Risks During Pregnancy Regarding Rh Status

There seems to be a lot of confusion where Rh status and pregnancy are concerned, so I thought I would make a chart for you to check against.

You have to remember though, that problems only occur when the positive baby or the positive Mother passes their own blood to a negative Mother or baby.

To avoid all problems completely you should only have children with someone who is the same Rh status as you. This is also not taking into account all the other factors in blood like Kell, Duffy and others which can also affect pregnancy.

Rh Negative Blood & Hypothyroidism

Did you know that the thyroid medication your Doctor gives you is synthetic?

Thyroid-S is natural and works much better.

Are you a Secretor or a Non-Secretor?

You may know your blood type – but do you know whether or not you're a secretor or a non-secretor? Most people have no idea that this blood typing sub-system even exists, but in truth, knowing which category you fall into can help you to make the most of your health.

The concepts of secretors and non-secretors were first introduced to the public by Dr. Peter D'Adamo's book Eat Right 4 Your Blood Type. In his book, Dr. D'Adamo posits that differences in blood type make people respond differently to various diets and medical treatments, and are the reason why some people are more vulnerable to certain illnesses and maladies than others. Each blood type, he says, has a distinct chemical reaction to lectins – substances found in foods. When a person eats a food containing lectins that are incompatible with his or her blood type, those lectins target a certain area and cause blood cells in that area to clump (or agglutinate), leading to uncomfortable symptoms. Continuing to ingest the offensive food will make the person susceptible to disease in the areas where the agglutination occurs.

Whether you're a secretor or a non-secretor is completely independent of your blood type, but just as important when it comes to understanding any metabolic dysfunctions and immune susceptibilities. Simply put, a secretor is a person whose body secretes its blood type antigens into its fluids – saliva, mucus, etc. A non-secretor does not. (Approximately 80% of the general population are estimated to be secretors.) And while no one blood type is better than the others, it is thought better to be a secretor than a non-secretor. The ability to secrete blood type antigens into your bodily fluids offers enhanced protection against outside factors such as potentially harmful microorganisms and the lectins from the food you eat. Secretors also have a more accomodating intestinal environment in which beneficial probiotic bacteria can thrive, since blood type can be used as a food source for such bacteria. Non-secretors on the other hand, because their bodies don't infuse their fluids with blood type antigens, have tendencies toward:

• Higher rates of oral disease, including more cavities – and, interestingly, habitual snoring
• Digestive problems, such as inflammation and ulcers
• A more prevalent rate of autoimmune disorders, such as multiple sclerosis
• Lungs that are more susceptible to environmental factors and cigarette smoking
• A greater risk of diabetes and heart disease
• A greater risk for recurrent urinary tract and Candida (yeast) infections
• An increased association with alcoholism
• More difficulty breaking down dietary fat and properly metabolizing calcium
• An increased intolerance to carbohydrates

Your “secretor/non-secretor” status, in conjunction with your blood type, also determines the viscosity and clotting time of your blood. So you see? Since many of your bodily functions and responses are influenced by your secretor status, knowing which you are can be a valuable tool in determining how to take the best care of yourself – and how to feel better than ever.

Source

Secretor status

Antigens are present in the blood and, in most individuals, in bodily fluids such as saliva. If antigens are present in your bodily fluids, you are known as a ‘secretor’. If they are not present in your bodily fluids, you are a ‘non-secretor’. This fact is important for the diet, so it is important that you find out your secretor status.

Some researchers have found a correlation between Rhesus status and Secretor status. If you are unable to determine your Secretor status, a general rule of thumb is that Rhesus + usually denotes a secretor, and Rhesus – usually denotes a non-secretor. This research has not been sufficiently documented at this stage, so if possible and if available in your country, a test for secretor status should be done at the same time as the test for your blood type.

Secretors are shown as ‘1’ and non-secretors as ‘2’, for example, A1 (secretor) or A2 (non-secretor).

Source


Find out more in the book Secrets of the Serpent Bloodline by Tau Tia L Douglass

Rh Negative Eye Colours

It is said that eyes can never lie, that when you look into someone's eyes you can see their true spirit. There are so many different colours and shades of eyes but Rh negatives do tend to have lighter eyes in general. They also tend to have mood eyes - changing colour depending on their mood and what they are wearing.

I decided to a survey to find out the most popular eye colours in Rh negatives and then a survey out in the public where anyone could answer.

Because all eye colours are made up from brown and blue, and the colour in between those is green I decided to make the survey more fair we should group certain shades in to one of these three groups, as follows:

Brown Eyes - Amber, Black.
Green Eyes - Hazel, Olive.
Blue Eyes - Grey, Violet.

