caregivers repeatedly. Precipitation – An overwhelmingly traumatic event that indicates the first use of dissociation as an escape or coping mechanism. Perpetuation – The continuing abusive phenomena link subsequent dissociative episodes with a common affective theme, eventually resulting in separate memories for each.  Over time, the patient begins to experience discrete life histories for each set of memories.  (Braun, 1990) Kluft’s and Braun’s model are similar.  The difference is in Kluft’s specific mention of the absence of a nurturing environment where the child might have the opportunity to heal.  This is implied in Braun’s “Perpetuation”. Essentially, the literature all points toward a common theme in the etiological background of patients with MPD.  This is an individual with a predisposition to dissociate, who grows up in a highly abusive environment where there is no opportunity for respite or escape, and the abuse is ongoing.  Braun reports that an estimated prevalence of MPD in the United States is 0.1% (Braun, 1990).  MPD has also been found to span generations (Kluft, 1991b).

https://www.nurseslearning.com/courses/nrp/NRP-1618/Section%203/index.htm#:~:text=Multiple%20Personality%20Disorder%20is%20described,the%20individual's%20ability%20to%20cope.

[Asylum: the Huge Psychiatric Hospital in the 19th century U.S]

[Article in Japanese]

Haruki Kazano 1

Affiliations expand

• PMID: 23234200

Abstract

The large-scale state psychiatric hospitals, referred to as "asylums," were built in the USA in the 19th century and generally have a bad reputation in Japan as institutions with an unpleasant environment for the patients. Asylums were not built for institutionalizing mental patients. The original meaning of the word asylum is a "retreat" or "sanctuary," and these institutions were originally built to act as sanctuaries for the protection of mental patients. The field of psychiatric medicine in western countries in the 19th century began to embrace the concept of "moral treatment" for mental patients, including no restraint of the patients and treating them in a more open environment. With this background, asylums were built according to the efforts of social activist Dorothea Dix with financial assistance from the Quakers. The psychiatrist Dr. Thomas Kirkbride had a large influence on asylum architecture, and believed that the hospital building and environment as well as location have healing effects on the patients, which he called the "therapeutic landscape". Kirkbridelater proposed an architectural plan that became the basis for subsequent mental hospital architecture, and many asylums were built according to this plan. As the architecture was considered part of the treatment, many leading architects and landscape architects at the time became involved in building asylums. In the later half of the 19th century, over 150 asylums were built across the USA. However, moral treatment fell out of favor toward the end of the 19th century, and the concept of therapeutic landscape was also neglected. The hospitals had many uncured patients, and caregivers became pessimistic about the efficacy of the treatments. Abuse and neglect of the patients were also common. The environment at the asylums deteriorated, which created the image of asylums that, we hold today. Many asylums have been demolished or abandoned. These early attempts at asylum failed due to insufficient treatment methods. However, the concept of the therapeutic landscape that comprehensively sees the architecture of the hospital building and landscape of the property as part of the treatment as well as the architectural beauty of asylum buildings may deserve reevaluation.

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So all of that is how the brain per the folds of it. Jace jace or dann howell is the one writing this. Its just kind of. That each of those things is the shape of a brain and how folds work if they were ilgrate worms cus they look the same. No offense to snakes. Its just kind of. So metaphorical but literally the same thing. Its just the action forms which means. He has multiple eprsonalities from  beinga bused eating a stink bug playing with toys and aging weird as a seven year treated as an adult. Whic means hes native american pochuatnus who was never once photographed as herself as historical photos we have. Its just kind of. Weird. Um. so yeah. Hes 7 forever, and hit 11 again because hed probably age regress as this person. And that changes his physical, but hes being age grown right row. Which is usually but not always a negative turned positive eventually of changing someoens age wrong. Mental age is real. It should always be treated as that its just never looks like that because it looks like steryptical age gap relationships often villanized as torture of it which is a disorder pedofilai but not tortured is just age agps. Kids can always kidn of consent as long as you dont take away the predetor or pedo. Lets takl about it.

Cureus. 2022 Feb; 14(2): e22131.

Published online 2022 Feb 11. doi: 10.7759/cureus.22131

PMCID: PMC8918204

PMID: 35308663

Voluntary Age Regression Entering “Headspace” in a Child With Post-traumatic Stress Disorder

Monitoring Editor: Alexander Muacevic and John R Adler

Alexander J O'Donovan,1 Hector Cardiel Sam,2 and Jasmin G Lagman2

Author information Article notes Copyright and License information PMC Disclaimer

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Abstract

In patients with post-traumatic stress disorder (PTSD), the use of coping mechanisms seems to correlate with higher levels of resiliency; however, in the age of the internet, patients may find it easier to discover new unhealthy skills that can hinder their treatment and further progress their symptoms. This report describes the case of a 12-year-old female with PTSD who was admitted for suicidal ideation and who presented with age regression that was voluntary in nature, characterized by reverting to the age of a six-year-old girl while her boyfriend took on a parental role for her. These behaviors were learned through her use of social media. This case demonstrates the use of maladaptive behaviors to cope with their trauma and the need for parental supervision on the use of the internet and social media by the younger population. 

