A genetic variant in the FUT2 gene controls whether or not you secrete your blood type into your saliva and other bodily fluids, such as your intestinal mucosa.
Whether you secrete your blood type plays a big role in the type of bacteria that dwell in our gut microbiome. Being a non-secretor can have both positive and negative impacts. For example, being a ‘non-secretor’ protects you from getting the norovirus – a.k.a. the dreaded stomach flu.
This article digs into the background science of secreting your blood type. Then it explains how to check your genetic raw data. Finally, we will wrap up with ‘lifehacks’ for dealing with being a non-secretor.
Non-secretors, the FUT2 gene, and health symptoms:
First, let me explain a little bit of the background science on being a ‘secretor’ or ‘non-secretor’ of your blood type – and then I’ll explain how to check your 23andMe or AncestryDNA raw data file for this information.
Oligosaccharides and Blood Type:
Oligosaccharides are a carbohydrate that consists of three to nine monosaccharides (simple sugars). You may be familiar with oligosaccharides as prebiotics in supplements or foods like chicory and Jerusalem artichokes.
Your body also makes oligosaccharides, and one of those oligosaccharides is what makes up your ABO blood type.
Yep – when you give blood, and they tell you that you have Type A or Type B blood, this means that your body produces a specific oligosaccharide that presents on your red blood cells.
What is a blood type secretor?
The FUT2 gene encodes the enzyme fucosyltransferase, which controls whether the oligosaccharides that make up your blood type will express in your bodily fluids (other than your blood).
For most people, the oligosaccharides that indicate your blood type are also found in your bodily fluids.
These bodily fluids that include most people’s blood type are:
- intestinal mucosa
- vaginal mucosa
But… About 20% of Caucasian and African populations are non-secretors of their blood type.
And it turns out that being a non-secretor affects how your body interacts with bacteria inside you and impacts your response to certain viruses.
Bifidobacteria, gut microbiome, and secretors:
Researchers consider Bifidobacteria to be one of the good guys when it comes to your gut microbiome. They are lactic and acetic acid-producing bacteria that help keep your immune system in check.
Bifidobacteria break down carbohydrates (specifically oligosaccharides) from the foods you eat. They also chow down on the oligosaccharides produced by our body in the intestinal mucosa. Your intestinal mucosa is what lines your intestines. It keeps your gut microbiome in the right place and away from your cells.
That is where secreting your blood type (an oligosaccharide) comes into play.
Pathogenic bacteria can’t get a grip:
Additionally, certain viruses, such as the norovirus, use the blood group glycans to attach to cells and enter them for infection. Thus, non-secretors are very unlikely to get sick from specific intestinal viruses.[ref][ref]
We’ll come back to this in a minute...first, check your genetic data to see if you are a secretor or a non-secretor.
Check your genetic raw data to see if you are a non-secretor
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FUT2 Gene: codes for fucosyltransferase enzyme
Check your genetic data for rs601338 (23andMe v4, v5; AncestryDNA (some)):
- G/G: blood type secretor
- A/G: blood type secretor
- A/A: non-secretor of blood type, lower amounts of bifidobacteria, resistance to norovirus
Members: Your genotype for rs601338 is —.
East Asian ancestry:
The SNP to check for secretor vs. non-secretor is different if you are of East Asian ancestry.
Check your genetic data for rs1047781 (23andMe v4, v5; AncestryDNA):
- A/A: “secretor” if Japanese or Korean ancestry
- A/T: “secretor” if Japanese or Korean ancestry
- T/T: “non-secretor” if Japanese or Korean ancestry[ref][ref][ref]
Members: Your genotype for rs1047781 is —.
Research on non-secretors:
So what’s the big deal about being a non-secretor? Well, a lot of it comes back to our body’s interactions with the microbiome.
Non-secretor microbiomes lack Bifidobacteria:
A 2011 study showed that non-secretors have significantly lower amounts of bifidobacteria in their gut microbiome. This makes sense because bifidobacteria are fed, in part, by the oligosaccharides in the intestinal mucosa. The same study showed that non-secretors also have a lower diversity of bacteria.[ref] Another study in 2014 confirmed those findings.[ref]
The good side of being a non-secretor: resistance to the norovirus!
