Food intolerances – using your genes to eat and live better?

The food you eat every day determines your health more than you might think, or at least it should. If you’re not eating the right food, you’re missing out on the nutrients your body needs and this can lead to all kinds of health issues.

We are what we eat and what we eat impacts us in a myriad of ways. From the time we’re born, our bodies are in a state of constant flux, with our food supply frequently shifting with the seasons, all of which is important to note when you’re trying to get the most out of your efforts to eat and live better.

I have a history of food intolerances. I used to get headaches, bloating, and diarrhea when I ate certain foods, and now I am a lot more careful about what I eat. You may have heard that food intolerances are hereditary, but does that mean that you can’t reverse them? Does it make sense to give up on the foods that make you feel good? Let’s explore some of the research on food intolerances and how they can affect our health.

Chapter 9

Intolerance to certain foodss were discovered.

This chapter will teach you the following:

We’ll look at the following topics in this chapter:

  • basic immune system and inflammatory reactions physiology;
  • what causes food allergies, intolerances, and sensitivities; how food allergies, intolerances, and sensitivities operate;
  • how our genes may influence these; and
  • what you may learn about your sensitivities to certain meals from genetic testing

We’ve looked at whether there is a single “optimal diet” in previous chapters. It should be evident by now that there isn’t.

There are two key factors to remember while you read:

  • While science is fascinating, and we have some intriguing genetic discoveries and topics for additional research, we still know a lot.
  • Just because a genetic test can tell you if you’re at risk for certain food sensitivities doesn’t imply it can provide you the “ideal” diet.

Also, keep in mind our normal warning:

There are many complex, linked aspects in most preferences, health risks, and hereditary features.

There is almost never a single gene that causes a specific outcome.

Any genetic information we provide is merely a starting point for further investigation.

Almost everyone has consumed something that “didn’t agree with us” in some fashion.

Of course, this does not imply that we are particularly sensitive.

It’s possible we should have said “no” before the third pound of suicide-spice chicken wings arrived.

Aside from situations where we should have known better, many people find that certain, seemingly harmless items — such as bananas, avocados, berries, shrimp, eggs, and so on — are simply awful for them.

We could call these “food sensitivities” or “food intolerances” in general, but we need to be careful with our terminology.

It’s critical to distinguish between a food allergy, a food sensitivity, a food intolerance, and a specific disease with a genetic basis, such as celiac disease or Crohn’s disease.

It’s also crucial to remember that, like other chronic diseases, these and associated digestive and immunological disorders are polygenic (meaning multiple genes play a role) and result from complicated interactions between genes, behaviors, and the environment.

Inflammation, antibodies, and immunoglobulins

An antibody is a type of protein produced by the immune system in response to the identification of a foreign substance known as an antigen by the immune system. Antibodies aid in the detection of infections (such as bacteria or viruses), allergies, and poisons.

Antibodies are also referred to as immunoglobulins and are abbreviated as “Ig.” IgA, IgD, IgE, IgG, and IgM are the five major antibodies.

Antibodies are Y-shaped proteins with a similar overall structure, but their tips differ significantly. This aids in the identification of a specific antigen.

Antibody structure and antigen binding sites

Antibody structure and antigen binding sites (Figure 9.1)

If our bodies believe a specific item or component of a food is toxic or foreign, they will produce a targeted antibody to protect us.

These immunoglobulins can build up over time as a result of frequent exposure, resulting in a physiological response. This reaction can be acute (rapid, abrupt, and typically dramatic) or chronic (ongoing, persistent, often lower-grade).

Inflammation is usually present as part of the reaction.

Inflammation can be localized, affecting only a small part of the body, such as a patch of skin. It can also be systemic, affecting many sections of our physiology including our respiratory system, joints, neurological system, and/or digestion.