Keywords: effects of social media, adolescent, coping mechanisms, age regression, posttraumatic stress disorder

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Introduction

The Diagnostic and Statistical Manual of Mental Disorders 5 (DSM-5) states that post-traumatic stress disorder (PTSD) has the essential feature of the "development of characteristic symptoms following the exposure to one or more traumatic events." In some individuals, the symptoms may reflect more fear-based and emotional behavior symptoms, while others may have anhedonic or dysphoric mood states predominate [1]. In people with PTSD, high levels of resilience are associated with a person's use of coping skills. According to Thompson et al., coping can be described as using cognitive strategies to alter one's environment or avoid internal stressors. These coping skills can be active or avoidant, choosing whether to internally modify the perceptions of the trauma or ignore it, respectively [2]. Some researchers argue that addressing and modifying these avoidant behaviors may reduce symptoms of PTSD [3,4]. However, further investigation is needed on the topic. This case report serves as an example of a unique avoidant coping mechanism in response to a childhood trauma.

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Case presentation

A 12-year-old female child with past psychiatric diagnoses of PTSD, anxiety, and depression presented to the inpatient facility with worsening depression, anxiety, and suicidal ideation. She had been having suicidal ideation for the past two months and eventually attempted suicide by overdosing on hydroxyzine due to family and school stressors. She endorsed depressed mood, poor energy, difficulty concentrating, irritability, changes in sleep (both increased and decreased depending on the day), poor appetite, anhedonia, increased guilt, and suicidal thoughts. The patient reported a history of sexual trauma within the past several months that she was uncomfortable disclosing to her treatment team, and Children and Youth Services were investigating the allegations at the time of admission. 

The patient shared with the team that when she was feeling stressed, anxious, or was experiencing flashbacks, she entered "headspace." She defined "headspace" as a mental space where she would become a "little," voluntarily regressing to the mental state of that of a young child around the age of six. She accomplished this by performing activities that someone at the desired age would perform, such as coloring, playing with clay, or cuddling. Her then 14-year-old boyfriend would also participate in these acts, playing the "daddy" figure who consoled and cared for the patient while she was in "headspace" and calling her names like "little princess," "little kitty," and "daddy's little girl." He would also purchase items like pacifiers and baby bottles for her to use while in this state. 

The patient's mother believed that there was a sexual nature to this voluntary age regression and believed that both the patient and her boyfriend were partaking in daddy dom/little girl (DDLG) role-play. According to the mother's research, DDLG is a form of sexual role play in which each member in the relationship takes on one of two roles: the "daddy dom," who acts as a caretaker, and the "little girl," who regresses in age to act of a child-like girl. The patient became defensive when this accusation was made and maintained that it was strictly non-sexual. She believed that it was therapeutic to return to an age before she experienced any of her traumatic events, and she said that she learned about it from her friends who also perform the activity, from social media apps such as Instagram, and from websites she discovered through Google searches on the topic. She was not ashamed of this coping mechanism, portraying her status as a "little" on the artwork she created during group sessions and talking about it openly amongst her peers with excitement and pride.

The patient was previously diagnosed with anxiety and depressive disorders and was seeing a therapist for the past few months. There were no significant medical issues. Family history was significant for a history of anxiety in a second-degree relative. There were no issues with developmental history, and social history was significant for parental separation within the past two years. Her parents do not get along well. The patient's mother's boyfriend moved in with them a few months prior to this admission. She was attending regular classes, but her grades were deteriorating. 

During this hospital stay, she reported classic symptoms of trauma, which included nightmares as well as flashbacks of witnessing domestic violence in the home, with an inability to intervene. She wanted all avoidance with the alleged perpetrator, and she had persistent symptoms of insomnia, irritability, and difficulty concentrating since experiencing her trauma. Once she became more comfortable with the treatment team, she provided additional details on the previously reported sexual trauma. Individual therapy and family meetings focused on the unstable home environment as well as her fear of being in contact again with the alleged perpetrator. As she was already on fluoxetine, this medication was continued, and the dose was increased to address the worsening of depression and anxiety. Individual and family therapy focused on safety planning and addressing her fears, leading to improvement in her anxiety. Extensive psychoeducation was done regarding the danger of excessive reliance on social media and the use of unreliable therapeutic interventions by non-experts or websites and how it can negatively impact her treatment. This was initially faced with resistance. Resolution of her age regressive behaviors was noted after family meetings where she was able to express her fears and concerns to her mother. They expressed understanding that her preferred coping mechanism was non-evidenced based, after which there were clinical improvements. Trauma-focused cognitive-behavioral therapy (TF-CBT) was recommended in the outpatient to address the ongoing symptoms of PTSD, with which she agreed to participate. 

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Discussion

As exhibited by her known traumatic event, nightmares, preferred avoidance of the alleged perpetrator, decreased concentration, and increased irritability, we believe our patient fits the ICD-10 criteria for PTSD [5]. Current treatments for PTSD consist of pharmacotherapy, psychotherapy, or a combination of both. For pharmacotherapy, selective serotonin reuptake inhibitors (SSRIs) are generally regarded as the first-line therapy, specifically for fluoxetine or paroxetine. The serotonin/norepinephrine reuptake inhibitor venlafaxine is also seen as a common recommendation for first-line pharmacotherapy [6]. A systematic review conducted by Martin et al. in 2021 found that one-third of guidelines recommended psychotherapy over pharmacotherapy, and all chose cognitive-behavioral therapy (CBT) as first-line [6]. Our patient was maintained on fluoxetine while inpatient and recommended for trauma-focused CBT outpatient as part of her therapy per these guidelines.