Here are the results within the Rh negative study group.

Chart Created by & © Copyright Tia L Douglass 2012 All Rights Reserved

As you can see in the Rh negative study group green is the highest, closely followed by blue and brown is the lowest. This points to the original Rh negatives having blue eyes. Brown is the dominant eye colour which normally over rides any other colour, then green, then blue. Seeing as blue is so high here it shows that those with Rh negative genes do carry the blue eyed gene strongly, as all green eyed people also carry it.

Here is the chart for the general public results, within Europe, Scandinavia, America and Australia.

Chart Created by & © Copyright Tia L Douglass 2012 All Rights Reserved

These results are harder to get a good picture from because it isn't a worldwide survey and seeing as the vast majority of the world has brown eyes. However this is including areas with the highest number of blue eyes.

What is interesting is how people seem to think that green eyes are rare, however there are lot of places in the world where the people have green eyes, and these areas show where our ancient bloodline families have visited the most, as the genes are still strong there, because as I said, all people with green eyes carry the blue eyed genes. Obviously after time an area left behind will slowly lose all green and blue eyes completely, so long as people are breeding with people with brown eyes, as they are the dominant genes.

We all have the same two eye colour genes. What gives us different eye colours are which variations of these genes we have.

One of these genes is called HERC2. It comes in two variations, brown and blue. The other gene, called gey, also comes in two versions -- green and blue.

Your eye colour depends on which combination of these versions you have as shown below:

So you can see how difficult it is for someone to have green or blue eyes, especially blue.

Chart Created by & © Copyright Tia L Douglass 2012 All Rights Reserved

Here is a map of all the places in the world where people carry the green eyed gene.

Most of the other areas are all brown eyed areas completely, with only Europe, Scandinavia, America, Russia and Australia having some blue eyes.

All Research & Graphics © Copyright Tau Tia L Douglass 2012-2015 All Rights Reserved

DO NOT COPY THIS WORK TO OTHER WEB SITES - JUST LINK TO IT

© Copyright Tau Tia Douglass All Rights Reserved - NO PART CAN BE USED WITHOUT WRITTEN PERMISSION

Find out more http://bloodtypepersonality.info/

Child Blood Type Calculator

Blood Type Genetic Basis:

In genetics, blood type gene has two alleles, each allele has genotype A, B or O. 
The A and B are dominant, and O is recessive. So allele A combined with allele O is type A.
Similarly, BO is type B, AA is type A, BB is type B, OO is type O, and AB is type AB.
If both parents have type A blood, then the alleles could be AA or AO, thus the allele A frequency is 75%, allele O frequency is 25% for both parents.
So the chance of alleles OO is 25% × 25% = 6.25%, 
alleles AA is 75% × 75% = 56.25%, 
alleles AO is 75% × 25% = 18.75%, 
alleles OA is 25% × 75% = 18.75%.
Since AA, AO and OA are blood type A, and OO is blood type O, thus their child has 6.25% chance to be blood type O and 93.75% chance to be blood type A. 

The +/- is called the rhesus factor, with + being dominant, and - being recessive.
So if both parents are -, the kids are always -, otherwise the kids might be + or -. 


Child Blood Type Estimate Table:

		Father's Blood Type
		A	B	AB	O
Mother's Blood Type
	A	A/O	A/B/AB/O	A/B/AB	A/O
	B	A/B/AB/O	B/O	A/B/AB	B/O
	AB	A/B/AB	A/B/AB	A/B/AB	A/B
	O	A/O	B/O	A/B	O

Parent Blood Type Estimate Table:

		Child's Blood Type
		A	B	AB	O
One Parent's Blood Type
	A	A/B/AB/O	B/AB	B/AB	A/B/O
	B	A/AB/O	A/B/AB/O	A/AB	A/B/O
	AB	A/B/AB/O	A/B/AB/O	A/B/AB	Impossible
	O	A/AB	B/AB	Impossible	A/B/O

Source: http://www.endmemo.com/medical/bloodtype.php

Mules Are Rh Negative!!

OK, so you know how these memes start. Some ill-informed person decides to start a rumour without checking the facts and then posts it up on the internet. Soon it is all over, and people copy and paste is everywhere and the source of the disinformation is soon lost.

However, being as this blog deals in facts only I thought I would put to bed the idea that mules have Rh-negative blood once and for all.

