Friday, 25 January 2013

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.


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).

Tuesday, 15 January 2013

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

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

Saturday, 12 January 2013

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

Parent Blood Type Estimate Table:
Child's Blood Type

Friday, 11 January 2013

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.

On these fantasy sites they also use the fact mules are sterile as a way of comparing it to Rh neg women having trouble to have 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) need 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 amount 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 reproduce this way, but 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 the 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 positives. 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.


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



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.


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.


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.


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 sclerosisCrohn's diseaseceliac 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].

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 18305142rs2476601(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.

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.


[1] Type 1 diabetes among sardinian children is increasing -
[2] DNA of Sardinians -
[3] Diabetic Disorders linked to Diabetes Type 1 -
[4] SNP Rs2476601 -
[5] Linking PTPN22 with HLA-B27 -

Research by Tia L Douglass of NATA

Saturday, 5 January 2013

Are you from the most ancient bloodline?

Asks Dr Pinna.

"If you have a “RED GENE” freckles, light skin, reddish hair, that is a sign.

High intelligence is also a Neanderthal trait. The Neanderthals had large craniums and therefore more brains. They survived through the Ice Ages which required the ability to adapt to hunger and to be able to kill large animals. This meant they had good skills in team work."

By David Noel

From a combination of old and new evidence, it appears that at last we have a satisfactory answer to the age-old question of ‘What Happened to the Neanderthals?’. If the current reasoning is correct, their descendants are still with us, and we call them the Basques.

Robert J Sawyer has recently published his book “Hominids” [2], a fictional account of an interaction between Sapiens humans and Neanderthals, but drawing on the latest scientific research about Neanderthals.

This research included studies of DNA extracted from bones of Neanderthal remains. The account mentions five months of painstaking work to extract a 379-nucleotide fragment from the control region of the Neanderthal’s mitochondrial DNA, followed by use of a polymerase chain reaction to reproduce millions of copies of the recovered DNA.

This was carefully sequenced and then a check made of the corresponding mitochondrial DNA from 1,600 modern humans: Native Canadians, Polynesians. Australians, Africans, Asians, and Europeans. Every one of those 1,600 people had at least 371 nucleotides out of those 379 the same; the maximum deviation was just 8 nucleotides.

But the Neanderthal DNA had an average of only 352 nucleotides in common with the modern specimens; it deviated by 27 nucleotides. It was concluded that Homo sapiens and Neanderthals must have diverged from each other between 550,000 and 690,000 years ago for their DNA to be so different.

In contrast, all modern humans probably shared a common ancestor 150,000 or 200,000 years in the past. It was concluded that Neanderthals were probably a fully separate species from modern humans, not just a subspecies: Homo neanderthalensis, not Homo sapiens neanderthalensis.

Looking now at the evidence for the theory that the Basques are descended principally from Neanderthals, everything suddenly falls into place, and the supposition becomes almost self-evident.

Location: The ‘home country’ of the Neanderthals is well known to have been western Europe. One source says that they “dominated this area for at least a quarter of a million years”. Many of the best Neanderthal specimens have originated from the Iberian Peninsular. The Basque Country, lying on the western side of the Pyrenees and on the border between Spain and France, fits in neatly with this location.

Note: According to more recent sources Neanderthal originated in the Tigris area, and have been found in Israel. This is not to say a lot of them didn't settle in, or were pushed into the Basque area.[11]

The Basques are well-known to have distinctive body characteristics. Kurlansky says “Ample evidence exists that the Basques are a physically distinct group. There is a Basque type with a long straight nose, thick eyebrows, strong chin, and long earlobes” [1].

Basque skulls tend to be built on a different pattern. In the early 1880s, a researcher reported “Someone gave me a Basque body and I dissected it, and I assert that the head was not built like that of other men” [1].

These qualitative differences are indicative, but quantitative evidence, with presence or absence of features, or items being present in different numbers, has greater weight in deciding whether specimens belong to the same or different species. Powerful quantitative evidence comes from a consideration of blood factors.

Human blood is classified according to various parameters, the most important of which are ABO and Rhesus characteristics. In ABO, blood may contain the ‘A’ factor (giving A-group blood), the ‘B’ factor (B-group), both ‘A’ and ‘B’ (AB blood), or neither (O blood). The A and B factors act like antibodies, and if blood containing one or both of them is transferred to a person whose blood does not already contain them, adverse reactions occur. Group O blood contains neither antibody and can typically be transferred without reaction to any recipient.

Some 55% of Basques have Group O blood, one of the highest percentages in the world [3].

Even stronger evidence comes from the Rhesus factor, discovered only in 1940. The blood of most humans (and, apparently, all other primates [6]) contains this factor, and is called Rhesus-positive or Rh+ blood. Blood lacking this factor is called Rhesus-negative.