Non-secretor status plays a role in infectious diseases as well. One big advantage of being a non-secretor is resistance to some viruses that cause what is commonly called the ‘stomach flu’.
- The norovirus and the rotavirus are much, much less likely to infect a non-secretor. Around 99% of non-secretors are protected from getting these infections![ref][ref]
- Children who are non-secretors are less likely to have diarrheal diseases. Some research indicates that just carrying one copy of the non-secretor allele can reduce the risk of diarrheal diseases in children.[ref]
- H. pylori colonization is also less in non-secretors.[ref] H. pylori bacteria resides in the stomach and can cause ulcers and stomach cancers.
Non-secretors are at an increased risk for certain diseases:
Secretor status also plays a role in non-infectious diseases, possibly through interactions with the gut microbiome. Non-secretors have a higher relative risk of:
- Type 1 diabetes[ref],
- alcohol-induced pancreatitis[ref],
- Crohn’s disease[ref][ref]
- adverse outcomes in premature infants[ref]
- symptoms from e. Coli infections[ref]
- slightly higher risk of the mumps[ref]
Keep in mind that this increase in risk is simply a statistical connection with relative risk. Being a non-secretor does not mean that you will automatically get diabetes or pancreatitis.
B12 Levels in non-secretors:
Non-secretors also often have higher serum B12 levels. It may not truly reflect the amount of B12 being transported into the cells, so a methylmalonic acid test may give you a better indication of your B12 status.[ref]
Oligosaccharides in breast milk:
Your microbiome began to develop at birth. An infant’s microbiome is, in part, colonized from the mother, and bifidobacteria usually make up a large part of an infant’s microbiome.
Breast milk contains oligosaccharides that feed the baby’s microbiome. Non-secretor mothers do not produce the 2′-FL oligosaccharide in their breastmilk, thus possibly impacting the baby’s microbiome.[ref]
Interestingly, babies born via C-section to non-secretor mothers have altered microbiomes.[ref]
The effects on non-secretor status can also influence breastfed babies of non-secretor mothers. A 2015 study found that “Infants fed by non-secretor mothers are delayed in the establishment of a bifidobacteria-laden microbiota. This delay may be due to difficulties in the infant acquiring a species of bifidobacteria able to consume the specific milk oligosaccharides delivered by the mother.”[ref]
In other words, if your mom is a non-secretor, your gut microbiome may be altered a little bit.
Related article: Leveraging your gut microbiome to change your gene expression
Lifehacks for non-secretors:
If you are a non-secretor, you may want to minimize the ‘downside’ while enjoying the fact that you are unlikely to get the norovirus.
Probiotics containing bifidobacteria:
Some clinicians recommend that bifidobacteria-containing probiotics are good for non-secretors. RenewLife’s Ultimate Flora has a high count of several types of bifidobacteria. VSL #3 is another probiotic that has good reviews and contains bifidobacteria. BifidoMax from Custom Probiotics is another probiotic with high bifidobacteria counts.
Prebiotics containing 2′-FL (2′-Fucosyllactose):
Mothers who are non-secretors do not produce the 2′-FL oligosaccharide in their breastmilk. This oligosaccharide is now available as a prebiotic via online and other sources. Various strains of bifidobacteria use 2′-FL as a food source, and those bifidobacteria then increase the amount of short-chain fatty acids produced in the gut microbiome.[ref]
Thus, combining bifidobacteria probiotics and a 2′-FL prebiotic may be beneficial for increasing short-chain fatty acids in the gut. (I’m making some assumptions here – but it may be worth trying if you are a non-secretor with gut problems…)
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Aghdassi, Ali A., et al. “Genetic Susceptibility Factors for Alcohol-Induced Chronic Pancreatitis.” Pancreatology: Official Journal of the International Association of Pancreatology (IAP) … [et Al.], vol. 15, no. 4 Suppl, July 2015, pp. S23-31. PubMed, https://doi.org/10.1016/j.pan.2015.05.476.
Azad, Meghan B., et al. “FUT2 Secretor Genotype and Susceptibility to Infections and Chronic Conditions in the ALSPAC Cohort.” Wellcome Open Research, vol. 3, Sept. 2018, p. 65. PubMed Central, https://doi.org/10.12688/wellcomeopenres.14636.2.
