Where is your blood type from?

We have learned a good deal about how common each of the ABO blood types is around the world. The patterns can thus be traced to specific regions, migrations and intermingling of various civilizations in human history.This can be seen with the global frequency patterns of the type B blood allele (shown in the map below). Note that it is highest in Central Asia and lowest among the indigenous peoples of the Americas and Australia. However, there are relatively high frequency pockets in Africa as well. Overall in the world, B is the rarest ABO blood allele. Only 16% of humanity have it.

Distribution of the B type blood allele in native populations of the world

The A blood allele is somewhat more common around the world than B. About 21% of all people share the A allele. The highest frequencies of A are found in small, unrelated populations, especially the Blackfoot Indians of Montana (30-35%), the Australian Aborigines (many groups are 40-53%), and the Lapps, or Saami people, of Northern Scandinavia (50-90%). The A allele apparently was absent among Central and South American Indians.

Distribution of the A type blood allele in native populations of the world

The O blood type (usually resulting from the absence of both A and B alleles) is very common around the world. About 63% of humans share it. Type O is particularly high in frequency among the indigenous populations of Central and South America, where it approaches 100%. It also is relatively high among Australian Aborigines and in Western Europe (especially in populations with Celtic ancestors). The lowest frequency of O is found in Eastern Europe and Central Asia, where B is common.

As we’ll see later, type O is considered the original blood flowing in both Neandertal and Cro-Magnon primates.

Distribution of the O type blood allele in native populations of the world


Blood type fortunes: looks legit!

In Japan (and some other East Asian countries), the ABO blood types are thought to be related to personality. On the one hand, surveys of self-reported blood types and self-reported personality have shown some association. On the other hand, surveys of personality traits have shown no ability to predict blood type.[4] Thus, the evidence of an association is about as persuasive as astrological sign.

If personality ‘differs’, why not other diet differences? Peter D’Adamo prominently proposed an ABO-basedblood type diet.

Blood type and personality in Japan

A belief that blood types influenced personality in Japan arose in the early 20th century, partially as a response to European style “scientific racism“. In Japan, the several blood types are distributed more evenly than they are among Europeans; ascribing personality types to blood types indicated a more adaptable mix of traits in the Japanese race. In the 1930s, the hypothesis was investigated for military use in breeding better soldiers.[5] The blood type beliefs were revived in the 1970s as a form of personality testsimilar to astrology, by Masahiko Nomi, as a sort of pop psychology. According to Nomi,

  • Type O blood is for “warriors”. They are confident, self-determined, optimistic, self-centered, cold, doubtful, and unpredictable.
  • Type A blood is for “farmers”. They are earnest, sensible, reserved, patient, fastidious, stubborn, and tense.
  • Type B blood is for “hunters”. They are passionate, active, creative, strong, irresponsible, unforgiving, and bohemian.
  • Type AB blood is for “humanists”. They are cool, controlled, rational, sociable, critical, indecisive, and irresponsible.[6]

The personalities ascribed to the several blood types carry forth stereotypes that ultimately backdate themselves to the abiding influence of Japanese feudalism. Japan saw itself as a society of samurai (type O) and peasants (type A), the most frequent blood types in Japan; with a smaller number of merchants and artisans (type B) and intellectuals (type AB).[7]

Books promoting these beliefs about blood type sell well in Japan. On the Japanese language Wikipedia, most articles about celebrities contain information about their blood types. Dating websites and social networks in East Asia often include the opportunity to share the user’s blood type. Anime and manga often describe characters by blood type. Employment applications may call on the applicants to indicate their blood type. The belief has spread to neighboring areas including Korea and Taiwan.

Blood types Diet

This is based on improperly correlating the idea that your blood type is linked to your genotype, and that A type blood, for example, is linked to reduced ability to digest meat.The blood type diet is a type of fad diet that claims that your blood type affects how you digest different kinds of food, and thus what you should eat is determined by your blood type.


The diet was founded by Peter D’Adamo (a naturopathicdoctor“) and published under the catchy-titled Eat Right 4 Your Type. It was founded based on the evolutionary theory of blood type. Although the diet ignores factors such as Rhesus negative/positive and other rarer sub-types, D’Adamo claims that 90% of the properties of the blood are due to the ABO groups.


There are four primary blood groups in the ABO system. Types A, B, AB and O. For each group, a different diet is recommended for healthy living. Each is also very scientifically assigned a cool comic book villain nickname.

