Abraham Lincoln Marfan syndrome
According to medical scholars, Marfan syndrome is a health condition instigated by inherited genetic defect tissues with the autosomal dominant mode of transmission. The heritable genetic defect is separated from the gene FBN1 present on chromosome 15, coding the fibrillin. The anomalies in the protein fibrillin cause a myriad of distinct clinical defects where the problems affecting cardiac, ocular, and musculoskeletal prevail. Of all the clinical defects of Marfan syndrome, aortic root dilatation, and dissection are the most severe as, through history, they have been anticipated as the causative factors in early patient demise. The gene occurring in the protein fibrillin gene inflicts pleiotropic aspects, which influences the massive range of phenotypic features immuted from a single gene mutation (Boritt & Borit, 1983). This paper explores the Abraham Lincoln Marfan syndrome by reflecting on the proposed historical explanations for variations in findings. It demonstrates the application of evidence-based resources in the research study to comprehend and assess MFS.
The history of Abraham Lincoln linked to MFS
Abraham Lincoln was the sixteenth president of the United States and was known for his dedication to leadership. The president was born in Laure County, Kentucky, in the early 19th century. Most scholars of the post-modern century were interested in researching Lincoln as he was not only a crucial figure in the politics of the United States, and his impact on making America great, but also his physical features amazed medics. Drawing from the historical aspect of MFS, Dr. A. M. Gordon was the first person to describe the condition in 1962, nearly 30 years after the assassination and death of Lincoln. The argument of Dr. Gordon was based on the physical assessment, where he compared the physical features of Lincoln t that of his mother, Nancy, and linked it to the symptoms of MFS. Irrespective of the clear evidence shown on the Marfan syndrome symptoms in Lincoln, he was never known to have a heart murmur, nor did he present loose joints. Additionally, during his autopsy, the condition of aortic anomalies was not mentioned as he did not show ocular defects, which are usually associated with Marfan syndrome.
Propose Historical Explanations for Variations in Findings
MFS was first described in the early 20th century by pediatrician Antoine-Bernard Marfan. In 1962, approximately five decades after the discovery of MFS, Dr. A. M. Gordon suggested the possibility that Lincoln had Marfan syndrome. Dr. Gordon, a Cincinnati physician, based his argument on the physical appearance of Lincoln and corresponded his physical features to his mother’s tall and skinny appearance. In 1964, Harold Schwartz published an article about his 7-year-old Patient, who was diagnosed with MFS. The Individual’s ancestry was traced back to Mordecai Lincoln II, the great-grandfather of Lincoln (Markets & Begkas, 2022). This inflicted an intense debate on the possibility of Lincoln inheriting MFS from his lineage.
The diagnostics of Lincoln having MFS were supported by Gordon and Schwartz, basing their argument on the reviewed skeletal structure of Lincoln. Similarly, Dr. J. Willard Montgomery opposed the likelihood of Lincoln having MFS by mentioning his physical strength and athletic prowess of Lincoln. Using physical observational reference, Schwartz contributed to the debate in 1972 by using an anecdote from the photograph of Lincoln where the foot of the crossed leg late president appeared blurry in the picture. Noah Brooks, a newspaper person, proposed that the throbbing of the arteries might have caused the motion in Lincoln’s leg. Irrespective of the clear evidence of MFS on Lincoln, the late president was not known to have loose joints, nor did he have a heart murmur. After his death, the autopsy did not mention aortic abnormalities and was not anticipated to present ocular abnormalities, a disorder associated with MFS.
The studies on American presidents by Dr. John Sotos, a cardiologist, suggested a new argument on Lincoln’s genetics concerning the presently revealed marfanoid syndromes. Sotos believed that the marfanoid syndromes mutations reflect the alteration of the growth factor-beta receptor. One prime marfanoid syndrome is manifold endocrine neoplasia type 2B (MEN2B)- a cancerous disorder featured by elements including; pheochromocytoma, mucosal neuromas, marfanoid habitus, and medullary thyroid cancer. Sotos applies information on Lincoln’s and Nancy Hanks’s physical features to make his assessment and arguments. According to the article, “Lincoln’s mother suffered from the marfanoid disorder and that the MEN2B disorder may have been passed to Lincoln through genes”.
Consequently, DNA testing of the president was suggested in the late 1990s but was disputed after scientists denoted the presence of the MFS gene. Various objects and elements from the night of his assassination would have been used in the testing, including the pistol ball, locks of hair, and more. However, the committee of geneticists, forensic scientists, and lawyers established in 1991 ruled that testing Lincoln’s DNA was because not only the technicality involved, given the various mutations found in the Marfan families, but also because this would infringe the privacy of Lincoln. This means we cannot conclusively say Lincoln had MFS genes because of a lack of DNA testing.


