[Anonymous]

Hi, it’s good to see whites who care about rh negative blood. I am O negative. Many people ask others what their “sign” is. I ask them their blood type.

[Sudoku]

Another 0 Rh- here. Although I view it much like white skin, blue eyes, blonde /red hair, another interesting trait that white people carry but with no special relevance otherwise. The only additional interest is due to the impact it had on birth rates historically.

It annoys me that so much fake info gets spread about Rh- blood online, as it makes it difficult to find the real info. When I began looking into it (specifically, due to health issues that Rh- women in my family share), I had to wade through all the alien / reptilian / angel / whatever else videos. Plus the fake 15% figure that gets copy pasted everywhere. It got a bit irritating.

My personal theory is that it just evolved when white people were more cut off from other groups in areas such as the Caucus mountains. If you have a smaller population breeding with each other over a long period of time, you are more likely to get traits like that continuing through the group. Then when they come into contact with other groups, those traits decrease in number if individuals from the different groups are able to effectively reproduce and it is easier for the Rh+ trait to spread to the next generation. Unlike blonde hair or blue eyes, which (as far as I know) don’t have any impact on how many viable offspring a couple produces.

Rh- women used to have a natural ‘barrier’ against producing Rh+ children with Rh+ men they met. So at first it was easier for the Rh- trait to continue (Rh- men could have an equal number of Rh- and Rh+ offspring with Rh+ women, but Rh- women had fewer surviving Rh+ offspring with Rh+ men). But since the invention of the RhoGAM shot, the Rh+ trait has had more chance to spread (less second, third, fourth+ children with Rh+ blood getting sick or dying before/during birth or in childhood) and I imagine eventually it will disappear entirely.

So finding another Rh- partner isn’t important unless you care about the Rh- blood trait continuing in future. O Rh- blood is useful for donating to other blood type patients in emergencies. So there’s that. But I’m guessing artificial 0 Rh- will be created in future, so there won’t be any need for the real stuff. I think there’s only 4-6% of the global population left that are Rh- anyway (the 15% figure was ONLY for the USA and based on a study done back in 2001, and the widespread use RhoGAM plus non-white immigration plus low native birthrates will have reduced numbers in higher Rh- populations even further). And the % of 0 Rh- globally is even lower. So I think it’s a done deal at this point.

• This reply was modified 2 years, 3 months ago by Sudoku. Reason: spelling
• This reply was modified 2 years, 3 months ago by Sudoku.

[Trey]

Blood Groups and Red Cell Antigens – by Laura Dean, MD
Bethesda (MD): National Center for Biotechnology Information (US); 2005.

“Blood Groups and Red Cell Antigens is a guide to the differences in our blood types that complicate blood transfusions and pregnancy. It accompanies the dbRBC, a new NCBI resource that contains clinical and DNA data about human red blood cells.”
https://www.ncbi.nlm.nih.gov/books/NBK2261/
https://www.ncbi.nlm.nih.gov/books/NBK2261/pdf/Bookshelf_NBK2261.pdf

some quotes from sections of this book:

Chapter 5 The ABO blood group

Frequency of ABO blood group antigens
A: 43% Caucasians, 27% Blacks, 28% Asians
B: 9% Caucasians, 20% Blacks, 27% Asians
A1: 34% Caucasians, 19% Blacks, 27% Asians
Note: Does not include AB blood groups (1).

Frequency of ABO phenotypes
Blood group O is the most common phenotype in most populations.
Caucasians: group O, 44%; A1, 33%; A2, 10%; B, 9%; A1B, 3%; A2B, 1%
Blacks: group O, 49%; A1, 19%; A2, 8%; B, 20%; A1B, 3%; A2B, 1%
Asians: group O, 43%; A1, 27%; A2, rare; B, 25%; A1B, 5%; A2B, rare
Note: Blood group A is divided into two main phenotypes, A1 and A2 (1).

Chapter 7 The Rh blood group

“The significance of the Rh blood group is related to the fact that the Rh antigens are highly immunogenic. In the case of the D antigen, individuals who do not produce the D antigen will produce anti-D if they encounter the D antigen on transfused RBCs (causing a hemolytic transfusion reaction, HTR) or on fetal RBCs (causing HDN). For this reason, the Rh status is routinely determined in blood donors, transfusion recipients, and in mothers-to-be.

Despite the importance of the Rh antigens in blood transfusion and HDN, we can only speculate about the physiological function of the proteins, which may involve transporting ammonium across the RBC membrane and maintaining the integrity of the RBC membrane.”