Redness, swelling, rashes, hives, or a mix of these symptoms can often be seen as inflammation develops in real time. Inflammation can also be detected chemically by the presence of certain chemicals such as interleukins (IL), histamine, prostaglandins, and so on.

Our genes, of course, influence the expression of all of these.

Immune and inflammatory responses come in a variety of forms.

It might be difficult to distinguish between different forms of food-related immune and inflammatory responses since their symptoms (such as stomach pain or diarrhea) are so similar. Furthermore, persons can have multiple health issues (for instance, a food allergy plus celiac disease).

Allergies to foods

An allergen is a substance that triggers a histamine reaction, often known as an immunoglobulin E (IgE) immunological response. When white blood cells (mast cells and basophils) are exposed to an allergen, histamine molecules are released, causing an inflammatory reaction such as:

  • hives;
  • swelling;
  • respiratory problems; and
  • a reduction in blood pressure that occurs suddenly

Allergies are often described as “sudden and severe.” IgE levels rise quickly, but then fall swiftly, usually vanishing within a few days (though it can last up to a week or two).

Food allergies, like other allergies, appear to be passed down through families. This shows that our allergy risk is inherited to some extent.

Sensitivity to foods

Food sensitivities are more commonly associated with symptoms such as abdominal pain and bloating, which are caused by immunoglobulin G (IgG) rather than IgE, as in allergies. IgG responses are more time consuming than IgE responses, taking hours or even days to manifest.

IgG levels are higher in people with inflammatory bowel syndrome / illness (IBS / IBD), Crohn’s disease, and ulcerative colitis than in healthy controls. Other tissues that IgG antibodies can infiltrate and harm include the pancreas, thyroid, respiratory system, kidney, lymph nodes, and salivary glands.

Food intolerance

Other types of food intolerances, such as lactose intolerance (seen below), are often caused by a lack of the appropriate enzymes (for instance, lactase). We can’t digest some foods effectively if we don’t have enough of a specific enzyme.

Symptoms of autoimmunity

Celiac illness is a type of celiac disease that and gluten sensitivity

Gluten is a protein that can be found in wheat, rye, and barley. Prolamins are a type of storage protein made up of two proteins: gliadin and glutenin. (Hordeins are barley prolamins, secalins are rye prolamins, and avenins are oat prolamins.)

Gluten is the protein that gives wheat its elasticity and viscosity, allowing it to be used to make bread, pasta, and other baked foods.

You’ve probably heard the terms “gluten intolerance” and “gluten allergy.” You may have heard that gluten is the source of all disease and dysfunction in humans. (Get out of here, money and power!) Gluten is the town’s new gangster!)

Humans, like everything else, are diverse.

Some people, especially those with strong immune systems, appear to be able to eat anything. They happily eat from the bread basket, crumbs dropping from their mouths, seemingly undisturbed.

Others have reported intolerance to gluten and other comparable proteins found in wheat. Perhaps their joints pain a little; perhaps they have a stuffy nose; perhaps they have a rash on their skin.

Even trace levels of gluten or the proteins in other grains cause a significant, rapid reaction in a few people.

Gluten and other grain protein sensitivity, like other food sensitivities, can manifest itself in a variety of ways, ranging from moderate to severe.


Of obviously, genetics plays a role in at least some of this. However, we do not yet know all of the elements at play.

Celiac disease

Gluten causes Celiac disease, which is an autoimmune illness. Because it’s autoimmune, the immune system assaults the body’s own healthy tissues, symptoms can extend across the entire system.

Genes linked to autoimmune can play a variety of roles, as we saw in our chapter on metabolism and thyroid autoimmunity. Many autoimmune illnesses share genetic components, and there is no unique “autoimmunity gene,” as seen here.

Our risk for celiac disease appears to be polygenic, like with most diseases. Genetic factors are thought to account for roughly 55 percent of celiac disease cases, according to study.