There is limited literature on DDLG and voluntary age regression. The available information on the web comes mostly from personal accounts of people or groups engaging in these behaviors. However, the idea of regression as a response to a traumatic experience is certainly not new. Studies have described adolescents developing late-onset secondary enuresis following a traumatic experience, such as a car accident [7,8]. Other common regressive behaviors seen by hospitalized psychiatric patients include crying, engaging in baby talk, sucking on objects or body parts, assuming the fetal position, and needing a comforting object, like a stuffed animal, among others [9]. These regressive behaviors seen in hospital patients are usually involuntary and are a result of various psychiatric disorders such as major depressive disorder, catatonia, psychotic disorders, delirium, borderline personality disorder, or substance abuse disorders. While studies addressing the prevalence of regression in hospitalized patients are lacking, the number of patients referred to as "agitated" while inpatient can also help infer that number of regressing patients may be misclassified [9]. 

The difference between our patient's presentation of regression and the regression as described in the existing literature is that the former is voluntary. Where regression may be a clinical feature of many medical, psychiatric, or neurologic disorders, age regression, when done voluntarily, may hinder treatment. Negative coping skills learned from the internet or friends, with no therapeutic studies done in the past, can be detrimental to patients. In the case of this patient, she found herself in an abusive situation with her partner because of this dominant role he had over her decisions. She avoided talking about different stressors in her life with people other than her partner, including her mother, with whom the patient still claimed she felt close. Instead, she repressed her traumas and stressors and underwent voluntary age regression by entering a "headspace." This act of pretending to be a different age and ignoring the trauma and stressors in her life hindered her ability to develop positive coping mechanisms and benefit from her initial management of her PTSD. 

PTSD is becoming a growing problem for children, adolescents, and college-aged individuals [10,11]. Kilpatrick et al. found in 2003 that the six-month prevalence was estimated to be 6.3% in female adolescents and 3.7% in male adolescents [12]. As numbers of children and adolescents with PTSD increase over time, new variations of coping mechanisms may manifest, both positive and negative. A study found that all avoidant coping strategies were negatively correlated with the concept of resilience and positively correlated with further progression of PTSD symptoms [2]. As seen in this case, subordination and submissiveness are also associated with increased anxiety and depression [13].

As clinicians, it is important to acknowledge some of the coping mechanisms patients will adopt to manage their trauma. As the growing influence of the internet and subgroups that can be found on it expands, people will find ways to use it to cope with their stressors. Studies have found that those with problematic internet use are more likely to have maladaptive coping strategies and use immature, neurotic, and autistic fantasy defenses [14]. Understanding some of the ways the internet can influence patients to try new and possibly negative coping mechanisms is important for clinicians to be aware of to better understand their patients and provide appropriate and timely intervention. 

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Conclusions

PTSD is becoming more frequently diagnosed in children and adolescents in recent years. Coincidentally increasing in recent years has been society's use of the internet. As this happens, patients living with PTSD may gain access to coping mechanisms that could be unhealthy in nature and lead to further harm. Voluntary age regression and submissiveness are techniques that can easily be discovered through the internet and social media and are two of those starting to be used by adolescents as a method of self-management for their stressors. Since no therapeutic studies have been done on these techniques, they can potentially worsen PTSD symptoms and negatively impact a patient's treatment and recovery. Healthcare professionals, parents, and other personnel working with children and adolescents may benefit from being aware of these negative techniques used by our younger population so that they may help guide them to seek more evidence-based practices.

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Notes

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

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Human Ethics

Consent was obtained or waived by all participants in this study

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References

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8918204/

WHAT IS ABDL? THE TRUTH ABOUT ADULT BABIES & DIAPER LOVERS

• by jezebelnight

• May 6, 2021

Recently I wrote about a kink known as DDLG. I explained what DDLG is, how it is practised, addressed some common misconceptions about DDLG, as well as showcasing some of the cutest DDLG products on the store.

Today I’m talking about a different community within the kink scene, one that is just as misunderstood as DDLG, if not more, and one that has its very own set of confusing letters to describe it. 

I’m talking about ABDL.

What is ABDL? The Truth About Adult Babies & Diaper Lovers

What is ABDL?

 

ABDL is an acronym that stands for ‘adult baby’ and ‘diaper lover’ and describes a community of people in the wider kink community. 

If you are into ABDL, you can be one of these things, or you can be both; just like how somebody who is in the BDSM community may be into bondage but not sadism, somebody in the ABDL community may be a diaper lover but not an adult baby, and vice versa.

Let’s break down exactly what it means to be an adult baby or a diaper lover…

 

What is an adult baby?

 

An adult baby is an adult who chooses to return mentally to a childlike state, either for fun or eroticism. In scientific terms, this is called ‘paraphilic infantilism.’