Identification of Pathophysiology of Marfan syndrome
The concept of Marfan syndrome diagnosis is ensured on the characteristics manifestations, specifically on aortic root dilatation or mitral valve prolapse, the separation and ectopia lentis, dural ectasia, and skeletal findings. When an individual has MFS, it means that they have some defect in the gene encoding the fibrillin structure, called fibrillin-1 or gene FBN1. The MFS gene is often inherited through a modification pattern known as “autosomal dominant.” The concept of “autosomal dominant” relates to similar disorders among the genders. Studies by Asano, et al., (2022) shows that Individuals with MFS can pass the genes to their offsprings regardless of the children’s gender. 50% genes of a parent having MFS are passed to the children. From this percentage, in 25% of the incidences, the occurrence of new gene defects may be instigated.
Marfan syndrome is reflected as a “variable expression” inherited gene disorder as its symptoms differ among people with it. For some people, the condition expresses at birth, while in others, it reflects in teenage or even adulthood. Various medical scholars in the post-modern world studied different molecules present in the extracellular matrix, as this would assist in elucidating the effects and causes of MFS. The studied molecules encompass but are not limited to collagen, fibrillin, elastin, and hyaluronic acid. The studies showed that mutation occurs in the fibrillin gene, mainly affecting cysteine deposits within the microfibril (Asano, et al., 2022). This means that the gene mutations are anticipated as the causal agents of abnormal protein compacted because of the modification of bonding between cysteine deposits, which then causes the production of defective microfibril.
The defective microfibril is a critical component in the formation of Cystic medial necrosis (CMN), a condition that affects the large arteries, particularly the aorta. The CMN is branded by the deposition of mucopolysaccharides in the tunica media of the arteries vessels, leading to the loss or reduction of muscle and elastic fibers through the degeneration of the cystic media aortic. The degeneration of Cystic medial aortic occurs when mucopolysaccharide cysts deposits and raptures vascular smooth muscle cells. The proposition release of variable degradation, cytokines, MMP, and prostaglandin derivatives weaken the aortic walls. When these factors integrate with the condensed collagen reduces the structural stability of the aorta, leading to aneurysmal dilatation. The alteration or reduction of fibrillin-1 structures can instigate the release of TGF-beta that is confiscated. This means that MFS is fostered by vascular remodeling induced by the integrated effect of MMP-2, expanded TGT-beta, structural microfibril modifications, and MMP-9 overexpression.
Clinical Manifestation of MFS
Clinical manifestation of the disease requires various health assessments, including a physical examination of an individual. Because of the variable expressivity of MFS, it anticipated that there is no single sign that’s pathognomic. The clinical manifestation is founded on typical abnormalities, such as a tall and thin build and kyphoscoliosis, which are linked to physical assessment (Reilly, 2000). The cardiac, skeletal, and ocular systems are typically professed upon Marfan syndrome diagnostic criteria. Nonetheless, the disorder sometimes affects other tissues, encompassing the respiratory tract, skin, skeletal muscle, fascia, and fats. In the prospective study by Verma (2017), the physical assessment elements having maximum diagnostic results were denoted: Pectus carinatum, Craniofacial characteristics, Severe hindfoot valgus, and Thumb and wrist signs. Taking a physical assessment of Abraham Lincoln’s Marfan syndrome based on the four described features, the diagnostics showed that Lincoln had MFS.
Although the anticipated condition of Marfan syndrome Lincoln was diagnosed after assassination and death, there are various clinical manifestations different scholars and medics have drawn from Lincoln’s physical assessment and anticipations by people who knew him or his lineage. From the description of different people, Lincon was a six feet four inches tall man with long legs and limbs. His shoulders are described as “slightly slumped.” From this description, Lincoln had excessive growth of long bones, one prime physic used in depicting the President (Boritt & Borit, 1983). Lincoln’s height and ungainly shows that he had limited joint mobility. Nonetheless, since he had eyesight issues as he suffered from double vision instigated by intermittent vertical hypertropia, most scholars argued that MFS probably caused the intermittent vertical hypertropia.
From the clinical manifestations depicted, the president probably suffered from MFS, a condition resulting in uneven overgrowth or symptoms such as double vision, long bones, and limited joint mobility, which indicates the possibility of having MFS. The medical diagnosis is grounded on the reports of Lincoln as an ungainly individual with long legs, limbs, and a big head. Besides, it said that Lincoln had aortic inflation (AI) condition, which reflects in the pathophysiology of MFS. The pathophysiology of MFS is a multifaced process instigated by vasculogenesis and fostered by various structural microfibril alterations, encompassing MMP-2 and MMP-9 overexpression and excess TGF-beta. The clinical manifestation and claims tend to verify the possibility of Lincoln having MFS.
Healthcare Planning, Intervention, and Evaluation for Marfan syndrome
Marfan syndrome is a spectrum of disorders also referred to as a connective-tissue disease caused by inheritable genetic defects in an autosomal dominant manner resulting from gene FBN1 mutation. Various studies show that MFS incidences range from 1 in 5000 to 2-3 in 10,000 persons. The MFS disorder is critical when left untreated or not well managed in a patient as it inflicts a considerable shift in cognitive abilities and emotions (Jimenez, et al., 2022). Patients, families, and friends of the patients and healthcare providers need to have early identification of the MFS problem through the various symptoms and establish a suitable treatment plan encompassing psychotherapy, medications, a healthy lifestyle, and a regular healthcare schedule (Mbwasi, et al., 2022).