Not unexpectedly, studies have discovered correlations between celiac disease and various genes involved in immunological and inflammatory responses, such as:

  • The C-C chemokine receptor type 3 is designated by the code CCR3. Chemokines are a sort of cytokine, or cell signaling molecule, that instructs other cells to migrate to a certain location, such as the infection site. The CCR3 protein is abundantly expressed in immune system cells such as eosinophils and basophils (white blood cells), T-helper cells, and airway epithelial cells.
  • HLA-DQ, which we’ll go over in more detail later.
  • Interleukin 12A (IL12A) is a gene that codes for a protein (interleukins are a family of cytokines). T-helper cells’ activity are directed by IL12A.
  • Interleukin 18 receptor accessory protein (IL18RAP) is a gene that genes for interleukin 18 receptor accessory protein. It plays a role in IL-18 binding and signaling. Inflammatory bowel and Crohn’s illnesses, as well as leprosy and atopic dermatitis, have all been associated to variations in this gene.
  • MYO9B is a gene that genes for myosin IXB, a protein that helps keep the intestinal lining intact. Inflammatory bowel disease has also been linked to it. People with MYO9B variations may have greater intestinal permeability, sometimes known as “leaky gut.”
  • PFKFB3, a gene that encodes a protein involved in cancer progression, circadian clocks, autophagy, and insulin signaling.
  • Protein kinase C (PRKCQ) is a protein involved in T-cell immune system signaling.
  • Protein tyrosine phosphatase, receptor type K (PTPRK) is a protein that is involved in cell growth, differentiation, migration, and division. The presence of this protein has been linked to the development of some cancers.
  • Regulator of G-protein Signaling 1 (RGS1) is a gene that has been used as a marker of intestinal tissue quality in colorectal cancer research. It’s also been connected to multiple sclerosis and mental health (along with IL12A).
  • Remember SH2B3 from Chapter 6’s discussion of metabolism and autoimmune thyroid disease? He’s reappeared!
  • TAGAP is a gene that codes for a T-cell signaling protein that, like the other genes on this list, has been associated to autoimmune diseases such rheumatoid arthritis, Type 1 diabetes, and multiple sclerosis.
  • THEMIS-coded proteins are involved in T-cell maturation, can be found in lymphoid organs, and are abundant in celiac disease.

These genes, as well as others like them, are likely to have a role in a range of immune system functions.

Type 1 diabetes and celiac disease, for example, share HLA-DQ, IL2/IL21, CCR3, and SH2B3 SNPs in European populations. Vitamin D also appears to have an interaction with IL2RA and TAGAP.

Of course, there isn’t a test for this.

Just to give you an idea, it’s difficult.


In Chapter 6, we discussed the human leukocyte antigen (HLA) gene complex, which codes for major histocompatibility complex (MHC) proteins in humans.

Our immune system is regulated by these proteins, which are located on the surfaces and membranes of cells.

HLA-DQ is a sort of protein found on the membranes of antigen-presenting cells, which alert other immune system cells (such as T cells) that there’s a problem (such as a pathogen) and that it’s time to go to work.

The HLA-DQ2/DQ8 heterodimers appear to be the most important genetic risk factor for celiac disease (molecular complexes of two macromolecules stuck together).

When immune cells with HLA-DQ2 or DQ8 on their membranes come into contact with gluten (for example, in the small intestine), the immune system may mistakenly tell the immune system to fight the threat, which in this case is healthy tissues. This causes celiac disease symptoms including stomach pain and diarrhea.

Other genetic variants, as we’ve seen, may also play a role. So far, a few dozen factors have been identified. Some genes appear to be affected only in adults or children with celiac disease, implying that the genetic expression of the disease may differ with age.

Although not everyone with genetic abnormalities will develop celiac disease, the majority of celiac disease patients appear to have certain genetic variants in common.

For example, 23AndMe uses an SNP called rs2187668 in one of the genes encoding HLA-DQ2.5 to test for a subtype of HLA-DQ2 called HLA-DQ2.5.