Frequency of Rh antigens
D: 85% Caucasians, 92% Blacks, 99% Asians
C: 68% Caucasians, 27% Blacks, 93% Asians
E: 29% Caucasians, 22% Blacks, 39% Asians
c: 80% Caucasians, 96% Blacks, 47% Asians
e: 98% Caucasians, 98% Blacks, 96% Asians (1)

Frequency of Rh phenotypes
Rh haplotype DCe: most common in Caucasians (42%), Native Americans (44%), and Asians (70%)
Rh haplotype Dce: most common in Blacks (44%)
Rh D-negative phenotype: most common in Caucasians (15%), less common in Blacks (8%), and rare in Asians (1%) (1)
————

“It was wrongly thought that the agglutinating antibodies produced in the mother’s serum in response to her husbands RBCs were the same specificity as antibodies produced in various animals’ serum in response to RBCs from the Rhesus monkey. In error, the paternal antigen was named the Rhesus factor. By the time it was discovered that the mother’s antibodies were produced against a different antigen, the rhesus blood group terminology was being widely used. Therefore, instead of changing the name, it was abbreviated to the Rh blood group.”

—- the following section is complete quote of that section from the book: —-

Basic biochemistry

Common Rh phenotypes

“” The most common Rh haplotype in Caucasians, Asians, and Native Americans is DCe. In Blacks, the Dce haplotype is slightly more common (1).

In Caucasians, the Rh D-negative phenotype results from a deletion of the RHD gene. About 15% of Caucasians are Rh D-negative.

In Africans, there are three molecular backgrounds that give rise to the Rh D-phenotype which is found in 8% of the population. One is the RHD gene deletion that is common in Caucasians. The other two mechanisms are inheriting a RHD pseudogene (contains a duplication of nucleotides that introduces a premature stop codon) or inheriting a RHD hybrid gene (contains nucleotide sequences from the RHCE gene, produces no D antigen and abnormal C antigen) (3)

Uncommon Rh phenotypes

The D antigen contains over 30 epitopes. Variations of the D phenotype arise when these epitopes are only weakly expressed (“weak D phenotype”) or when some are missing (“partial D phenotype”).

Weak D: all D antigen epitopes are present but are underexpressed

“Weak D” is a Rh phenotype found in less than 1% of Caucasians and is only slightly more common in African Americans (2). It is typically caused by a single amino acid switch in the transmembrane region of the RhD protein. This disrupts how the RhD protein is inserted into the RBC membrane, reducing the level of expression of RhD. In most cases, adequate levels of D antigen are present and because there has been no change in D epitopes, the formation of anti-D is prevented. Therefore, individuals with the weak D phenotype can receive Rh D-positive blood.

Partial D: some D antigen epitopes are missing

In contrast, people who have been identified as having the “partial D” phenotype should not receive Rh D-positive blood but in practice, people with partial D are difficult to identify. This phenotype is usually caused by the creation of a hybrid RhD and RhCE protein. The hybrid protein is similar enough to RhD to be correctly inserted in the RBC membrane, but it lacks several epitopes found on the complete RhD protein. If a person with the partial D phenotype encounters the complete D antigen on transfused RBCs, they may form anti-D and suffer from a transfusion reaction. “”
——–

Function of Rh proteins

“The Rh antigens are thought to play a role in maintaining the integrity of the RBC membrane—RBCs which lack Rh antigens have an abnormal shape.

Individuals with the rare Rhnull phenotype caused by the deletion of RHAG have RBCs that do not express any of the Rh antigens because they cannot be targeted to the RBC membrane. The absence of the Rh complex alters the RBC shape, increases its osmotic fragility, and shortens its lifespan, resulting in a hemolytic anemia that is usually mild in nature. These patients are at risk of adverse transfusion reactions because they may produce antibodies against several of the Rh antigens”

Clinical significance of Rh antibodies

“Whereas most blood types are determined by red cell antigens that differ by one or two amino acids, the Rh blood group contains the D antigen which differs from the C/c and E/e antigens by 35 amino acids. This large difference in amino acids is the reason why the Rh antigens are potent at stimulating an immune response (4).

The majority of antibodies formed against the Rh antigens are of the IgG type. They are capable of causing significant HTR and HDN. Rh antibodies rarely, if ever, bind complement, and therefore RBC destruction is mediated almost exclusively via macrophages in the spleen (extravascular hemolysis).”

Molecular information

Gene

“The Rh locus is located on the long arm of chromosome 1 (on 1p36-p34). It contains the RHD and RHCE genes, which lie in tandem. The RHD and RHCE genes are structural homologs and result from a duplication of a common gene ancestor.

RHD and RHCE each contain 10 exons and span a ~75-kb DNA sequence. The RHD gene is flanked by two 9-kb, highly homologous sequences called “Rhesus boxes” (14, 15). It is thought that unequal homologous recombination confined to the Rhesus boxes is a common cause of the deletion of the RHD gene, which is found in up to 40% of the population.”

Protein

“The RHD and RHCE genes each encode a transmembrane protein over 400 residues in length that traverses the RBC membrane 12 times. The RhD protein only differs from the common form of the RhCE protein by about 35 amino acids.”