The Basques are well-known to have the highest percentage (around 33%) of Rhesus-negative blood of any human population [2], and so are regarded as the original source of this factor. In the United States, some 15% of the ‘European’ population are Rh-negative, while the percentage in the ‘Asian’ and ‘Black’ population is much less than this.

Possession of Rh-negative blood can be a major disadvantage for a human population. A Rh-negative woman who conceives a Rh-positive child with a Rh-positive man will typically bear her first child without special problems. However, because of intermingling of fluids between mother and foetus, the first pregnancy builds up antibodies to Rh+ blood in the woman which typically attack the blood of her subsequent Rh+ children, causing them to miscarry, be stillborn, or die shortly after birth (infant haemolytic disease [6]).

Note: If Rh negatives breed only with each other, there are no problems at all.[12]

The scenario so far then is this. Around 600,000 years ago, in southern Europe, a species of man separated off from the ancestral line, and we call this species Homo neanderthalensis, the ‘N-people’. The blood of this species contained none of the factors A, B, or Rh.

Note: Neanderthals evolved and came out of Tigris area, not Africa.[11]

Much later, possibly around 200,000 years ago in Africa, the main human line had picked up the A, B, and Rh factors (possibly from other primates, the Rhesus factor is named after the Rhesus monkey or macaque), and by then could be classed as Homo sapiens, the ‘S-people’.

In competition between related species or races, antibodies in their blood are a powerful genetic advantage for those who possess them when competing against those who don’t. History has many examples of European settlers who quite unintentionally won out against native populations because the latter had no antibodies against diseases such as measles which the Europeans brought with them.

In the present scenario, a woman of the N-people (Basque, Rh-) who partnered with a man of the S-people (non-Basque, Rh+) would be likely to bear no more than a single child of the partnership. ‘Mixed marriages’ in humans are not usually genetically disadvantageous, but in this case they would be. The effect would be a continuing reduction in the N-people population as ‘mixed’ couples produced only a single child, half the nominal population-maintenance rate.

There are other physical characteristics of humans which are typically associated with Rh-negative blood, but which in the present scenario would be regarded as belonging to the N-people. These include early maturity, large head and eyes, high IQ [6], or an extra vertebra (a ‘tail bone’ — called a ‘cauda’), lower than normal body temperature, lower than normal blood pressure, and higher mental analytical abilities [5].

Rh Negative Blood & HLA B27

By Matt McGrath

In the human immune system, the HLA (human leucocyte antigen) family of genes plays an important role in defending against foreign invaders such as viruses.

The authors say that the origins of some HLA class 1 genes are proof that our ancient relatives interbred with Neanderthals and Denisovans for a period.

“Getting these genes by mating would have given an advantage to populations that acquired them.”

At least one variety of HLA gene occurs frequently in present day populations from West Asia, but is rare in Africans.

“The HLA genes that the Neanderthals and Denisovans had, had been adapted to life in Europe and Asia for several hundred thousand years, whereas the recent migrants from Africa wouldn't have had these genes,” said study leader Peter Parham from Stanford University School of Medicine in California.

“So getting these genes by mating would have given an advantage to populations that acquired them.”

Dr. Pinna says:

The HLA gene which provides our white cells in our immune system with the ability to recognize viruses and perhaps cancers was a gift from our Neanderthal ancestors.

Neanderthals interbred with Europeans and Chinese but not with Africans. This is very important from a medical point of view.

Since the HLA (HUMAN LEUKOCYTE (WHITE CELL) ANTIGEN) protects against viruses, we find the most deadly viruses in Africa. For example, the famous EBOLA virus.Why? Because Africans do not have the ability to defend against and eradicate this virus. The viruses found in Europe and China are rather mild, such as mumps, measles and German measles.Also, Africans have less defenses against cancers caused by viruses. Here is a report from the Guardian, U.K:

“The difference is that a disproportionate number of cancers in Africa are caused by infections, such as the hepatitis viruses (B and C), which cause liver cancer, or the human papillomavirus (HPV), which causes 98% of cervical cancers. The worldwide average for infection-related cancers is about 22%; in Africa, the figures are much higher: 40% of cases in women and 30% in men.”

European and Chinese interbreeding with Neanderthals was a gift from God. Not only did it give us red hair and big brains, but also a way to fight viral infection.

HLA B27 & Arthritis

Arthritis is a term for any of more than one hundred diseases that produce swelling in a joint, accompanied by pain and stiffness. The most common forms of arthritis are osteoarthritis (the degeneration of a joint) and rheumatoid arthritis ("the great crippler," inflammation of a joint that erodes bone and cartilage). Other forms include ankylosing spondylitis (inflammation of spinal joints, mainly affecting young men), infectious arthritis (caused by invading microorganisms), and chronic Lyme arthritis (which appears in some people who contract Lyme disease). Lupus, an autoimmune disease, also has elements of arthritis, with painful and often swollen joints.