Animals have different blood and antigens to humans. Animals do get Hemolytic disease which can be caused when human Rh negatives and positives have children together. However, that does not mean to say it is the same antigen that causes it in animals too.

Neonatal isoerythrolysis (NI) is an immune-mediated hemolytic disease seen in newborn horses, mules, cattle, pigs, cats, and, rarely, in dogs. NI is caused by ingestion of maternal colostrum containing antibodies to one of the neonate’s blood group antigens. The maternal antibodies develop to specific foreign blood group antigens during previous pregnancies, unmatched transfusions, and from Babesia and Anaplasma vaccinations in cattle. Cats are unique in that blood type B cats have naturally occurring anti-A antibodies without prior exposure, and their kittens that are type A develop hemolysis after nursing. In horses, the antigens usually involved are A, C, and Q; NI is most commonly seen in Thoroughbreds and mules. Neonates with NI are normal at birth but develop severe hemolytic anemia within 2-3 days and become weak and icteric. Diagnosis is confirmed by screening maternal serum, plasma, or colostrum against the paternal or neonatal RBC. Treatment consists of stopping any colostrum while giving supportive care with transfusions. If necessary, neonates can be transfused with triple-washed maternal RBC. NI can be avoided by withholding maternal colostrum and giving colostrum from a maternal source free of the antibodies. The newborn’s RBC can be mixed with maternal serum to look for agglutination before the newborn is allowed to receive maternal colostrum.

         http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/10203.htm

On these fantasy sites, they also use the fact mules are sterile as a way of comparing it to Rh-neg women having trouble having babies with Rh positives.

A mule is the product of two different species (a horse and a donkey) mating with each other. Mules are always sterile because horses and donkeys have different chromosome numbers.

For the mule, having parents with different chromosome numbers isn't a problem. During mitotic cell division, each of the chromosomes copies itself and then distributes these two copies to the two daughter cells. In contrast, when the mule is producing sperm or egg cells during meiosis, each pair of chromosomes (one from Mum and one from Dad) needs to pair up with each other. Since the mule doesn't have an even number of homologous pairs (his parents had different chromosome numbers), meiosis is disrupted and viable sperm and eggs are not formed.

Neanderthals and the simians they mixed genes with did have different amounts of chromosomes, but the two smallest ape chromosomes were combined into a single, larger human chromosome.

Most ape and human chromosomes are identical. The 9th and the 14th ape chromosomes, when combined, are like a palindrome of the human 12th chromosome. That is, when viewed on a chromatic scale if the ape chromosomes (9 + 14) are joined and flipped over, the result would look just like the human #12 chromosome.

That's what makes apes so genetically close to human beings, despite the difference in the number of chromosomes, and once the chromosomes had been joined and Sapiens were created it was possible for them to breed with Neanderthals. Some of the Neanderthals did breed with the new Sapiens, and that produced the Cro-Magnons. It was harder for them to reproduce this way, but it was possible, even though the Rh factor was different.

Even though Neanderthals and the Simians started out not being able to breed with each other, after genetic engineering it was possible. The Sapiens could of course breed very easily between themselves. 

Two people with Rh-negative blood can have children normally, as can two Rh-positive. The only problems occur when the parents are incompatible and it doesn't matter which way round it is.

Like so:

Father	Mother	Result
Rh Negative	Rh Negative	Normal
Rh Positive	Rh Positive	Normal
Rh Positive	Rh Negative	Problems
Rh Negative	Rh Positive	Problems

By Tia L Douglass of NATA

Rh Negative Related Health Genetics

Sardinian Lady

Rh Negative Blood Linked To The High Amount of Diabetes Type 1 in Sardinians.

Type 1 diabetes among Sardinian children is increasing: the Sardinian diabetes register for children aged 0-14 years (1989-1999).

Casu A, Pascutto C, Bernardinelli L, Songini M.

Source

Department of Internal Medicine, Azienda Ospedaliera Brotzu, Via Peretti, Cagliari, Italy.

Abstract

OBJECTIVE:

The Sardinian type 1 diabetes register represented the basis to determine the most recent trends and the age distribution of type 1 diabetes incidence among Sardinians <15 years of age during 1989-1999. Part of the data (1989-1998) has been already published by the EURODIAB Group with a lower completeness of ascertainment (87%). The geographical distribution of type 1 diabetes risk was also investigated.