  • Blood group O: The Hunter; stated to be the earliest human blood group. D’Adamo recommends a higher protein intake for people of this type.
  • Blood group A: The Cultivator; claimed to be a more recent blood type that has evolved since agriculture. As a result, the diet claims group A people should avoid meat and consume vegetables instead.
  • Blood group B: The Nomad; D’Adamo claims that people with group B blood can indeed thrive on dairy products due to it being associated with a healthy and highly evolved immune system.
  • Blood group AB: The Enigma; As a combination of types A and B, it is considered the most recently evolved blood type. As a result Eat Right 4 Your Type suggests a diet part way between that of A and B.

Rh blood group system

From Wikipedia, the free encyclopedia
“Rh-” redirects here. For the Siddharta album, see Rh- (album). For the band, see The RH Factor.

The Rh blood group system (including the Rh factor) is one of thirty-five current human blood group systems. It is the second most important blood group system, after ABO. At present, the Rh blood group system consists of 50 defined blood-group antigens, among which the five antigens D, C, c, E, and e are the most important. The commonly used terms Rh factor, Rh positive and Rh negative refer to the D antigen only. Besides its role in blood transfusion, the Rh blood group system—specifically, the D antigen—is used to determine the risk of hemolytic disease of the newborn (or erythroblastosis fetalis) as prevention is the best approach to the management of this condition.

Rh factor[edit]

An individual either has, or does not have, the “Rh factor” on the surface of their red blood cells. This term strictly refers only to the most immunogenic D antigen of the Rh blood group system, or the Rh− blood group system. The status is usually indicated by Rh positive (Rh+ does have the D antigen) or Rh negative (Rh− does not have the D antigen) suffix to the ABO blood type. However, other antigens of this blood group system are also clinically relevant. These antigens are listed separately (see below: Rh nomenclature). In contrast to the ABO blood group, immunization against Rh can generally only occur through blood transfusion or placental exposure during pregnancy in women.

History of discoveries[edit]

The rhesus blood type named after the rhesus monkey was first discovered in 1937 by Karl Landsteiner and Alexander S. Wiener. The significance of the discovery was not immediately apparent and was only realized in 1940, after subsequent findings by Philip Levine and Rufus Stetson.[1] This serum that led to the discovery was produced by immunizing rabbits with red blood cells from a rhesus macaque. The antigen that induced this immunization was designated by them as Rh factor to indicate that rhesus blood had been used for the production of the serum.[2]

In 1939, Phillip Levine and Rufus Stetson published in a first case report the clinical consequences of non-recognized Rh factor, hemolytic transfusion reaction and hemolytic disease of the newborn in its most severe form.[3] It was recognized that the serum of the reported woman agglutinated with red blood cells of about 80% of the people although the then known blood groups, in particular ABO were matched. No name was given to this agglutinin when described. In 1940, Karl Landsteiner and Alexander S. Wiener made the connection to their earlier discovery, reporting a serum that also reacted with about 85% of different human red blood cells.[4]

Based on the serologic similarities Rh factor was later also used for antigens, and anti-Rh for antibodies, found in humans such as the previously described by Levine and Stetson. Although differences between these two sera were shown already in 1942 and clearly demonstrated in 1963, the already widely used term “Rh” was kept for the clinically described human antibodies which are different from the ones related to the rhesus monkey. This real factor found in rhesus macaque was classified in the Landsteiner-Wiener antigen system (antigen LW, antibody anti-LW) in honor of the discoverers.[5][6] It was recognized that the Rh factor was just one in a system of various antigens. Based on different models of genetic inheritance, two different terminologies were developed; both of them are still in use.

The clinical significance of this highly immunizing D antigen (i.e. Rh factor) was soon realized. Some keystones were to recognize its importance for blood transfusion including reliable diagnostic tests, and hemolytic disease of the newborn including exchange transfusion and very importantly the prevention of it by screening and prophylaxis.

The discovery of fetal cell-free DNA in maternal circulation by Holzgrieve et al. led to the noninvasive genotyping of fetal Rh genes in many countries.

Population data[edit]

The frequency of Rh factor blood types and the RhD neg allele gene differs in various populations.