This subtype is found in approximately 15% of the general population but over 90% of persons with celiac disease, albeit only about 3% of people with this exact variation will acquire celiac disease.

rs6822844, an SNP in a gene block (KIAA1109/Tenr/IL2/IL21) that, along with another SNP in the same area (rs13119723), is highly linked to autoimmune disease, particularly celiac disease, is also tested by 23andMe.

Celiac disease’s prevalence varies with area and demographic, as it does with many chronic diseases with a strong genetic component.

Celiac disease is most common among people of European ancestry (North America, Europe, Australia, and parts of South America), as well as in people of Indian ancestry. It is relatively uncommon in most Asian native communities.

Despite this, the prevalence of celiac disease is rapidly growing. This suggests that additional physiological or environmental factors (such as the health or variety of our gut flora) may be involved.

Getting diagnosed with celiac disease is a difficult process. Patients must consume more gluten in order to build enough antibodies to show up on a lab test. If you already have a sensitivity, you can picture how that feels. If you have a bee venom allergy, it’s like having to get stung by even more bees.

As a result, genetic testing is a lot more pleasant alternative in this scenario. However:

  • The answer would remain the same: eliminate gluten from one’s diet.
  • Gluten sensitivity that isn’t caused by celiac disease (sensitivity to gluten without overt antibodies) appears to exist, according to research.
Non-celiac gluten sensitivity

Wheat and other grains are problematic for the majority of our co-author Krista’s extended family. They have rashes on their skin, coughs and sneezes, and sometimes gastrointestinal hemorrhage (in worst cases). You’d think this would be an apparent case of celiac disease caused by genetics, and it might be in some cases.

Krista also avoids wheat because the link between it and inflammatory symptoms is well-established. Krista’s 23andMe celiac risk test, however, revealed that she had half the typical risk of celiac disease based on a few key markers.

So, what’s the deal?

Is Krista’s family made of entirely of hypochondriacs who despise pasta?

Is there a different explanation?

Many other frustrated people who know they don’t react well to wheat may have been advised that they don’t have true celiac disease and should therefore stop whining (so to speak).

In fact, we’re learning that non-celiac gluten sensitivity (NCGS) might be a concern as well.

We don’t observe the same molecular indicators (such immunoglobulin A, or IgA, antibodies) or intestinal tissue loss that we see in full-blown celiac disease with NCGS, but we do see inflammation.

There is currently no direct-to-consumer test for NCGS, but we can look in research labs to see if inflammatory markers (such interleukins or immune system proteins) are raised.

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However, more than half of persons with NCGS have genetic variants that are identical to those seen in those with full-blown celiac disease, and both NCGS and celiac disease sufferers are substantially more likely to have these variants than the general population.

What we discovered in our research

Each copy of a thymine (T) increases celiac risk in the HLA-DQA rs2187668 SNP examined by 23andMe. As a result, TTs (thymine-thymine) are the most vulnerable.

We had no TTs in our sample, but CT (cytosine-thymine) was found in roughly 16% of it, indicating a somewhat higher risk.

Several people stated that they were “definitely” wheat intolerant. Four of them got a celiac test, indicating that they had adequate wheat intolerance symptoms to rule out celiac disease.

None of these wheat-intolerant people, however, were CTs. All of them were CCs, celiac disease’s lowest-risk group.


  • All of the participants who stated they were “definitely” intolerant to wheat were CCs, which are the people who, in theory, shouldn’t have any issues.
  • A few respondents stated that they were “definitely” not intolerant and could easily break croissants. The most were, predictably, CCs, but one was a CT.

What does this mean to you?

