User:TamerGorashi/Sickle cell trait

Normally, a person inherits two copies of the [[gene]] that produces [[beta-globin]], a [[protein]] needed to produce normal hemoglobin ([[hemoglobin A]], genotype AA). '''According to ''StatPearls'', sickle cell trait occurs when an individual inherits “one normal hemoglobin gene and one sickle hemoglobin gene,” resulting in the AS genotype.'''

Normally, a person inherits two copies of the [[gene]] that produces [[beta-globin]], a [[protein]] needed to produce normal hemoglobin ([[hemoglobin A]], genotype AA). '''According to ''StatPearls'', sickle cell trait occurs when an individual inherits “one normal hemoglobin gene and one sickle hemoglobin gene,” resulting in the AS genotype.'''

The sickle cell trait can be used to demonstrate the concepts of co-dominance and incomplete dominance. An individual with the sickle cell trait shows incomplete dominance when the shape of the red blood cell is considered. '''''StatPearls'' explains that sickle cell trait is a carrier condition in which “both normal hemoglobin and hemoglobin S are present in red blood cells,” supporting a co-dominant pattern of expression'''. This is because the sickling happens only at low oxygen concentrations. With regards to the actual concentration of hemoglobin in the circulating cells, the alleles demonstrate co-dominance as both 'normal' and mutant forms co-exist in the bloodstream. Thus it is an ambiguous condition showing both incomplete dominance and co-dominance.^{[''[[Wikipedia:Citation needed|citation needed]]'']}

The sickle cell trait can be used to demonstrate the concepts of co-dominance and incomplete dominance. An individual with the sickle cell trait shows incomplete dominance when the shape of the red blood cell is considered. This is because the sickling happens only at low oxygen concentrations. With regards to the actual concentration of hemoglobin in the circulating cells, the alleles demonstrate co-dominance as both 'normal' and mutant forms co-exist in the bloodstream. Thus it is an ambiguous condition showing both incomplete dominance and co-dominance.

Unlike the sickle-cell trait, [[sickle-cell disease]] is passed on in a recessive manner. Sickle cell anemia affects about 72,000 people in the United States. Most Americans who have sickle cell anemia are of African descent. The disease also affects Americans from the [[Caribbean]], [[Central America]], and parts of [[South America]], [[Turkey]], [[Greece]], [[Italy]], the [[Middle East]] and East India.

Unlike the sickle-cell trait, [[sickle-cell disease]] is passed on in a recessive manner. Sickle cell anemia affects about 72,000 people in the United States. Most Americans who have sickle cell anemia are of African descent. The disease also affects Americans from the [[Caribbean]], [[Central America]], and parts of [[South America]], [[Turkey]], [[Greece]], [[Italy]], the [[Middle East]] and East India.

There also have been studies that show changes in the globin genes. There have been noted changes in the beta-globin sequence, to what is known as the sickle hemoglobin.^{[''[[Wikipedia:Citation needed|citation needed]]'']}

There also have been studies that show changes in the globin genes. There have been noted changes in the beta-globin sequence, to what is known as the sickle hemoglobin.^{[''[[Wikipedia:Citation needed|citation needed]]'']}

The significance of the sickle-cell trait is that it does not show any symptoms, nor does it cause any major difference in blood cell count. '''The trait confers about 30% protection against malaria ^{[''[[Wikipedia:Please} clarify|clarification needed]]''] and its occurrence appears to have risen tremendously in [[Africa]], [[India]] and the Middle East.''' Some findings also show the reduction of the sickle-cell trait in those who retain much more fetal hemoglobin than usual in adulthood. Fetal hemoglobin likely plays a role in the prevention of sickling. Elevated fetal hemoglobin levels have been observed in populations where sickle-cell disease is prevalent.  

The significance of the sickle-cell trait is that it does not show any symptoms, nor does it cause any major difference in blood cell count. '''There are about 30% of people who carry the sickle cell trait that are naturally protected against malaria. With malaria and sickle cell trait occurrences appearing to have risen in [[Africa]], [[India]] and the Middle East.'''{{Cite web |title=How the sickle cell trait protects against malaria |url=https://www.datelinehealthafrica.org/how-the-sickle-cell-trait-protects-against-malaria-a-simplified-scientific-explanation |access-date=2026-04-20 |website=www.datelinehealthafrica.org |language=en-US}} Some findings also show the reduction of the sickle-cell trait in those who retain much more fetal hemoglobin than usual in adulthood. Fetal hemoglobin likely plays a role in the prevention of sickling. Elevated fetal hemoglobin levels have been observed in populations where sickle-cell disease is prevalent.  