It describes a kind of ‘age-play,’ which is a specific form of fantasy role play where a partner embodies a person of a different age than their actual chronological age. 

According to Ignacio Rivera in The Ultimate Guide to Kink (which is a fantastic book btw), age-play can be progressive (where someone pretends to be older than they actually are) or regressive (where they pretend to be younger than they actually are).

Somebody who is an adult baby is therefore engaging in regressive age-play (not to be confused with age regression, which is a defence mechanism related to trauma and has nothing to do with kink). 

Something that may surprise you is that adult babies are often not role-playing as babies at all! 

Adult babies do not necessarily regress all the way back to the state of being a baby, with many ‘adult babies’ identifying as toddlers, children and even teenagers! Not only that, but the age of an adult baby is not static and can fluctuate – while an adult baby may be a bratty schoolgirl one day, she may turn into a helpless newborn the next, a pouty teenager the next, and so on.

 

ABDL accessories, costumes and behaviours

 

Someone who is an adult baby might like to use various props when they are age-playing. For age-players, the right costumes and accessories can really help them get in (and stay in) their ‘little’ headspace.

ABDL products can include pacifiers, colouring books, bottles of milk, cribs, sippy cups, and of course, diapers. 

ABDL costumes can include babygros, dungarees, school uniforms, frilly ankle socks, childish dresses and more.

ABDL behaviours could include anything from throwing a tantrum at bedtime to sucking on a pacifier, playing with dolls, crawling on the floor, becoming non-verbal (if role-playing as a baby), sucking on a lollipop, adopting a more childlike voice and lots, lots more.

Every adult baby is completely unique and different, just like every adult is completely unique and different!

You can visit our Lolita collection to see our range of DDLG and ABDL products – currently we don’t have many ABDL products on the store yet (pacifiers, diapers etc.) but I plan to add some in the near future so watch this space!

 

Our Kawaii ABDL Dungarees!

Partners of adult babies

 

The partner of an adult baby is often referred to as a ‘caregiver’ and is usually (but not always) a dominant figure in the relationship.

During play, they may take on the role of a stern school teacher, a nurturing mommy figure, a dominant daddy or a cruel babysitter. 

However, sometimes this power dynamic can shift and the adult baby can often find themselves being the one in control – think a manipulative schoolgirl blackmailing her perverted teacher into giving her good grades or a toddler tormenting his babysitter until she cries.

Again, these roles are always subject to change, and as long as both parties are fully on-board, the sky really is the limit when it comes to ABDL role-play and the characters that can be created within it.

 

What’s in a name?

 

Now that we have a rough idea of what it means to be an adult baby, it is important to know that the actual term ‘adult baby’ is not favoured by everyone in the ABDL community. 

There are a couple of reasons for this.

First, someone who embodies the mindset of a twelve year old when they are playing may not feel as though the term ‘adult baby’ describes them accurately, and find it frustrating when members outside of the kink community automatically assume that they enjoy acting like a baby. 

An age-player named Emma, known as @ABDLgirl on Twitter, told Bold Pleasures that ‘I don’t really like the term. I know I’m “ABDLgirl” and stuff but it’s easy to use; it’s a term that most people know nowadays, but I think it’s too narrowed down. I actually prefer the term “age-play” because you can have so many facets, and the term “ABDL” – adult baby, diaper lover – I don’t consider myself to be an adult baby – more like an adult little girl.’ 

Even some people that do enjoy role playing as a baby may not like the term ‘adult baby’ due to the negative connotations it carries (more on that later), and feel as though they may be stigmatised if they use it.

This is why many people in the ABDL scene prefer to use the catch-all term ‘age-play,’ feeling as though it is a much more accurate description of what they do, as well as being less confusing for people outside the scene to understand.

Another popular term used for somebody who age-plays as someone younger than they actually are is ‘little.’ ‘Little’ is a great way to describe a regressive age-player because being ‘little’ could be anything from a baby upwards, and it doesn’t hold as much stigma as ‘adult baby.’

 

Okay, okay. Enough about ‘adult babies,’ or ‘age-players,’ or ‘littles’ or whatever. What is a diaper lover?!

 

Well, I’m glad you asked!

A ‘diaper lover’ is somebody with a fetish for diapers (or nappies, to my UK readers). This means that they find diapers (and the act of wearing them) a turn-on.

They may become aroused by the soft material of the diaper against their skin, or they might enjoy soiling the diaper and being spanked and scolded (or nurtured and changed) by their caregiver. 

An adult diaper lover may not have any desire to act like a baby, and age-play may not be a part of their kink at all. 

For example, a submissive man with a humiliation kink may enjoy being ‘forced’ to wear a diaper in public by his Domme, or a coprophilia fetishist may enjoy the more ‘dirty’ aspect of soiling his diaper.

There are many reasons why adult diaper lovers enjoy wearing diapers, but for now it is just important to know that a diaper lover is not necessarily also an adult baby (although they could be).

 

Adult babies may or may not also be diaper lovers

 

ABDL – what it’s NOT

 

In ‘The Ultimate Guide to Kink,’ Mollena Williams says that ‘your fantasies do not have to be politically correct. They do not have to be socially acceptable.’ 