Population data for the Rh D factor and RhD neg allele[13]
Population Rh(D) Neg Rh(D) Pos Rh(D) Neg alleles
Basque people[14] 21–36% 65% ∼ 60%
other Europeans 16% 84% 40%
African American ∼ 7% 93% ∼ 26%
Native Americans ∼ 1% 99% ∼ 10%
African descent < 1% > 99% 3%
Asian < 1% > 99% 1%


If both of a child’s parents are Rh negative, the child will definitely be Rh negative. Otherwise the child may be Rh positiveor Rh negative, depending on the parents’ specific genotypes.[15]

The D antigen is inherited as one gene (RHD) (on the short arm of the first chromosome, p36.13–p34.3) with various alleles. Though very much simplified, one can think of alleles that are positive or negative for the D antigen. The gene codes for the RhD protein on the red cell membrane. D− individuals who lack a functional RHD gene do not produce the D antigen, and may be immunized by D+ blood.

The epitopes for the next 4 most common Rh antigens, C, c, E and e are expressed on the highly similar RhCE protein that is genetically encoded in the RHCE gene, also found on chromosome 1. It has been shown that the RHD gene arose by duplication of the RHCE gene during primate evolution.[citation needed] Mice have just one RH gene.[16]

The RHAG gene, responsible for encoding Rh-associated glycoprotein (RhAG) is found on chromosome 6a.

The polypeptides produced from the RHD and RHCE genes form a complex on the red blood cell membrane with the Rh-associated glycoprotein.

Blood Group AB Is Associated with Increased Risk for Severe Dengue Disease in Secondary Infections

Why certain individuals progress to severe dengue disease is unknown. In this study, blood groups associated with dengue disease were investigated. ABO phenotypes were identified by use of serum from 399 patients with dengue-virus infection who participated in a cohort study. ABO blood-group frequencies were similar in primary versus secondary dengue-virus infections. However, in secondary infection, individuals with blood group AB were likely to have dengue hemorrhagic fever grade 3 than either grades 1 and 2 combined (corrected P value, <.0001; odds ratio, 0.097 [95% confidence interval, 0.03–0.33]) or dengue fever (corrected P value, <.0001; odds ratio, 0.119 [95% confidence interval, 0.04–0.37]). To our knowledge, this is the first report demonstrating an association between ABO blood group and the severity of dengue disease.

Infection with dengue virus is a serious emerging health threat and has commanded considerable medical and public-health concern worldwide [1]. Today, dengue disease is considered to be, in terms of morbidity and mortality, the most important arthropod-borne human viral disease [1]. Globally, it has been estimated that 50–100 million new dengue-virus infections occur annually. Among these, there are 200,000–500,000 cases of potentially life-threatening dengue hemorrhagic fever (DHF)/dengue-shock syndrome (DSS), characterized by thrombocytopenia and increased vascular permeability [1]. The death rate associated with the more severe form of DHF/DSS (DHF grades 3 [DHF3] or 4 [DHF4]) is ∼5%, mainly in children <15 years of age [1].

The dengue viruses are mosquito-borne viruses of the Flaviviridae family. Four genetically related but distinct serotypes, designated “DENV-1,” “-2,” “-3,” and “-4,” circulate worldwide [1]. Infection with any serotype can be either asymptomatic or lead to 1 of the 4 clinical scenarios of increasing severity: undifferentiated fever, dengue fever (DF), DHF, and DSS [2]. Infection with one serotype leads to lifelong immunity to that serotype but to only partial and temporary immunity to the others; circulation of >1 serotype increases the risk of secondary infections and of DHF and DSS [2].

DF results from the bite of a mosquito carrying infectious dengue virus and is an acute self-limited disease comprising 5–7 days of fever, headache, myalgia, bone/joint pain, and rash, often accompanied by leukopenia. Occasionally variable degrees of thrombocytopenia and cutaneous hemorrhage are observed. Infrequently, DF may be accompanied by unusual bleeding complications that may cause death [1].

The clinical features of DHF are similar to those of DF during the early febrile phase, but, at defervescence, patients develop the pathophysiologic hallmarks of plasma leakage, because of increased vascular permeability and abnormal hemostasis [1]; studies of samples collected during and after the acute disease suggest that immune and inflammatory molecules play a role in increasing the permeability of blood vessels [3]. The risk factors for DHF are complex and poorly understood. Secondary infections, which occur commonly in areas where dengue disease is endemic, have proven to be one of the main risk factors for severe dengue disease [2, 4]; and this has led to the antibodydependent enhancement theory [2]. In addition, other probable risk factors for DHF are the infecting virus’s strain/serotype, the age of the patient, and the genetic background of the patient [2]; however, none of these factors alone accounts for the risk of DHF in patients with dengue-virus infections.