Bai, Yaqiang, et al. “Fucosylated Human Milk Oligosaccharides and N-Glycans in the Milk of Chinese Mothers Regulate the Gut Microbiome of Their Breast-Fed Infants during Different Lactation Stages.” MSystems, vol. 3, no. 6, Dec. 2018, pp. e00206-18. PubMed, https://doi.org/10.1128/mSystems.00206-18.
Bunesova, Vera, et al. “Fucosyllactose and L-Fucose Utilization of Infant Bifidobacterium Longum and Bifidobacterium Kashiwanohense.” BMC Microbiology, vol. 16, no. 1, Oct. 2016, p. 248. PubMed, https://doi.org/10.1186/s12866-016-0867-4.
Bustamante, Mariona, et al. “A Genome-Wide Association Meta-Analysis of Diarrhoeal Disease in Young Children Identifies FUT2 Locus and Provides Plausible Biological Pathways.” Human Molecular Genetics, vol. 25, no. 18, Sept. 2016, pp. 4127–42. PubMed, https://doi.org/10.1093/hmg/ddw264.
Graziano, Vincent R., et al. “Norovirus Attachment and Entry.” Viruses, vol. 11, no. 6, May 2019, p. 495. PubMed Central, https://doi.org/10.3390/v11060495.
Günaydın, Gökçe, et al. “Association of Elevated Rotavirus-Specific Antibody Titers with HBGA Secretor Status in Swedish Individuals: The FUT2 Gene as a Putative Susceptibility Determinant for Infection.” Virus Research, vol. 211, Jan. 2016, pp. 64–68. PubMed, https://doi.org/10.1016/j.virusres.2015.10.005.
Ihara, K., et al. “FUT2 Non-Secretor Status Is Associated with Type 1 Diabetes Susceptibility in Japanese Children.” Diabetic Medicine: A Journal of the British Diabetic Association, vol. 34, no. 4, Apr. 2017, pp. 586–89. PubMed, https://doi.org/10.1111/dme.13288.
Korpela, Katri, et al. “Fucosylated Oligosaccharides in Mother’s Milk Alleviate the Effects of Caesarean Birth on Infant Gut Microbiota.” Scientific Reports, vol. 8, Sept. 2018, p. 13757. PubMed Central, https://doi.org/10.1038/s41598-018-32037-6.
Kudo, T., et al. “Molecular Genetic Analysis of the Human Lewis Histo-Blood Group System. II. Secretor Gene Inactivation by a Novel Single Missense Mutation A385T in Japanese Nonsecretor Individuals.” The Journal of Biological Chemistry, vol. 271, no. 16, Apr. 1996, pp. 9830–37. PubMed, https://doi.org/10.1074/jbc.271.16.9830.
Leccioli, Valentina, et al. “A New Proposal for the Pathogenic Mechanism of Non-Coeliac/Non-Allergic Gluten/Wheat Sensitivity: Piecing Together the Puzzle of Recent Scientific Evidence.” Nutrients, vol. 9, no. 11, Nov. 2017, p. 1203. PubMed Central, https://doi.org/10.3390/nu9111203.
Lewis, Zachery T., et al. “Maternal Fucosyltransferase 2 Status Affects the Gut Bifidobacterial Communities of Breastfed Infants.” Microbiome, vol. 3, 2015, p. 13. PubMed, https://doi.org/10.1186/s40168-015-0071-z.
Magalhães, Ana, et al. “Muc5ac Gastric Mucin Glycosylation Is Shaped by FUT2 Activity and Functionally Impacts Helicobacter Pylori Binding.” Scientific Reports, vol. 6, May 2016, p. 25575. PubMed, https://doi.org/10.1038/srep25575.
Mankelow, Tosti J., et al. “Blood Group Type A Secretors Are Associated with a Higher Risk of COVID‐19 Cardiovascular Disease Complications.” Ejhaem, vol. 2, no. 2, May 2021, p. 175. www.ncbi.nlm.nih.gov, https://doi.org/10.1002/jha2.180.
Mills, Susan, et al. “Precision Nutrition and the Microbiome Part II: Potential Opportunities and Pathways to Commercialisation.” Nutrients, vol. 11, no. 7, June 2019, p. 1468. PubMed Central, https://doi.org/10.3390/nu11071468.