Just like DDLG, ABDL is a hugely misunderstood kink, even within the kink community!

Anything involving age-play is a huge taboo in society, with critics of ABDL and DDLG claiming that adults are just not meant to act like children, especially in a sexualised environment. 

To the uninitiated, ABDL is just a cover for paedophilia and child sex abuse, with paedophiles acting out their disgusting fantasies in a role play scenario rather than with actual children.

Let me be very clear – paraphilic infantilism is absolutely not related to paedophilia or any form of child sexual abuse. 

Adult babies are not attracted to children, nor do they want to form relationships with children. 

They want to take on the role OF a child, rather than be WITH a child. 

A 1993 series of case studies by sexologists Ray Blanchard and Kurt Freund corroborates this, noting that while paedophiles were attracted to children due to the desire for a child sexual partner, infantalists (age-players) imagined themselves as children and adopted the objects of childhood or infancy to increase the power difference between their partners and themselves.

Sexologist Gloria Brame goes one step further than this, stating that ‘infantilists who recognise and accept their sexuality – and its possible roots in infantile trauma – tend to be acutely protective over real children.’

As far as the ‘Big’ (partner of an adult baby goes), their attraction to their ‘little’ is also a far cry from being attracted to a child. While they may enjoy caring for their little in a pretend, role-play environment, they are attracted to ADULT bodies, not children’s.

There is also no evidence to say that adult babies are mentally ill, or suffer in any way as a result of their preferences. 

Age-play is really just that – play and fantasy between consenting adults who do not condone coercion, violence and sexual abuse any more than the average person does.

 

Why do people enjoy ABDL?

 

Many of you may be wondering, why do people enjoy ABDL? What’s in it for them?

Well, why do people like any of the things they like?

People like things because ultimately, those things make them happy.

For example, I like watching horror movies because doing so makes me happy.

If I wanted to, I could come up with a myriad of reasons why horror movies make me happy – I get excited by the jump scares, I’m interested in the paranormal, I find it funny when the people I’m watching with get scared, I like being able to yell at the TV when the protagonist ventures down into the dark and spooky basement…the list goes on.

I have no way of knowing whether the things that I like about horror movies are the same things that other horror movie buffs enjoy, and honestly, it doesn’t really matter.

Horror movie fans enjoy horror movies because horror movies entertain them, which in turn makes them happy.

That’s all there is to it.

It’s the same with ABDL.

Adult babies and diaper lovers do the things they do because they derive a sense of happiness from them.

 

What’s so fun about an adult baby fetish?

 

Some people like to age-play because they like to return to a time of simplicity, where they didn’t have any responsibilities and they could just play all day without having to worry about work, bills, deadlines, and all the other fun things that come with being an adult.

Some people enjoy being in a vulnerable state and having a caregiver nurture them, making them feel protected and loved.

Some people may have had an abusive or neglectful childhood and find that age-play gives them the innocence and sense of warmth that they were never able to receive as a child.

For some, they may work in a very high-powered job where they are the one calling the shots all day. Age-play allows them to surrender that control and relax, entering an almost meditative state of being.

Ignacio Rivera says that for them, age-play takes them to ‘wonderfully enlightening places as well as deep, dark ones.’

They go on to say that age-play can also ‘sexualise a forbidden inter-generational relationship or explore a wide variety of D/s power dynamics.’ 

 

Many adult babies enjoy pacifiers

And what about diaper lovers?

 

For diaper lovers, their feelings may be slightly different, but ultimately lead to the same sense of fulfilment and happiness.

Maybe they enjoy the thrill of having a secret, of wearing something underneath their clothes that nobody else knows about. This is exciting to them, which in turn, is a turn-on.

Maybe they enjoy being an adult in baby diapers because adults should not wear diapers. It is taboo. It is forbidden. It is this sense of the taboo that draws them towards diapers.

Perhaps they feel embarrassed, degraded or humiliated when they choose to wear diapers – or, even better – when a dominant female ‘forces’ them to wear a diaper as a punishment or humiliation tool (consensually of course).

Some adults in baby diapers like soiling their nappy – sometimes even in public – because it makes them feel dirty and disgusting, and it is this feeling that they enjoy.

They may enjoy having their diaper changed by a ‘caregiver’ or female dominant. This may evoke feelings of shame and humiliation (something they enjoy), or it may make them feel loved and cared for.

Whatever the specific reason why somebody enjoys age-play or wearing diapers, the underlying motives are the same – doing these things makes them feel good. It makes them feel happy.

After all, what is any human being motivated by, if not a quest for happiness?

 

There are many reasons why someone may enjoy wearing diapers

ABDL and aftercare

 

Aftercare is very important in the BDSM community and it describes the practice of the Dom taking physical and mental care of the sub after a ‘scene.’ 

In this case, the sub would usually be the adult baby or the diaper lover, but as I explained earlier, it doesn’t always have to be this way.

Aftercare gently pulls the sub back into the ‘real world,’ and is particularly helpful if the sub has undergone a gruelling BDSM scene with corporal punishment, humiliation, degradation etc. After all, BDSM can be really physically and emotionally taxing.

Aftercare is also especially important when it comes to age-play because age-play can put both the ‘top’ and the ‘bottom’ (the dominant and the submissive) in a very intense and vulnerable headspace.