Neanderthal skeletons show signs of arthritis, as do Egyptian mummies. Ancient Greek and Roman physicians wrote detailed descriptions of arthritic conditions and methods of treatment. In fourteenth- and fifteenth-century Europe, gout became common among members of the upper classes, and an outbreak of rheumatoid arthritis swept through the masses of Europe during the Industrial Revolution. By the early nineteenth century, rheumatoid arthritis had been recognized as a distinct condition, separate from gout. Augustin Landre-Beauvais gave rheumatoid arthritis its first complete clinical description in 1800; in 1859 Alfred Garrod (1819-1907) distinguished gout by the presence of uric acid.

While the disease had been known for centuries, its cause remained unknown. Some thought arthritis was the result of an infectious disease, such as gonorrhea or tuberculosis. In 1900 twophysicians, Frederick J. Poynton (1869-1943) and A. Paine, discovered a bacteria in a group of children afflicted with rheumatism. They speculated that rheumatic arthritis could be the result of an immune reaction to an invading microorganism. In 1940 researchers found an rheumatoid factor, an antibody-like substance, in the blood of arthritis patients. Further study showed that rheumatic infections were caused by a group A streptococcus, so the rheumatoid factor was indeed an immune system response to that bacteria. Current research focuses on the relationship between specific genetically coded HLA molecules (an element of the immune system) and the occurrence of various types of arthritis. For example, the HLA-B27 molecule is common in people with ankylosing spondylitis.[14]

HLA B27 & CCR5-Δ32

According to Randall Johnson at the Baylor College of Medicine in Houston, "Only 7% of the US population tests positive for the HLA-B27 gene; this gene, found only in persons with Rh-Negative blood, can trigger the immune system to operate overtime at WARP SPEED in times of medical emergency."

Note: HLA-B27 is also sometimes found in those who are Rh negative recessive.

The HLA-B27 Genetic Marker is said to have protective properties that guard against the progression of HIV. It is said, that people with this gene do not have the right proteins for the HIV virus to bind with. The HLA-B27 Marker is most often found in people with O- Blood. 

CCR5-Δ32 is a deletion mutation of a gene that has a specific impact on the function of T cells. At least one copy of CCR5-Δ32 is found in about (5-14%) of people of Northern European and in those of Northern European descent. There also is a small minority (1%) with the same mutation amongst Southern Europeans or Balkan Peninsula. It has been hypothesized that this allele was favored by natural selection during the Black Death for Northern Europeans.

The allele has a negative effect upon T cell function, but appears to protect against smallpox and HIV. Yersinia pestis (the bubonic plague bacterium) was demonstrated in the laboratory not to associate with CCR5. Individuals with the Δ32 allele of CCR5 are healthy, suggesting that CCR5 is largely dispensable. However, CCR5 apparently plays a role in mediating resistance to West Nile virus infection in humans, as CCR5-Δ32 individuals have shown to be disproportionately at higher risk of West Nile virus in studies, indicating that not all of the functions of CCR5 may be compensated by other receptors.

While CCR5 has multiple variants in its coding region, the deletion of a 32-bp segment results in a nonfunctional receptor, thus preventing HIV R5 entry; two copies of this allele provide strong protection against HIV infection. This allele is found in 5–14% of Europeans but is rare in Africans and Asians.

HLA-B27 is an inherited gene marker that is associated with a number of related rheumatic diseases. They share in common, certain features like spinal and peripheral arthritis, skin and GI disorders, anterior chamber eye disease, psoriasis like skin lesions, as well as inflammation and joint pain. This gene is found with highest prevalence in patients with ankylosing spondylosis, reactive arthritis, and patients with the combination of peripheral arthritis and either psoriasis or inflammatory bowel disease. 

Neanderthals have been found with skeletal deformities known to be caused be ankylosing spondylitis and Arthritis.[13]


Neanderthals carried HLA-B27 which offers protection from certain diseases, however it also causes autoimmune diseases. CCR5-Δ32 deletion is also linked in with O negative blood. They originate in Neanderthals and are not often found in Africa. If you have Rh negative blood, you are blessed with some of the genes from our most ancient families.

Research by Tia Douglass & Andre Heyrman of NADA.

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


[1] Mark Kurlansky, The Basque History of the World, Penguin Books, New York, 2001.

[2] Robert J. Sawyer, Hominids, Tor Books, 2002.

[3] FAQs About Basque and the Basques,

[4] David Noel, Matrix Thinking, BFC Press, 1997. Chapter 104, Syston Boundaries and SIOS. Also at:

[5] The Rh-negative Factor and ‘Reptilian Traits’,

[6] Blood of the Gods,

[7] Philip Lieberman, Eve Spoke: Human Language and Human Evolution, W W Norton, 1998

[8] What is Basque?,

[9] Basque Pronunciation,

[10] Homo neanderthalensis,

[11] List of Neanderthal sites,

[12] What does it mean to be Rh negative?

[13] La Chapelle-aux-Saints 1 (also known as "The Old Man") is a partial skeleton of the species Homo neanderthalensis,

[14] Arthritis,