[Dios Rey Æλ]

It is true that a White woman that is rh negative should probably find another White man who is also rh negative as well.

This are the factual and true reasons…

Rh incompatibility:

Rh incompatibility is a condition that develops when a pregnant woman has Rh-negative blood and the baby in her womb has Rh- positive blood.

Causes:
During pregnancy, red blood cells from the unborn baby can cross into the mother’s blood through the placenta.

If the mother is Rh-negative, her immune system treats Rh-positive fetal cells as if they were a foreign substance. The mother’s body makes antibodies against the fetal blood cells. These antibodies may cross back through the placenta into the developing baby. They destroy the baby’s circulating red blood cells.

When red blood cells are broken down, they make bilirubin. This causes an infant to become yellow (jaundiced). The level of bilirubin in the infant’s blood may range from mild to dangerously high.

Firstborn infants are often not affected unless the mother had past miscarriages or abortions. This would sensitize her immune system. This is because it takes time for the mother to develop antibodies. All children she has later who are also Rh-positive may be affected.

Rh incompatibility develops only when the mother is Rh-negative and the infant is Rh-positive. This problem has become less common in places that provide good prenatal care. This is because special immune globulins called RhoGAM are routinely used.

Symptoms:
Rh incompatibility can cause symptoms ranging from very mild to deadly. In its mildest form, Rh incompatibility causes the destruction of red blood cells. There are no other effects.

After birth, the infant may have:

Yellowing of the skin and whites of the eyes (jaundice)
Low muscle tone (hypotonia) and lethargy
Exams and Tests:
Before delivery, the mother may have more amniotic fluid around her unborn baby (polyhydramnios).

There may be:

A positive direct Coombs test result
Higher-than-normal levels of bilirubin in the baby’s umbilical cord blood
Signs of red blood cell destruction in the infant’s blood
Treatment:
Rh incompatibility can be prevented with the use of RhoGAM. Therefore, prevention remains the best treatment. Treatment of an infant who is already affected depends on the severity of the condition.

Infants with mild Rh incompatibility may be treated with phototherapy using bilirubin lights. IV immune globulin may also be used. For infants severely affected, an exchange transfusion of blood may be needed. This is to decrease the levels of bilirubin in the blood.

Outlook (Prognosis):
Full recovery is expected for mild Rh incompatibility.

Possible Complications:
Complications may include:

Brain damage due to high levels of bilirubin (kernicterus)
Fluid buildup and swelling in the baby (hydrops fetalis)
Problems with mental function, movement, hearing, speech, and seizures
When to Contact a Medical Professional:
Call your health care provider if you think or know you are pregnant and have not yet seen a provider.

Prevention:
Rh incompatibility is almost completely preventable. Rh-negative mothers should be followed closely by their providers during pregnancy.

Special immune globulins, called RhoGAM, are now used to prevent RH incompatibility in mothers who are Rh-negative.

If the father of the infant is Rh-positive or if his blood type is not known, the mother is given an injection of RhoGAM during the second trimester. If the baby is Rh-positive, the mother will get a second injection within a few days after delivery.

These injections prevent the development of antibodies against Rh-positive blood. However, women with Rh-negative blood type must get injections:

During every pregnancy
After a miscarriage or abortion
After prenatal tests such as amniocentesis and chorionic villus biopsy
After injury to the abdomen during pregnancy
Alternative Names:
Rh-induced hemolytic disease of the newborn; Erythroblastosis fetalis

Patient Instructions:
Newborn jaundice – discharge:
Your baby has been treated in the hospital for newborn jaundice. This tells you what you need to know when your baby comes home.

When Your Child Was in the Hospital
Your baby has newborn jaundice. This common condition is caused by high levels of bilirubin in the blood. Your child’s skin and sclera (whites of his eyes) will look yellow.

Some newborns need to be treated before they leave the hospital. Others may need to go back to the hospital when they are a few days old. Treatment in the hospital most often lasts 1 to 2 days. Your child needs treatment when their bilirubin level is too high or rising too quickly.

To help break down the bilirubin, your child will be placed under bright lights (phototherapy) in a warm, enclosed bed. The infant will wear only a diaper and special eye shades. Your baby may have an intravenous (IV) line to give them fluids.

Rarely, your baby may need treatment called a double volume blood exchange transfusion. This is used when the baby’s bilirubin level is very high.

Unless there are other problems, your child will be able to feed (by breast or bottle) normally. Your child should feed every 2 to 2 ½ hours (10 to 12 times a day).

The health care provider may stop phototherapy and send your child home when their bilirubin level is low enough to be safe. Your child’s bilirubin level will need to be checked in the provider’s office, 24 hours after therapy stops, to make sure the level is not rising again.

Possible side effects of phototherapy are watery diarrhea, dehydration, and skin rash that will go away once the therapy stops.