During this time, you should check in with your partner that they are okay, that their physical and emotional needs have been met, and you can ask them how the scene was for them and if there was anything that they didn’t like. For some, checking in once is enough, but others might need to be checked on every hour, or a few days after the scene to make sure that they are still okay.

Aftercare looks different for everybody, but making a cup of tea, having a cuddle and having a laugh and a joke together are all great ways of getting the natural dynamic of your relationship back and coming back down to earth.

 

What is ABDL? The Truth About Adult Babies & Diaper Lovers | Final Thoughts

I hope that I’ve managed to clear up some of the confusion about ABDL, age-play, diaper fetishes and more in this post! ABDL is not my personal idea of a good time, but I absolutely abhor kink shaming and it is a sword that I am prepared to die on (okay, maybe not literally but u know what I mean).

Just because you don’t like something or don’t understand something, it doesn’t make it ‘wrong’ or ‘weird.’

I don’t understand why my boyfriend is so obsessed with FIFA, but hey, he probably doesn’t get my true crime obsession either.

Every single person on this planet likes something that other people may consider weird (or even taboo), and if you take away one thing from this article, let it be this – adult babies and diaper lovers are not weird, f****d up or strange. They are not paedophiles, they are not abusers and they do not have something wrong with them.

People in the ABDL community just like what they like, and that’s all there is to it.

Jezebel xoxo

 

Its jst not all fetishes are sexy. Some are platonic obsesive hobbies. https://jezebelbynight.com/what-is-abdl-adult-babies-diaper-lovers/ judging by her face she will develop arhcins if you do that feitsh to much thats probably the case and theirs a reason i say this liike that. Its chance theory. Its just. Unfortunately each age would be a separate identity. And this article is by jason. So he probably time travel to hang out with hismelf like he says its about tehctonic plates in teh earth its how time works. We proved that. Just apply it to earth quakes and sodium equatses phoslpihoe or e = mc2

Early case studies of individuals exhibiting these behaviors were reported in the 1960s and 1970s. These cases included a 29-year-old male who wore diapers and rubber pants regularly and would masturbate and urinate while wearing them (Tuchman & Lachman, 1964), that of a 20-year-old male who wore diapers and would orgasm when he defecated in them (Malitz, 1966), a 17-year-old male who wore diapers (also often accompanied with erections and masturbation), ate baby food, and drank from a baby bottle (Dinello, 1967), and a 20-year-old male with brain damage who wore diapers and women’s wigs and drank out of a baby bottle, behaviors that led to erection and ejaculation (Bethell, 1974). More recently, several cases have been reported on men wearing, urinating, and defecating in diapers, but also using baby toys, sucking on pacifiers, crawling, using bottles, sleeping with blankets, and expressing desires to become a baby, be treated like a baby, and have their diapers changed (Croarkin, Nam, & Waldrep, 2004; Evcimen & Gratz, 2006; Kise & Nguyen, 2011; Lehne & Money, 2003; Pandita-Gunawardena, 1990; Pate & Gabbard, 2003; Sanders, 1997). The sexual behaviors associated with some diaper-wearers do not always coincide with those who act like babies; for example, Caldwell (2008) reported a case in which the subject urinated, defecated, and masturbated while wearing diapers, but did not engage in any other baby-like behaviors. Evcimen and Gratz (2006) described a patient who wished to be a baby and wore diapers, but denied using the diapers for any sexual gratification. Although there are not many cases of diaper fetishism/adult babies in the literature, a simple search on the internet suggests that there is a large number of adults who role-play as babies and use items related to infancy, such as diapers. Members of this online community generally refer to themselves as adult babies (AB), those who enjoy role-playing as infants, and diaper lovers (DL), those who wear diapers voluntarily but may not engage in other baby-like behaviors. As a group, they are referred to as Adult Baby/Diaper Lovers (ABDL).

Given the lack of literature on the ABDL community and the tendency to pathologize such behaviors (Moser, 2005), the purpose of this study was to provide descriptive information on these individuals. Exploratory analyses were also planned to gain a greater understanding of individuals who belong to the ABDL online community. Because fetish behaviors could function to reduce anxiety or negative mood states (Coleman, 2000), one research question focused on the degree to which ABDL behavior was associated with negative mood states. Research has suggested a person’s relationship with or attachment to a parent may relate to ABDL interests (Caldwell, 2008; Dinello, 1967; Malitz, 1966). Per this body of research, greater levels of insecure attachment would typically be associated with greater levels of ABDL behaviors. Thus, a second research question focused on the degree to which attachment to a parent was associated with ABDL behavior. Based on clinical experiences from one of the authors, a third research question focused on discerning two possible subgroups within the ABDL community: persons focused on role play behavior and persons who were primarily interested in sexual arousal in their ABDL behavior.