RESEARCH DESIGN AND METHODS:

The new cases of type 1 diabetes in children aged 0-14 years in Sardinia were prospectively registered from 1989 to 1999 according to the EURODIAB ACE criteria. The completeness of ascertainment calculated applying the capture-recapture method was 91%. Standardized incidence rates and 95% CI were calculated assuming the Poisson distribution. Trend of type 1 diabetes incidence was analyzed using the Poisson regression model. Maps of the geographical distribution of type 1 diabetes risk for the whole time period and separately for 1989-1994 and 1995-1999 were produced applying a Bayesian method.

RESULTS:

A total of 1214 type 1 diabetic patients were registered yielding to an overall age- and sex-standardized incidence rate of 38.8/100000 (95% CI 36.7-41.1). There was a male excess with an overall male-to-female ratio of 1.4 (1.3-1.8). The increase of incidence during the 11 years analyzed was statistically significant (P = 0.002) with a yearly increasing rate of 2.8% (1.0-4.7). No evidence of an effect of age and sex on this trend has been found. The geographical distribution of type 1 diabetes relative risk (RR) showed that the highest risk areas are located in the southern and central-eastern part of the island and the lowest risk in the northeastern part, even if most of these differences were not statistically significant. This geographical distribution seemed to remain mainly the same between 1989-1994 and 1995-1999.

CONCLUSIONS:

The homogeneity of diabetes risk and the increase of incidence over the age-groups in the Sardinian population stress the role of an environmental factor uniformly distributed among the genetically high-risk Sardinians.[1]

Sardinian DNA

About 42% of the Sardinians belong to Y-chromosome haplogroup I. The second most common Y-chromosome haplogroup among Sardinian male population is the haplogroup R1b (22% of the total population) mainly present in the northern part of the island. Sardinia also has a relatively high distribution of Y-chromosome haplogroup G (11%), which is also found in the Caucasus, the Pyrenees and the Alps, in particular Tyrol area. Other haplogroups show lower frequencies.

Note: These health problems then seem to be related to the I haplogroup and Rh negative blood parts of the island, but not R1b areas.

The most common mtDNA haplogroups in Sardinia are H (H1 and H3) and V who are also particularly common in the iberian peninsula. Some subclades typical of Sardinia and rare in the rest of Europe are:

The subclade U5b3a1 of Haplogroup U (mtDNA), about 4% of the female population in Sardinia belongs to this haplotype. One other interesting anomaly is the presence of H13a of Haplogroup H (mtDNA) is present in the island at around 9.2%. As this is an extremely rare subclade normally present in the Caucasus, its worthy of further investigation.[2]

RH blood groups and diabetic disorders: is there an effect on glycosylated hemoglobin level?

Hum Biol. 2000 Apr;72(2):287-94.

Gloria-Bottini F, Antonacci E, Bottini N, Ogana A, Borgiani P, De Santis G, Lucarini N.

• Recent cloning of RH genes has elucidated their structure, suggesting that RH proteins are part of an oligomeric complex with transport function in the erythrocyte. This observation prompted us to investigate a possible relationship between the RH system and the glycosylated hemoglobin level (Hb A(1c)) in diabetes. This compound is considered an important indicator- of glycemic control in diabetic disorders. We studied 278 subjects with non-insulin-dependent diabetes mellitus (NIDDM) from the population of Penne, Italy. Glycemic and glycosylated hemoglobin (Hb A(1c)) levels are associated with RH phenotype. Glucose and Hb A(1c) levels are increased in DCcEe subjects and decreased in ddccee subjects as compared to the mean values for other genotypes. Sex, age at onset of disease, duration of disease, and age of patients were also considered. Correlation analysis suggests that these variables influence glycemia directly and Hb A(1c) indirectly. The RH system, on the other hand, seems to influence the Hb A(1c) level directly. Preliminary data on 53 children with insulin-dependent diabetes mellitus (IDDM) from Sardinia seem to confirm the relationship between RH and Hb A(1c) observed in NIDDM. Since glycosylated hemoglobin is found inside red blood cells, the relationship between RH genetic variability and Hb A(1c) level suggests that RH proteins may influence glucose transport through red cell membrane and/or hemoglobin glycation.[3]

Type 1 Diabetes is linked to other genetic traits of Rh Negatives through SNP data:

SNP Rs2476601

This SNP, located in the PTPN22 gene and also known as R620W, or 1858C>T, may influence Rheumatoid Arthritis and other autoimmune diseases, including but not limited to, multiple sclerosis, Crohn's disease, celiac disease and type-1 diabetes.

In an expanded follow-up study of >6,000 controls and 6,000 patients, the heterozygote odds ratio for type-1 diabetes for this SNP was recalculated to be 1.98 (CI 1.82-2.15). [PMID 17554260]

rs2476601 was confirmed in another 2007 study to be a risk factor for RA [PMID 17804836].

