Effects of Warfarin/tPa [important]

Espaa_

Ku sali nabiga {scw}
@Espaa_

Chatgpt confirmed I'm VKORC1*2 Homozygote however the SNP rs61742245 is unfindable in my raw data.

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@giire12 Looks like 23andme doesnt genotype this mutation at all. Its incomplete. Doesnt shock me though because it is quite rare to get A/A so they dont really have a basis to test for it. Its quite sad as Somalis have this allele at a rate of 17% which is very high. i did ask chatgpt and this is what it gave me:

IMG_4272.jpeg


As for your result, it fits with the study. You are now the second person with VKORC1*2. You have a higher risk of dementia than @giire12 [not a lot just based on this gene, blood pressure is literally more of a factor than this]. Thank you so much for posting these results brother, i appreciate it!
 

Espaa_

Ku sali nabiga {scw}
One thing it did is that chatgpt was able to find i have recent admixture that Gedmatch and illustrative would mistaken me as ethiopians and eritreans

View attachment 360136

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View attachment 360138

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This next infromation it gave me was suprising but i suspect its likely not true.

Somali Grouprs9923231rs9934438rs7294rs17708472Profile Summary
Interior Nomads (e.g., Darod, Hawiye inland)C/C (wild-type)G/GG/GG/GFully East African VKORC1*1, normal warfarin dose
Northern Coastal (Zeila, Berbera)C/T (mixed)A/GA/G or G/GA/GMinor VKORC1*2 presence, moderate sensitivity
Southern Coastal (Benadiri, Reer Hamar)C/T or even T/T (rare)A/G or A/AA/GA/G or A/AHigher Eurasian influence, higher sensitivity
Barawani / Bajuni (Swahili-linked)C/T or T/TA/G or A/AA/AA/G or A/AStrong Eurasian + Bantu Swahili mixture, more sensitive
Ogaden (Deep Pastoralist)C/CG/GG/GG/GAlmost pure VKORC1*1, resistant to warfarin sensitivity
@TheLand This is very interesting [take it with a grain of salt]. It doesnt make sense how bajunis which are bantu admixed carry more non african alleles than ethnic somalis which do. Only difference id be able to see is a tiny tiny % between northerners and southerners and people in galbeed but not enough to make a tangible difference

thanks for posting this 🙏. I will write an email to whoever wrote this abstract because it has inconsistencies

this emphasises a need for more testing within our populations
 
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Espaa_

Ku sali nabiga {scw}
I'll need to read up on this, it seems I don't have Asp36Tyr(rs61742245) nor does my granny, she has the AG genotype.

rs9934438 AA → you are likely more sensitive to warfarin → need lower doses.
rs2359612 AA → the effect is less clear, but not dramatically different from normal for most people.
AG interesting. I would like to ask how you tested it. We have found some stuff in raw data from 23andme but it doesnt seem to contain this segment.
 
Somalis have a unique pharmacological profile. We're an understudied population, too.

I posted that specific study around when it came out (I think another guy did the same time), and focused more on the diabetes susceptibility.


Somalis really don't have Natufian-derived ancestry, and the autoimmune architecture in populations can shift through internal selection, drift, and whatnot. It is not 1:1. We're neither Natufian nor Nilotic, and we've had a stable Cushitic ancestry signature for ~8000 years. That is ample time to develop unique adaptation directions that make us respond differently to specific environmental pressures.

For example, we have only 23-24% of lactase persistence genetics that are mapped, but over 75% can consume milk. There are a lot of things we don't understand. Dinkas have high consumption yet have 0%. Take the Nubians. They have much lower milk consumption -- similar to Europeans-- their lactase persistence frequency matches the milk consumption, where experience of malabsorption arises for those that lack these LP alleles.

For intermediate populations, you can see phenotype expressions that can fluctuate widely between two hypothetical poles, with several unique pathways also adding to the dimensions. Certain traits of Somalis in the genetic diversity could be entirely African or Eurasian. There has to be genomic research. Ashkenazi Jews have a unique response to things as well, and they are punching above their demographic weight in their public health concerns, being relatively overrepresented.
 