What to Expect at Home
If your child did not have jaundice at birth but now has it, you should call your provider. Bilirubin levels are generally the highest when a newborn is 3 to 5 days old.

If the bilirubin level is not too high or not rising quickly, you can do phototherapy at home with a fiber optic blanket, which has tiny bright lights in it. You may also use a bed that shines light up from the mattress. A nurse will come to your home to teach you how to use the blanket or bed and to check on your child.

The nurse will return daily to check your child’s:

-Weight
-Intake of breast milk or formula
-Number of wet and poopy (stool) diapers
-Skin, to see how far down (head to toe) the yellow color goes
-Bilirubin level
You must keep the light therapy on your child’s skin and feed your child every 2 to 3 hours (10 to 12 times a day). Feeding prevents dehydration and helps bilirubin leave the body.

Therapy will continue until your baby’s bilirubin level lowers enough to be safe. Your baby’s provider will want to check the level again in 2 to 3 days.

If you are having trouble breastfeeding, contact a breastfeeding nurse specialist.

When to Call the Doctor
Call your baby’s health care provider if the infant:

-Has a yellow color that goes away, but then returns after treatment stop
-Has a yellow color that lasts for more than 2 to 3 weeks
Also call your baby’s provider if you have concerns, if the jaundice is getting worse, or the baby:
-Is lethargic (hard to wake up), less responsive, or fussy
-Refuses the bottle or breast for more than 2 feedings in a row
-Is losing weight
-Has watery diarrhea
Alternative Names
Jaundice of the newborn – discharge; Neonatal hyperbilirubinemia – discharge; Breastfeeding jaundice – discharge; Physiologic jaundice – discharge

Sources: https://medlineplus.gov/ency/article/001600.htm#:~:text=If%20the%20mother%20is%20Rh,baby’s%20circulating%20red%20blood%20cells.
Second source: https://medlineplus.gov/ency/patientinstructions/000296.htm

[Trey]

i understand the desire to pass on your Blood to your Children and Race however this topic is based on a lie that was invented and named by 2 jew “scientist”… here is a White paper on this topic that clearly states this issue is NOT the reason the Woman’s body tries to kill the baby in the womb of the RH- Mother. https://www.ncbi.nlm.nih.gov/books/NBK2269/ i would only ask this be read to the end for the actual reasons the Mother’s Body rejects the baby. also for the actual reality of the so called Rhesus factor. i am not here to attack anyone at all i am only trying to dispel a jew lie used to divide the White Race. thank you…

[Astoria]

O rh negative woman here. Thank you for creating this. I often wonder if I should search for an rh negative partner to have children with, as I heard that carrying an rh positive baby can have detrimental effects, however, searching for an rh negative partner greatly limits the dating pool that I can choose from.

[Anonymous]

Appreciate you creating this thread explaining the importance of our blood type (I am also Rh O-, myself). It’s such an intriguing subject – the absence of rhesus originated in Europe but we don’t understand how it evolved. I wonder if other Rh negatives also have this feeling of not “belonging” on this planet or part of this society.

[Dios Rey Æλ]

Hello, I am O rh negative and I am glad that this group exist for other Whites and I start the first topic of this forum for my tipe of blood and for the people who have it as well… There could be more topics for every specific letter with RH negative but this one I will do it only for the Whites O RH negatives. it is very important to know the blood of your couple no matter if you are a White man or White woman.

Why is O negative blood important and special? O negative blood is often called the ‘universal blood type’ because people of any blood type can receive it. is often called the universal donor as well… This makes it vitally important in an emergency or when a patient’s blood type is unknown. Now the O negative blood can only receive blood of his own type… O Negative blood is often used for premature infants and babies who need blood transfusions.

Only 7% of the population are O negative so they are rare. However, the need for O negative blood is the highest because it is used most often during emergencies.

Basques (north of Spain and south of France) have the highest concentration of type O negative in the world — more than 50 percent of the population of O rh negative — with an even higher percentage in remote areas where the language is best preserved, such as Soule.

O rh negative is most found in european caucasians… therefore Whites.

Another curiosity is that we can preserve our own blood refrigerated to donate to our own self…

Another curiosity is that the monarchy of the United Kingdom is O rh negative such as the brunnete Queen Elizabeth, brunnete Prince Charles and his redhaired sons with the blondie Diana.

Rh negative people in general not only O but as well the A negative B negative and AB negative have no rhesus monkey factor therefore the name rh negative…

Final Curiosity is that most of the genius rockers of the Club 27 who died at 27 years old by different reaons are O rh negative like the vocalist of The Doors, Vocalist/Guitarrist of Nirvana, Composer of the Rolling Stones, Janis Joplin solist vocalist too to say some of them.

• This topic was modified 3 years, 9 months ago by Dios Rey Æλ.

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