Whole genome sequence analysis has identified a single origin of the sickle trait, with one haplotype ancestral to all sickle-cell variants. This haplotype is thought to have originated in the Sahara during the [[Holocene Wet Phase]] around 7,300 years ago. Sickle cell variants descended from this ancestral haplotype comprise five haplotypes named after toponyms or ethnolinguistic groups (the Arabian/Indian, [[Benin]], [[Cameroon]], [[Central African Republic]]/[[Bantu languages|Bantu]], and [[Senegal]] variants), and another designation earmarked for atypical sickle-cell haplotypes. Their clinical importance is because some are associated with higher HbF levels (e.g., Senegal and Saudi-Asian variants tend to have milder disease).

Whole genome sequence analysis has identified a single origin of the sickle trait, with one haplotype ancestral to all sickle-cell variants. This haplotype is thought to have originated in the Sahara during the [[Holocene Wet Phase]] around 7,300 years ago. Sickle cell variants descended from this ancestral haplotype comprise five haplotypes named after toponyms or ethnolinguistic groups (the Arabian/Indian, [[Benin]], [[Cameroon]], [[Central African Republic]]/[[Bantu languages|Bantu]], and [[Senegal]] variants), and another designation earmarked for atypical sickle-cell haplotypes. Their clinical importance is because some are associated with higher HbF levels (e.g., Senegal and Saudi-Asian variants tend to have milder disease).

In some cases, athletes with sickle cell trait do not achieve the same level of performance as elite athletes with normal hemoglobin (AA). Athletes with sickle cell trait and their instructors must be aware of the dangers of the condition during anaerobic exertion especially in hot and dehydrated conditions. In rare cases, exercise-induced dehydration or exhaustion may cause healthy red blood cells to turn sickle-shaped, which can cause death during sporting activities.

In some cases, athletes with sickle cell trait do not achieve the same level of performance as elite athletes with normal hemoglobin (AA). Athletes with sickle cell trait and their instructors must be aware of the dangers of the condition during anaerobic exertion especially in hot and dehydrated conditions. In rare cases, exercise-induced dehydration or exhaustion may cause healthy red blood cells to turn sickle-shaped, which can cause death during sporting activities.

'''A peer-reviewed study by Buchanan et al. (2020) found an “increased risk of exertional death in NCAA athletes” with sickle cell trait, particularly before the introduction of screening policies'''. In recent years the [[NCAA]] has partnered with the [[American College of Sports Medicine|ACSM]] and issued a joint statement, warning athletes about both the prevalence and the potential risk factors of sickle cell trait. The NCAA has also recently encouraged athletes to become aware of their sickle cell trait status, as the trait itself does not typically result in symptoms under normal conditions but can become dangerous during extreme physical activity similar to the daily training that athletes undergo.<sup>[''[[Wikipedia:Citation needed|citation needed]]''] '''Buchanan et al. (2020) also found that exertional deaths decreased after screening, noting a “reduction in sudden deaths following the implementation of mandatory sickle cell trait screening and preventive policies.”'''