Method

Participants

The final sample included 1,795 male and 139 female participants. Participants were recruited from community ABDL websites (e.g., diaperspace.com, bedwettingabdl.com, adisc.org). To preserve anonymity, no personally identifying information, including IP addresses, was collected. From the initial 2,849 participants, 69 were deleted because they were younger than 18 years old, 6 were deleted because consent was lacking, 353 were eliminated because only the age and consent form were completed, and 404 were eliminated because no data beyond demographic information were provided. Another 83 were eliminated because they identified as intersex, transsexual, or transgendered individuals. We elected to focus on the males and females only for the current article. A response rate of 73 % was estimated by dividing the approximate number of participants who completed the survey (2,849 minus 353 and 404) by the 2,849 participants who started the survey.

The resulting participants ranged in age from 18 years to over 80 years (M = 30.7, SD = 12.36). Table 1 shows demographic information by sex. The majority of the participants were males (93 %) who were attracted to females only. Female participants tended to be sexually attracted to both males and females (43 %) or males only (34 %). Regarding household structure, the majority of participants grew up in a two-parent household (male–female) with one brother or sister. Thirteen percent of the male participants (n = 224) and 17 % of the female participants (n = 23) reported no siblings. The highest level of formal education varied considerably (see Table 1), but most participants had received at least a high school diploma. Income levels ranged from less than $25,000 per year to over $100,000 per year, but the largest group of participants among males and females reported making less than $25,000. Participants with a job (n = 1,484) had spent about 6 years at their current position (M = 6.24, SD = 7.24).

Table 1 Demographic information by sex

Full size table

Procedure

With the approval of website administrators, an advertisement with a link to the survey on SurveyMonkey was posted on each participating website. The advertisement requested that viewers complete a survey to help a therapist at the University of Minnesota gain more accurate information about the ABDL community. The survey was available for 8 weeks.

Participants were informed that the survey was completely anonymous and confidential, that there was no compensation to completing the survey, and that there was no penalty for stopping at any time during the survey. Participants consented to take part in the study by clicking on the link to the survey, reading a consent form, affirming that they understood the consent form (a yes/no query), and verifying that they were 18 years or older. Early in the survey, another item querying participants’ age served as a manipulation check to confirm that the participants were indeed over 18. The survey began with a demographic questionnaire and then moved into specific questions relating to the participants’ ABDL interests, desires, behaviors, and fantasies as well as questions regarding how these practices have affected their lives and relationships. Next, participants were asked about their relationships with their mother and father. Finally, participants completed two additional questionnaires: adult attachment (Wei, Russell, Mallinckrodt, & Vogel, 2007) and a shortened version of the Profile of Mood States (Shacham, 1983). At the close of the survey, participants were thanked for their participation.

Measures

Participants were asked to give their age, gender identity, sexual orientation, household structure (i.e., number and gender of parents growing up), and number of siblings. They were also asked their education level, current job, length of time at their current job, and income.

Frequency of ABDL Behaviors

Participants were asked at what age they became interested in ABDL, at what age they started practicing, and how long they had been practicing. They also indicated if they were currently practicing ABDL. Participants were asked how often they wore diapers in a typical day (i.e., hours), week (i.e., days), and month (i.e., days). Using a typical month time frame, participants were also asked how often they practiced ABDL sexual behaviors

While that is physoclogiral its just age and identity and self are three things that make up a human mind so its probably mentally, religiously and physically as this theory were about to prove

Religion = 6

Age = 7 through alphabet system

S = 1 e = 2

Solve for e

= 45 over 192 + 10 = 1 heart over twelve equals debauchery - 10 = 11.92 = 1 + 2 = 3.14567

https://link.springer.com/article/10.1007/s10508-013-0241-7

How to Record Cassette Tapes

By legodano in CircuitsAudio130,176148

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Introduction: How to Record Cassette Tapes

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Cassettes are an old medium for recording things such as music, but hi-fi enthusiasts like myself still record to them to the sound quality and the fun experience that recording them is. In this Instructable I will show how to record music on to a cassette tape with use of a hi-fi receiver and a tape deck. This will also go over tape bias for different types of cassettes as well as Dolby noise reduction and receiver setup.

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Step 1: Getting the Right Tape

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When recoding music, it's best to record on blank tapes. You can find tapes at places like hardware stores or thrift stores, or buy them in bulk online. I bought the two chrome tapes still wrapped in plastic at my local hardware store and the other at a thrift store.
There are four types of cassette tapes. They are:

Type I (shown): Standard ferric oxide magnetic tapes, called Type I, normal bias, or ferric tapes, etc.
Type II (shown): made of chromium dioxide formula, called Type II, high bias, or chrome tapes. These record better highs, and sound generally better than Type I tapes.
Type III: FeCr formulation. These tapes combined the formulas for Type I and Type II as an experiment to make the ultimate tape, combining the bass response of the I and the highs of the II, these were unpopular and are generally rare.
Type IV: Known as metal tapes, they used a direct metal formulation instead of oxide particles. By far the best sound quality, but are generally more expensive than Type I or II.

How a deck tells the tape apart for playing is the notches on the top (shown above). Chrome tapes have extra notches next to the write-protect tabs.

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Step 2: Getting the Tools and Materials

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Tools required for this method:
1. A tape deck

2. A receiver (for playback) with speakers

3. A device to record from

4. RCA audio cables

5. Power, a strip cord is recommend

Note: Some receivers, such as mine, have outlets in the back for AC power. These can be used to power your audio equipment, as shown above. I have my tape deck and turntable plugged in, and everything runs fine.