Morrow, Ardythe L., et al. “Fucosyltransferase 2 Non-Secretor and Low Secretor Status Predicts Severe Outcomes in Premature Infants.” The Journal of Pediatrics, vol. 158, no. 5, May 2011, pp. 745–51. PubMed, https://doi.org/10.1016/j.jpeds.2010.10.043.
Mottram, Lynda, et al. “FUT2 Non-Secretor Status Is Associated with Altered Susceptibility to Symptomatic Enterotoxigenic Escherichia Coli Infection in Bangladeshis.” Scientific Reports, vol. 7, Sept. 2017, p. 10649. PubMed Central, https://doi.org/10.1038/s41598-017-10854-5.
Rivière, Audrey, et al. “Bifidobacteria and Butyrate-Producing Colon Bacteria: Importance and Strategies for Their Stimulation in the Human Gut.” Frontiers in Microbiology, vol. 7, June 2016, p. 979. PubMed Central, https://doi.org/10.3389/fmicb.2016.00979.
Ruas-Madiedo, Patricia, et al. “Mucin Degradation by Bifidobacterium Strains Isolated from the Human Intestinal Microbiota.” Applied and Environmental Microbiology, vol. 74, no. 6, Mar. 2008, pp. 1936–40. journals.asm.org (Atypon), https://doi.org/10.1128/AEM.02509-07.
Taylor, Steven L., et al. “Infection’s Sweet Tooth: How Glycans Mediate Infection and Disease Susceptibility.” Trends in Microbiology, vol. 26, no. 2, Feb. 2018, p. 92. www.ncbi.nlm.nih.gov, https://doi.org/10.1016/j.tim.2017.09.011.
Tong, Maomeng, et al. “Reprograming of Gut Microbiome Energy Metabolism by the FUT2 Crohn’s Disease Risk Polymorphism.” The ISME Journal, vol. 8, no. 11, Nov. 2014, pp. 2193–206. PubMed, https://doi.org/10.1038/ismej.2014.64.
Tu, Li-Tzu, et al. “Genetic Susceptibility to Norovirus GII.4 Sydney Strain Infections in Taiwanese Children.” The Pediatric Infectious Disease Journal, vol. 36, no. 4, Apr. 2017, pp. 353–57. PubMed, https://doi.org/10.1097/INF.0000000000001446.
Velkova, Aneliya, et al. “The FUT2 Secretor Variant p.Trp154Ter Influences Serum Vitamin B12 Concentration via Holo-Haptocorrin, but Not Holo-Transcobalamin, and Is Associated with Haptocorrin Glycosylation.” Human Molecular Genetics, vol. 26, no. 24, Dec. 2017, pp. 4975–88. PubMed Central, https://doi.org/10.1093/hmg/ddx369.
Wacklin, Pirjo, Jarno Tuimala, et al. “Faecal Microbiota Composition in Adults Is Associated with the FUT2 Gene Determining the Secretor Status.” PLoS ONE, vol. 9, no. 4, Apr. 2014, p. e94863. PubMed Central, https://doi.org/10.1371/journal.pone.0094863.
Wacklin, Pirjo, Harri Mäkivuokko, et al. “Secretor Genotype (FUT2 Gene) Is Strongly Associated with the Composition of Bifidobacteria in the Human Intestine.” PLOS ONE, vol. 6, no. 5, May 2011, p. e20113. PLoS Journals, https://doi.org/10.1371/journal.pone.0020113.
Ye, Byong Duk, et al. “Association of FUT2 and ABO with Crohn’s Disease in Koreans.” Journal of Gastroenterology and Hepatology, vol. 35, no. 1, Jan. 2020, pp. 104–09. PubMed, https://doi.org/10.1111/jgh.14766.
Zhou, Feng, et al. “Association of Fucosyltransferase 2 Gene Variant with Inflammatory Bowel Diseases: A Meta-Analysis.” Medical Science Monitor: International Medical Journal of Experimental and Clinical Research, vol. 25, Jan. 2019, pp. 184–92. PubMed, https://doi.org/10.12659/MSM.911857.
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.