Nursing Care Plan
Nursing Diagnostics Goals Interventions Evaluation

i. Heart problems.




ii. Ineffective airway clearance Longterm To eliminate patient symptoms, expand functional status of the patient, and foster the patient’s quality of life Intergration of medication, and good lifestyle habits; entailing seating a low-fat, consistent physical exercise, good sleep, no smoking, and low-salt diet. After six months, thepatient had reduced cardiac workload, and improve cardiac function with effective fluid retention

To reducce airflow limitation, Avert and treat minor medical complications. Intergration of medication, and good lifestyle habits; entailing seating a low-fat, consistent physical exercise, good sleep, no smoking, and low-salt diet. -After three months the Patient had clear, open airways.
-The clear open airways indicated by normal breath sounds, normal rate and depth of respirations.

Shorterm To improve cardiac output for patients with MFS due to weak heart associated with conditions such as aortic aneurysm Influencing the use of mechanical circulatory support The patient effectivwly demostrates adequate cardiac output as evidenced b significant signs within the acceptable limits
Shorterm To improve ineffective airway clearance due to chest wall and spinal deformities, emphysema, pneumothorax, sleep apnea, and potentially increased incidence of asthma, bronchiectasis, and interstitial lung disease. -Assess the rate, rhyth, depth of respiration,muscle and chest movement
-Change position frequently
Ten hours after the application of theinterventions, the patient is able to maintain patent airway with breathing sounds clearing respiratory system within 12 to 15 breath per minute.


Asano, K., Cantalupo, A., Sedes, L., & Ramirez, F. (2022). Pathophysiology and Therapeutics of Thoracic Aortic Aneurysm in Marfan Syndrome. Biomolecules, 12(1), 128.
Boritt, G. S., & Borit, A. (1983). Lincoln and the Marfan syndrome: The medical diagnosis of a historical figure. Civil War History, 29(3), 212-229. https://doi.org/10.1353/cwh.1983.0002
Jimenez, Y., Paulsen, C., Turner, E., Iturra, S., Cuevas, O., Lay-son, G., … & Calderon, J. F. (2022). Exome Sequencing Identifies Genetic Variants Associated with Extreme Manifestations of the Cardiovascular Phenotype in Marfan Syndrome. Genes, 13(6), 1027.
Markeas, N. G., & Begkas, D. (2022). What is Abraham Lincoln’s connection to Marfan syndrome?. Acta Orthopaedica Et Traumatologica Hellenica, 73(3).
Mbwasi, R. M., Maugeri, A., Joel, H. N., Sadiq, A., Ahmad, B., & Hamel, B. C. (2022). Early Onset Marfan Syndrome with multivalvular insufficiency: Report from a tertiary hospital in Tanzania, and a review of the recurrent c. 7606G> A p. 0 variant in FBN1. European Journal of Medical Genetics, 104576.
Reilly, P. R. (2000). Abraham Lincoln’s DNA. Cold Spring Harbor, Nueva York, Cold Spring Harbor Laboratory Press.
Verma, A. K. (2017). An unusual presentation of Marfan’s syndrome. Journal of Medical Science And clinical Research, 5(11). https://doi.org/10.18535/jmscr/v5i11.155
Zeigler, S. M., Sloan, B., & Jones, J. A. (2021). Pathophysiology and pathogenesis of Marfan syndrome. Advances in Experimental Medicine and Biology, 185-206. https://doi.org/10.1007/978-3-030-80614-9_8

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