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Step 3: Setup

Make sure power is being sent to everything you have set up, the deck, receiver, etc. Then, take the RCA cables and connect the "out" or "playback" ports on the tape deck to one of the "in" ports on the receiver. This will make it so the deck send sound through the speakers connected to the receiver. You can test this setup with something like a CD player or iPod with the proper cables. Then, plug your preferred device into the "in" or "record" ports on the tape deck. Some receiver have an "out" jack for recording with tapes decks, and if yours has this then connect this to the tape deck using RCA cables. Make sure speakers are plugged in to the designated ports on your receiver.

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Step 4: Tape Bias

Tape bias changes how the sound is sent to the tape. With incorrect bias, a tape will sound muddy and poor. Shown is a diagram for tape bias for Onkyo tape decks, like the one I use to record. Depending on your deck, try and find a guide for bias if your deck has a knob for it.
For Type I tapes, bias does not need to be changed whatsoever and shouldn't be.
For Type II tapes, these are called "high bias" and bias should be adjusted so.
For Type IV, bias should also be set to "high bias" and adjusted from there.

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Step 5: Noise Reduction

A crucial point in recording is the use of Dolby Noise Reduction (NR). Noise reduction reduces background noise, the hiss of the magnetic tape itself. Most commercial recordings use Dolby type B noise reduction. Newer decks will have a switch for NR with a choice between type B and type C. Older decks that just say "Dolby Noise Reduction" will have type B only. Rarely, some high-end decks will have an option for Dolby S NR which is by far the best, but as said incredibly rare. For recording, I personally recommend Dolby C, as it sounds the best to my ears. Set your desired noise reduction before recording your tape.

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Step 6: Recording

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Now to recording. When you have a tape to record, make sure first that the write-protect tabs are present or the holes are covered, as this allows you to record to a tape. Shown above are three cassettes, a Type I with the tabs pushed in, a Type II with the tabs present, and a Type I with the holes taped over.
First, turn on your tape deck and receiver and make what you intend to record is plugged in to the deck. If you have the option, such as shown, activate the tape deck channel over the desired channel you want to record. I have mine set to the analog ports for the CD section, which is where I have my iPod plugged in.

Then, press the record button with a tape in and play your music. Do not press play on your deck. Adjust the volume on your tape deck for the best level of sound if able.
When everything is set, noise reduction, bias, and volume, reset your music and pause it. Press the record button if the record light isn't on, and press the play button to start the tape. Wait a second or two for the tape to get on the magnetic portion, and play your music. The music is now being recorded. Do not press anything else on your tape or receiver, and listen to what you're recording until it reaches the end of the tape. When the end of side one is reached, flip the tape and record more on side two.

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Step 7: Playback

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With your receiver still set to your tape deck, flip your cassette and play it from the beginning. Note the lack of a record light (shown above). You should hear your music coming from the tape!

You can play your cassette in a hi-fi setup with a tape deck, or listen to it on the go with a player like a Walkman (shown). On mobile players, however, there typically isn't automatic tape detection, so try to find a switch to set it to the correct tape type (shown). If everything was recorded correctly, your tape is finished.
Print some small album art to put on the sleeve, write down the track list, put a label on both sides of your tape, push in the write-protect tabs and your cassette is complete!
Shown above is a cassette I recorded off of two vinyl record, cassettes can record iPods, records, CD's and more. The sound quality of them, in my experience, is quite good compared to CD's and records and being able to play them on the go without risking skipping and damage is very convenient.

 Thats actually how you build an atomic bomb or drown a particle acceslor. An orgy is sex with kids or multiple people who are kid like or youthful. Its just has eating if its older. As what an orgy is which is not group sex. But has that. He plans tonight to spread arhcins on teh one day he can be getting them drunk on pepsi, after fasting for two days, and doing hypnosis amstubrating together through the spirit world, while listening to emo music to spread the fountain of eternal youth and they also have to buy a puppy shaped plushie named jace or something very emo as a toy to be jace and it will make them all have it XD, um xd is a theory haha is also a theory. So yeah it apparently can be spread under certain conditions. So yes. This is imortally. It just means you have to be infested with bugs at some point it as parasyest every parasye and go through tooth decay that fungus is proof of as evolutaitnry theory as to the history of mushrooms. T he friends are jc howard, morgan h offman, snow the salt queen, jason jason, danny, yes boy, joseph smith the historical figure, abram icons daughter and symbol. This is a weird timeline were living in. but hey atleast we have immortal kids who age backwards like merlin myth now. This is kind of cool mtuations are back thats theoritzed and hypothosiesd to end global warming. Put them all back in highschool.

A case study thats so totally magick or something by muse. About adam snowflake. Youtube braincake adamsnowflakarhvice diongoespew jeneifers body and thatguyintherainbows with his firends yandrefreak, dusthallow, and um tj kirk. And puzzling =kazzo and repzion.

[mpd]

[asylums]

[jesus]

[energy]

[paticle accesltors]

[teha tom bomb]

[how to burn a cassette tape]

Shape theories

so yeah it changes face and age. as forever young but i imagine its rather painful cus it cripples you.