  • Consult your doctor if you suspect you have celiac disease. Other tests can also confirm if you have active antibodies to gluten. Genetic testing can help you see if your risk of celiac disease is increased, but other tests can also confirm whether you have active antibodies to gluten.
  • Even if you don’t have celiac disease, research suggests that you may be sensitive to gluten or other similar proteins. This could be inherited, but it could also be caused by a range of other variables, including your lifestyle, gastrointestinal health, and surroundings.
  • Consider working with a nutrition coach or dietitian to come up with menus that suit gluten intolerance or other food sensitivities.

Food sensitivities

Lactose tolerance / lactase persistence

Lactase is an enzyme produced by the small intestine’s brush border cells that aids in the digestion of lactose, a sugar found in milk.

When we are born, almost everyone can digest lactose. We have to because breast milk is our sole source of nutrition. However, not everyone retains this capacity as they get older.

Lactase persistence, or the ability to generate lactase throughout adulthood, is nearly entirely dictated by our genes, while other factors (such as gut bacteria) can influence how we digest milk and dairy.

The lactase gene has remained quite widespread in Europeans, particularly northern and western Europeans (such as Scandinavians and Irish), which likely reflects the importance of milk and dairy diets for European cultures. The same can be said for specific farming populations in eastern/northern Africa, the Middle East, or northeast Asia, where dairy consumption and herding are common.

Other populations, such as those with Southeast Asian descent, who don’t consume as much milk and dairy, are less likely to possess this gene.

Lactose intolerance is, in fact, more of a global standard than an exception. According to some estimates, over 65 percent of adults globally are lactose intolerant.

Who can drink milk? Global rates of lactase persistence

Figure 9.2: Who is allowed to consume milk? Lactase persistence rates around the world

Lactose digestion is thought to have developed separately in different populations.


Many distinct alleles of LCT, the lactose tolerance gene, are known to alter this ability at the time.

These alleles are found in a variety of haplotypes. This indicates that the result (whether or not a person can digest lactose) is the same, but the cause (a specific gene mutation) varies depending on a person’s heritage.

Consider the following scenario:

  • Tibetans, who traditionally herded cattle and yaks, may have developed 13838G/A, 13906T/A, and 13908C/T variants independently.
Interesting tidbit!

Tibetans have also created a hybrid called a dzo by crossing domestic cattle (Bos primigenius) with yaks (Bos grunniens).

  • 13910*T (also known as rs4988235) is found in Europeans and is almost fully correlated with lactose tolerance. This variety is very never found in Sub-Saharan African people, yet it is found among Sudanese Fulani who moved from western Africa. It’s also found in populations in South America that have been colonized by Europeans.
  • 13907*G, an East African variant seen in Afro-Asiatic Beja and Afro-Asiatic Kenyan people.
  • 13915*G, the founder mutation for Saudi Arabians and Bedouins’ abnormally high lactase persistence, which may not be related to cow’s milk but rather camel’s milk. (Despite their great lactose tolerance, the typically European 13910*T mutation does not seem to show up in this population.)
  • −14009 T>G, one of a few Ethiopian variations.
  • In Kenya and Tanzania, 14010*C is usually found in a single haplotype (known as Nilo-Saharan, from people who lived along the Nile and Sahara).

Other potential variants that are still being investigated are:

  • −13779 G>C, found to date only in Amhara people (aka Abyssinians) originating in the northern and central highlands of Ethiopia.
  • Only seen among Ethiopian milk drinkers, 13806*G is really linked to non-digestion.
  • −13909 C>T, another European variation.

You may recall that in the previous chapter, we discussed ethnic ancestry. Surface traits (such as skin color) don’t reveal much about a person’s entire gene pool.

The finding that at least seven separate uncommon alleles are linked to lactase persistence in one small ethnic group supports this theory (Somali cattle herders from Ethiopia). Simply lumping this group into a large category termed “African” or “black” would be meaningless at best in terms of comprehending genetic variance.

Enhancers and MCM6

There is evidence that linked mutations in the minichromosome maintenance complex component 6 (MCM6) could possibly have a role, in addition to changes upstream of the LCT gene.