The important role that host genetics plays in determining the susceptibility to infectious pathogens in humans has long been known. Although predisposition to DHF or DSS determined by human leukocyte antigen (HLA) haplotype has been proposed by several researchers, no clear, specific polymorphisms have been unequivocally described for severe forms of dengue disease [5]. The ABO blood-group system is part of the innate immune system [6], and it has been shown that individuals with different ABO blood groups differ in their susceptibility or resistance to viral and bacterial infections and diseases [6, 7]. A relationship between blood groups and disease was first hypothesized by Kaipainen et al. during 1960 [8], and the gene involved in ABO blood groups was discovered in 1990 [6].

Material and methods. Serum samples were collected from children with acute febrile illnesses who were enrolled in a prospective study that has been described elsewhere [9]. The severity of DHF grading and diagnostic criteria followed World Health Organization guidelines. Acute dengue-virus infections were confirmed both virologically (by virus isolation and/or reverse-transcriptase polymerase chain reaction) and serologically (by ELISA for IgM/IgG) [9]. Standard hemagglutination assays were used to type the blood groups [6]. The protocol was approved by the Human Subjects Research Review Board, the Thai Ministry of Public Health, and the Institutional Review Board of the University of Massachusetts Medical School. Written, informed consent was obtained from the parent or guardian of each child.

All patients with confirmed dengue-virus infections were included in these analyses. We compared ABO blood-group frequencies in primary versus secondary infections, as well as in the analysis of associations with disease severity (DF vs. DHF), according to World Health Organization criteria. Theχ2 test for ABO blood groups (2×2 contingency tables) was used. P < .05 was considered to be significant. We used Bonferroni’s method to correct for multiple comparisons; this included correcting for blood groups (n = 4), primary versus secondary infections (n = 2), and number of groups of patients (DF, DHF1, DHF2, DHF3, all grades of DHF combined, and DF+DHF combined [n = 6]). Corrected P values (Pc) <.05 were considered to be highly significant. The odds ratio (OR) and 95% confidence interval (CI) were used to assess the predisposition risk of disease severity associated with a specific ABO blood group.

Results. The frequencies of each blood group in the sample population are presented in table 1 and were consistent with those in the general Thai population [10]. The distribution of each blood group among patients with DF was similar to that among patients with DHF. Secondary infections are known to be associated with a higher risk of development of severe disease, so each patient was assayed by IgM/IgG ELISA to determine whether he or she was presenting with a primary or secondary infection.Table 2 shows the results of these assays, stratified by ABO blood group. In primary dengue-virus infections, all 4 blood groups had similar susceptibility to severe disease—that is, to DHF3—and no correlation between blood group and disease severity was seen. In contrast, among patients with secondary dengue-virus infection, blood group AB’s association with DHF3 was similar to both its association with DF (Pc < .0001; OR, 0.119 [95% CI, 0.04–0.37]) and its association with DHF1 and DHF2 combined (Pc < .0001; OR, 0.097 [95% CI, 0.03–0.33]). Also notable in secondary dengue-virus infection was that blood group O was associated less with DHF3 than with DF (P = .0304); however, this difference was not statistically significant after correction for multiple comparisons (Pc = 1.5).

Table 1.

Table 2.

Discussion. The results of the present study suggest that, when associated with a secondary infection, blood group AB may be a risk factor predisposing for severe dengue disease. The innate immune system—consisting of NK cells, dendritic and mast cells, macrophages, natural antibody—producing B cells, the complement system, and the host genetic factors—clearly plays a role in elimination of viral infections [11]. Among these innate factors, a predisposition for an individual to be susceptible or resistant to phenotypes of infectious diseases and their clinical manifestations resides in host genetic factors [6]. Two genetic factors—HLA and ABO blood groups—have, to some extent, been demonstrated to play an important role in resistance or susceptibility to infectious diseases [6].

DHF/DSS has been documented in infants during their first dengue-virus infection [1]. Presumably the enhancement of dengue disease in infants is due to preexistent dengue antibody that is passively acquired, via cord blood, from mothers immune to dengue-virus infection [1]. One limitation of the present study is that no infants were included. Whether ABO blood groups will play a similar role in infants remains to be delineated. In the present cohort study, the incidence of DHF in children with primary dengue-virus infection was low (table 2). Factors contributing to DHF in these children are unknown; perhaps individual genetic background may play a critical role in these children [2, 6].