'''A peer-reviewed study found increased risk of exertional death in NCAA athletes with sickle cell trait, particularly before the introduction of screening policies'''. '''Sickle cell trait is the cause of death in military training and sports around the world. The study found that a legislative waiver was enacted in 2010 for athletes to complete screening or sign waivers to decline them.'''{{Cite journal |last=Harmon |first=Kimberly G |last2=Drezner |first2=Jonathan A |last3=Klossner |first3=David |last4=Asif |first4=Irfan M |date=2012-04 |title=Sickle cell trait associated with a RR of death of 37 times in national collegiate athletic association football athletes: a database with 2 million athlete-years as the denominator |url=https://bjsm.bmj.com/lookup/doi/10.1136/bjsports-2011-090896 |journal=British Journal of Sports Medicine |language=en |volume=46 |issue=5 |pages=325–330 |doi=10.1136/bjsports-2011-090896 |issn=0306-3674}} '''On that note,''' in recent years the [[NCAA]] has partnered with the [[American College of Sports Medicine|ACSM]] and issued a joint statement, warning athletes about both the prevalence and the potential risk factors of sickle cell trait. The NCAA has also recently encouraged athletes to become aware of their sickle cell trait status, as the trait itself does not typically result in symptoms under normal conditions but can become dangerous during extreme physical activity similar to the daily training that athletes undergo.<ref>{{Cite web |last=Writer |first=Staff |date=2025-06-11 |title=Sickle Cell Test Requirements for NCAA Athletes: What You Need to Know |url=https://www.consumersearch.com/health-beauty/sickle-cell-test-requirements-ncaa-athletes-need-know |access-date=2026-04-20 |website=ConsumerSearch.com |language=en-US}}

Normal [[hemoglobin]] (and hemoglobin S in the presence of oxygen) contains a [[Erythrocyte deformability|deformability]] characteristic that allows [[erythrocytes]] to essentially squeeze their way into smaller vessels, including those involved in [[microcirculation]] to the [[capillaries]] within muscle tissue as well as blood supply embedded within organ tissues. When hemoglobin S is deprived of oxygen, it can polymerize, which is what is proposed to cause the "sickled" cells. The sickled erythrocytes present a decreased deformability when compared to normal erythrocytes, leading to distress in circulation into the smaller vessels involved in microcirculation, particularly, in this case, the capillaries embedded in muscle tissue.^{[''[[Wikipedia:Citation needed|citation needed]]'']}

Normal [[hemoglobin]] (and hemoglobin S in the presence of oxygen) contains a [[Erythrocyte deformability|deformability]] characteristic that allows [[erythrocytes]] to essentially squeeze their way into smaller vessels, including those involved in [[microcirculation]] to the [[capillaries]] within muscle tissue as well as blood supply embedded within organ tissues. When hemoglobin S is deprived of oxygen, it can polymerize, which is what is proposed to cause the "sickled" cells. The sickled erythrocytes present a decreased deformability when compared to normal erythrocytes, leading to distress in circulation into the smaller vessels involved in microcirculation, particularly, in this case, the capillaries embedded in muscle tissue.^{[''[[Wikipedia:Citation needed|citation needed]]'']}

Naik, Rakhi P, and Carlton Haywood Jr. “Sickle cell trait diagnosis: clinical and social implications.” ''Hematology. American Society of Hematology. Education Program'' vol. 2015,1 (2015): 160-7. doi:10.1182/asheducation-2015.1.160

Naik, Rakhi P, and Carlton Haywood Jr. “Sickle cell trait diagnosis: clinical and social implications.” ''Hematology. American Society of Hematology. Education Program'' vol. 2015,1 (2015): 160-7. doi:10.1182/asheducation-2015.1.160

* This article is from PubMed which is a highly reliable and is a authoritative database for biomedical and life sciences literature and maintained by the U.S. National Library of Medicine

* This article is from PubMed which is a highly reliable and is an authoritative database for biomedical and life sciences literature and maintained by the U.S. National Library of Medicine

Buchanan, Benjamin K., ''et al.'' “Sudden Death Associated with Sickle Cell Trait Before and After Mandatory Screening.” ''Sports Health'', vol. 12, no. 3, May–June 2020, pp. 241–245

Buchanan, Benjamin K., ''et al.'' “Sudden Death Associated with Sickle Cell Trait Before and After Mandatory Screening.” ''Sports Health'', vol. 12, no. 3, May–June 2020, pp. 241–245

* This article is reliable because its a a peer-reviewed study showing incidence of exertional death in NCAA athletes before and after SCT screening policies.

* This article is reliable because it's a peer-reviewed study showing incidence of exertional death in NCAA athletes before and after SCT screening policies.

Brousseau, David C., et al. ''Sickle Cell Trait''. '''StatPearls''', StatPearls Publishing, National Center for Biotechnology Information, 2024,

Brousseau, David C., et al. ''Sickle Cell Trait''. '''StatPearls''', StatPearls Publishing, National Center for Biotechnology Information, 2024,