To make a little more sense, let’s go back a step, and start off by explaining what Secretor means using non-technical, plain-speak, OK lets-go!
A person who is a “Secretor” has cells in various locations throughout their body which release their blood-type antigens into bodily fluids, such as saliva and tears. As an example, they have cells in their tear ducts which can convert antigens into tears. Those very same antigens are also found in every other form of bodily fluid released by Secretors.
Am I More or Less Likely to be a Secretor?
Around 80% of people are Secretors*. The remainder of the population have a single gene which has undergone a mutation rendering it ineffective in terms of producing antigens in a free-floating form. They are therefore deemed non-secretors.
FYI – “Secretor status” is not another way of saying “blood type”, and our blood type has no bearing on the odds of us being a Secretor or not.
Does my Secretor Status indicate the potential for Illness or Disease?
If only it were that simple. Studies cited at the foot of this post highlight advantages and disadvantages of both Secretor Status types. Let’s take a look at some of the findings of those studies in the simplest possible terms.
It’s important to point out that the research [and the findings made] referenced below are not quantitative research, but discoveries made and reported by a limited number of credible peer reviewed studies.
- Interestingly, non-secretors seem to be less likely to get certain stomach illnesses, i.e. stomach ulcers and flu.* In particular stomach flu – studies reported that all of the people who became ill were Secretors, and a grand total of zero were non-secretors!
- The non-secretor type has been associated with some auto-immune diseases. The link between the non-secretor and inflammatory bowel disease being the most substantial.
- Studies link non-secretors with type 1 diabetes and psoriasis*.
- Secretors seem to be less likely to get yeast infections.*
- It has also been shown, (albeit not extensively), that Secretors are less likely to contract pneumonia or meningitis.*
Is it hard to test for Secretor Status?
No, it’s fairly simple and can be done from home. You can find out whether or not you are a Secretor by testing DNA or Saliva. We recommend a stand-alone Secretor Saliva Test as it’s more affordable and also easier to perform. This test is performed by nutriPATH™, an established laboratory serving practitioners for over 20 years here in Australia.
What’s the story with Blood Type Diets?
Blood Type Diets* should be approached with caution as they are mostly unproven. The premise of these diets is that our Secretor Status affects how we digest food and whilst that is plausible, the impact of Secretor Status with regard to our diet is not fully understood by science at this time.
Do I really need to know my Secretor Status?
What this all means is hard to understand. The question is, what would we change knowing your Secretor Status? Well, assuming you’re a healthy individual, it probably won’t affect the choices you make, but it may be fun to learn more about how our bodies work.
Gut Health is a very big deal these days with millions of dollars spent on research each year. It’s certainly possible our Secretor Status may yet be shown to play a larger role than previously understood. Until then, we just stay focused on eating well, sleeping well and the ultimate – hormone balance.
This information was brought to you by TestoChecker.
This post is not intended for use as clinical reference. Always see your GP (or other suitably qualified practitioner) with any concerns about your health.
Sources and Studies Cited:
- 80% of people are secretors: Kelly et al., “Sequence and Expression of a Candidate for the Human Secretor Blood Group α(1,2)Fucosyltransferase Gene (FUT2)”.
- Quantitative research defined: “The Function of Measurement in Modern Physical Science”. Kuhn, Thomas S. (1961). doi:10.1086/349468. JSTOR 228678.
- Non-secretors have lower risk of Norovirus infection (stomach flu): Thorven et al., “A homozygous nonsense mutation (428G–>A) in the human secretor (FUT2) gene provides resistance to symptomatic norovirus (GGII) infections”.
- Non-secretors have higher risk of meningitis: Blackwell et al., “Non-secretion of ABO antigens predisposing to infection by Neisseria meningitidis and Streptococcus pneumonia”.
- Non-secretors’ are linked to inflammatory bowel disease: Jostins et al., “Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease”.
- Non-secretor is linked to inflammatory bowel disease: McGovern et al., “Fucosyltransferase 2 (FUT2) non-secretor status is associated with Crohn’s disease”.
- Non-secretors have higher risk of pneumonia: Blackwell et al., “Non-secretion of ABO blood group antigens predisposing to infection by Haemophilus influenzae”.
- Being a non-secretor is linked to Crohn’s disease and psoriasis: Ellinghaus et al., “Combined analysis of genome-wide association studies for Crohn disease and psoriasis identifies seven shared susceptibility loci”.
- Being a non-secretor is linked to type 1 diabetes: Smyth et al., “FUT2 Non-secretor Status Links Type 1 Diabetes Susceptibility and Resistance to Infection”.
- Scientific reports non-supportive of blood type diets: Cusack et al., “Blood type diets lack supporting evidence: A systematic review”.
- Scientific reports non-supportive of blood type diets: Wang et al., “ABO genotype, ‘Blood-Type’ diet and cardiometabolic risk factors”.
- Non-secretors link to lower risk of Rotavirus infection (stomach flu): Imbert-Marcille et al., “A FUT2 Gene Common Polymorphism Determines Resistance to Rotavirus A of the P Genotype”.
- Non-secretors have lower risk of H. pylori infection (stomach ulcers): Ikehara et al., “Polymorphisms of Two Fucosyltransferase Genes (Lewis and Secretor Genes) Involving Type I Lewis Antigens Are Associated with the Presence of Anti-Helicobacter pylori IgG Antibody”.
- Non-secretors have higher risk of yeast infections: Chaim et al., “Association of Recurrent Vaginal Candidiasis and Secretory ABO and Lewis Phenotype”.