In ABO blood-group antigens, individuals who lack an antigen have natural antibodies with the ability to agglutinate cells carrying that antigen [6]. The antigens are carbohydrate in nature; the immundominant sugar in the case of the A determinant is N-acetyl-D-galactosamine, and that in the case of the B determinant is D-galactose. Galactosyltransferases are involved in the synthesis of these carbohydrates [6]. The antibody that recognizes these carbohydrates is primarily natural IgM. Interestingly, several dengue viral proteins have been shown to be glycosylated [12], and antibodies, particularly IgM, produced in patients with dengue-virus infection have been shown to cross-react with host cells [3]. Two earlier studies found no association between blood group and disease severity in patients with dengue-virus infection [13, 14]; however, either the collected data were incomplete [13] or not all patients in the study had laboratory-confirmed dengue-virus infection and a comparison group with DF was not included [14]. Therefore, whether the combination of ABO blood group and the level of natural IgM antibody circulating in individuals has an effect on dengue disease remains to be seen.

Additionally, a correlation between HLA and dengue disease has been reported; but no specific polymorphisms have been found to be unequivocally associated with disease severity [5]. It therefore is of interest to see whether there is any correlation between a polymorphism in the galactosyltransferase gene and dengue-disease severity.

A previous study of HLA and dengue-virus infection found that the infecting viral serotype influenced the strength of the association between specific HLA alleles and dengue-disease severity [15]. The potential influence of dengue viral serotype in association with disease severity and ABO group was analyzed. All 4 serotypes were circulating during the periods of the study, and the results suggest that, for blood groups O, A, and B, no serotype was associated with disease severity. Interestingly, in the present study we found that, for blood group AB, moresevere dengue disease seemed to be associated more with dengue serotypes 2, 3, and 4 than with dengue serotype 1 (data not shown). Blood group AB’s association with DHF versus its association with DF was not significantly different from that in the other blood groups. Because of the limitations of the sample size in the present study, further studies will be necessary to determine whether dengue serotype, HLA, and ABO are independent variables—and whether some blood subgroups are associated with a particularly high risk of dengue-virus infection.


We thank Dr. Henry A. F. Stephens (Institute of Urology and Nephrology, University College London), for his excellent technical support in the statistical analysis and for helpful discussions, and Drs. SuchitraNimmannitya (Queen Sirikit National Institute of Child Health, Bangkok) and Alan Rothman (University of Massachusetts Medical School, Boston), for their knowledgeable comments and suggestions regarding the manuscript.

Rh negative people more resistant to chikungunya

Rh positive blood groups are more susceptible to chikungunya fever over Rh negative individuals are resistant to it, a new study suggests. Also, people with ‘O’ positive blood group are more susceptible to infection by the virus than people of other blood groups, the research says.


The researchers studied genetic predisposition to chikungunya fever, based on blood group antigens, on 100 families affected by the disease. They conducted blood group (ABO) tests by focusing on individuals who were likely to have a risk of chikungunya and identified the blood group involved in susceptibility/resistance to chikungunya.

The individuals were screened under four groups — A, B, AB and O. The result obtained showed that all Rh positive blood group individuals were susceptible to chikungunya fever.

Among ABO groups, O +ve individuals were found to bemore susceptible to chikungunya than other blood groups. No blood group with Rh negative was affected with chikungunya, indicating more resistance to chikungunya.

Source: natureINDIA

Chikungunya (pronunciation: \chik-en-gun-ye click to hear pronunciationExternal Web Site Icon) virus is transmitted to people by mosquitoes. The most common symptoms of chikungunya virus infection are fever and joint pain. Other symptoms may include headache, muscle pain, joint swelling, or rash. Outbreaks have occurred in countries in Africa, Asia, Europe, and the Indian and Pacific Oceans. In late 2013, chikungunya virus was found for the first time in the Americas on islands in the Caribbean. Chikungunya virus is not currently found in the United States. There is a risk that the virus will be imported to new areas by infected travelers. There is no vaccine to prevent or medicine to treat chikungunya virus infection. Travelers can protect themselves by preventing mosquito bites. When traveling to countries with chikungunya virus, use insect repellent, wear long sleeves and pants, and stay in places with air conditioning or that use window and door screens

By natureINDIA chart showing which blood types is more likely to get the virus