• [PMID 16490755] confirms the association of rs2476601 rheumatoid arthritis
• [PMID 15674368] two copies of the PTPN22 R620W allele more than doubles the risk for RF positive RA

rs2476601 shows a 0.75 (r squared) correlation with rs6679677, a SNP in the RSBN1 gene associated with rheumatoid arthritis. [PMID 17554300]

[PMID 17934143]] Confirms association of rs2476601 with type-1 diabetes in a Sardinian population of 490 sporadic patients (794 families).

[PMID 18301444] In study of 332 Norwegian patients plus a meta-analysis, the rs2476601(A) allele was linked to autoimmune Addison's disease (p=0.003)

[PMID 18305142] rs2476601(A) has a higher relative risk in type-1 diabetes cases carrying lower risk HLA class II genotypes than in those carrying higher risk ones (p=1.36x10^-4 in a test of interaction).[4]

Linking PTPN22 with HLA-B27 which is associated with many autoimmune diseases, where as the SNP is associated with various others including Diabetes.

Confirmation of the genetic association of CTLA4 and PTPN22 with ANCA-associated vasculitis.

(PMID:19951419)

Carr EJ, Niederer HA, Williams J, Harper L, Watts RA, Lyons PA, Smith KG

Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB20XY, UK.

BMC Medical Genetics [2009, 10:121]

Type: Journal Article, Research Support, Non-U.S. Gov't
DOI: 10.1186/1471-2350-10-121 

BACKGROUND: The genetic contribution to the aetiology of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is not well defined. Across different autoimmune diseases some genes with immunomodulatory roles, such as PTPN22, are frequently associated with multiple diseases, whereas specific HLA associations, such as HLA-B27, tend to be disease restricted. We studied ten candidate loci on the basis of their immunoregulatory role and prior associations with type 1 diabetes (T1D). These included PTPN22, CTLA4 and CD226, which have previously been associated with AAV. METHODS: We genotyped the following 11 SNPs, from 10 loci, in 641 AAV patients using TaqMan genotyping: rs2476601 in PTPN22, rs1990760 in IFIH1, rs3087243 in CTLA4, rs2069763 in IL2, rs10877012 in CYP27B1, rs2292239 in ERBB3, rs3184504 in SH2B3, rs12708716 in CLEC16A, rs1893217 and rs478582 in PTPN2 and rs763361 in CD226. Where possible, we performed a meta-analysis with previous analyses. RESULTS: Both CTLA4 rs3087243 and PTPN22 rs2476601 showed association with AAV, P = 6.4 x 10-3 and P = 1.4 x 10-4 respectively. The minor allele (A) of CTLA4 rs3087243 is protective (odds ratio = 0.84), whereas the minor allele (A) of PTPN22 rs2476601 confers susceptibility (odds ratio = 1.40). These results confirmed previously described associations with AAV. After meta-analysis, the PTPN22 rs2476601 association was further strengthened (combined P = 4.2 x 10-7, odds ratio of 1.48 for the A allele). The other 9 SNPs, including rs763361 in CD226, showed no association with AAV. CONCLUSION: Our study of T1D associated SNPs in AAV has confirmed CTLA4 and PTPN22 as susceptibility loci in AAV. These genes encode two key regulators of the immune response and are associated with many autoimmune diseases, including T1D, autoimmune thyroid disease, celiac disease, rheumatoid arthritis, and now AAV.[5]

Conclusion

PTPN22 rs2476601 is associated with HLA-B27 which in turn is associated with Rh negative blood and all the related health problems, including but not limited to: Type 1 diabetes, autoimmune thyroid disease, celiac disease, rheumatoid arthritis, multiple sclerosis, Crohn's disease, psoriasis, ankylosing spondylitus.

These health problems are particularly virulent in those with ftDNA I and mtDNA H.

Sources

[1] Type 1 diabetes among sardinian children is increasing - ncbi.nlm.nih.gov/pubmed/15220238
[2] DNA of Sardinians - nature.com/ejhg/journal/v11/n10/full/5201040a.html
[3] Diabetic Disorders linked to Diabetes Type 1 - generativemedicine.org/wiki/wiki.pl/Rhesus_(Rh)_Blood_Group
[4] SNP Rs2476601 - snpedia.com/index.php/Rs2476601
[5] Linking PTPN22 with HLA-B27 - http://europepmc.org/articles/PMC3224698/?report=abstract

Research by Tia L Douglass of NATA