Espaa_

Ku sali nabiga {scw}
Somalis have a unique pharmacological profile. We're an understudied population, too.

I posted that specific study around when it came out (I think another guy did the same time), and focused more on the diabetes susceptibility.


Somalis really don't have Natufian-derived ancestry, and the autoimmune architecture in populations can shift through internal selection, drift, and whatnot. It is not 1:1. We're neither Natufian nor Nilotic, and we've had a stable Cushitic ancestry signature for ~8000 years. That is ample time to develop unique adaptation directions that make us respond differently to specific environmental pressures.

For example, we have only 23-24% of lactase persistence genetics that are mapped, but over 75% can consume milk. There are a lot of things we don't understand. Dinkas have high consumption yet have 0%. Take the Nubians. They have much lower milk consumption -- similar to Europeans-- their lactase persistence frequency matches the milk consumption, where experience of malabsorption arises for those that lack these LP alleles.

For intermediate populations, you can see phenotype expressions that can fluctuate widely between two hypothetical poles, with several unique pathways also adding to the dimensions. Certain traits of Somalis in the genetic diversity could be entirely African or Eurasian. There has to be genomic research. Ashkenazi Jews have a unique response to things as well, and they are punching above their demographic weight in their public health concerns, being relatively overrepresented.
If its okay, please link your post on diabetes susceptibility. [oh wait you did I didnt look closely enough] I personally do not want to make a post on it since I lowkey find it boring and I would be more than happy to add to your research![your research needs to come alive again, it needs a proper discussion] You are right in that somalis dont really descend from those populations and that we have our own unique genetic genome as in my research I struggled to explain the high frequency of VKORC1*4 as it neither comes from Natufian related ancestry nor Nilotic related ancestry.

genes are not the only thing ofc. This is the classic nature vs nurture argument/which came first the chicken or the egg argument. There are many many many many things that scientists havent even discovered yet as we are so complex subhanallah. Some things dont even make sense even in the human body like why do we have an appendix

Ashkenazi Jews are lowkey inbred with diseases that are unique to them. The BRCA genes is just one of many. Because of this, many geneticists studied their dna as its something unheard of in human populations. But yes you are right, they are wayyyy too overrepresented
 
If its okay, please link your post on diabetes susceptibility. [oh wait you did I didnt look closely enough] I personally do not want to make a post on it since I lowkey find it boring and I would be more than happy to add to your research![your research needs to come alive again, it needs a proper discussion] You are right in that somalis dont really descend from those populations and that we have our own unique genetic genome as in my research I struggled to explain the high frequency of VKORC1*4 as it neither comes from Natufian related ancestry nor Nilotic related ancestry.

genes are not the only thing ofc. This is the classic nature vs nurture argument/which came first the chicken or the egg argument. There are many many many many things that scientists havent even discovered yet as we are so complex subhanallah. Some things dont even make sense even in the human body like why do we have an appendix

Ashkenazi Jews are lowkey inbred with diseases that are unique to them. The BRCA genes is just one of many. Because of this, many geneticists studied their dna as its something unheard of in human populations. But yes you are right, they are wayyyy too overrepresented
I'm not an expert in this, and my understanding of diabetes is very limited. I think your post is important, and I'd look forward to your weekly posts.

Nurture and nature is the wrong perspective. There is no nurture without nature, and DNA only has function in the environment. We cannot test it without the constraints of the environment. There would be no use in doing it either. Then again, in many ways, in complex genetic systems that do not deal with narrow disease-gene pathways, let's say intelligence, it's impossible to completely control for DNA in a non-linear environment. Most studies on human intelligence that are not hyper-focused are fraudulent.

DNA only has function through the environment, and that is how we understand it in the first place. The environment gives DNA its dimensions and definitions, its range, and in a suite of genes, their polygenic conditions; those dimensions that equal behavior become wider and move according to the environment for adaptation, i.e., the parameters move within a broader system making the brain specialize in new requirements and acclimations, i.e., i.e, the flynn effect. But this is somewhat of a digression, so I'm going to end it here.
 

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