MCM6 has two of the regulatory areas for lactose digestion, despite the fact that it has no direct effect on lactose digestion.

You may recall that in Chapter 2, we discussed how genes are generated, the process that controls whether or not a gene is made, and the enhancer, a vital section of DNA.

Because you don’t want all the genes to be created at the same time, enhancers for individual genes are distinct. Depending on the situation, you want some to be turned on and others to be turned off.

If enhancers differ genetically, so may the expression of other genes.

This is what happens when the LCT gene interacts with MCM6. Some persons have an SNP (rs49882359) in the MCM6 gene that causes the LCT enhancer to become more active, resulting in the expression of the LCT gene and most lactase.

Sweepstakes, spreads, and picks

These genetic variations, as well as the other probable variations that have yet to be discovered, provide convincing evidence of convergent evolution, or the emergence of a trait more than once (rather than developing in a straight linear path).

Consider the concept of food in a “wrap” configuration as an example of convergent evolution.

Sushi hand rolls, rice paper wraps, dosas, crepes, burritos, shawarma, and other wrap-type meals, for example, have all originated separately in international cuisines. Sushi did not develop directly from burritos (though we now have the sushi burrito, another of Nature’s marvels).

In this example, distinct populations are capable of producing lactase, but through different mechanisms.

Some of these variations also show signs of a selective sweep. A selective sweep occurs when a certain variation becomes substantially more common in a population, to the point that the alternative is completely lost. A gene’s form is deemed to be “fixed” if it has been found in 100 percent of the population.

Selective sweeps occur when an advantageous mutation appears to be rare at first, but quickly spreads through the population, displacing genetic competition. This frequently occurs when environmental conditions shift in favor of a new mutation.

If the temperature suddenly changes, for example, genes that were previously neutral but now help the organism adapt to the new environment are likely to propagate.

Everyone with the genes for a furry coat, short limbs, and plenty of subcutaneous fat will be left standing when the Ice Age strikes, while those with the genes for squeaky-smooth-as-a-dolphin skin, lanky heat-dispersing limbs, and six-pack abs will be quickly wiped out.

Lactase persistence is an example of positive selection, which occurs when a genetic mutation encourages the evolution of novel phenotypes by providing a benefit. (Another sort of selection is purifying selection, which helps maintain the phenotypic of an established phenotype.)

Lactase persistence may have developed repeatedly across different groups because it was beneficial to pastoral populations that consumed a lot of milk and dairy from cows, sheep, goats, and camels.

This notion appears to be supported by genetic studies, as populations with higher lactase persistence also prefer to consume milk and dairy on a regular basis. (Imagine Northern Europe without cheese or yogurt — no Icelandic skyr, British Stilton, or Swiss fondue, for example.)

Lactase persistence does not appear to have been very strong in early humans. The genetic differences that allow some of us to like ice cream and milkshakes have only been around for a few thousand to 25,000 years (some estimates even put it around 3,000 years ago).

This shows that humanity actively adapted to agricultural advancements, commonly known as “figuring out how to get animals to stand still long enough for us to milk them.” Consistent nutritional pressure in a small population can actually help us create genetic changes rather quickly, possibly between 150-400 generations.

For certain populations, the milk-lactase persistence link isn’t true.

Despite ingesting dairy, Dinka and Nuer people in Sudan and Somalis in Ethiopia do not appear to have lactase persistence. Gut bacteria may also be assisting lactose-intolerant people who eat dairy but don’t seem to have any problems digesting it.

What we discovered in our research

The rs4988235 SNP of the LCT gene is tested by 23andMe. Lactose intolerance is more common in the GG (guanine-guanine) type.

Having the GG variant did appear to indicate dairy intolerance in this situation. GGs made up the majority of those who reported they had trouble digesting dairy.

As a result:

  • Lactose tolerance remained variable. One gut-of-steel GG reported they had no issues with dairy, while others said their tolerance was inconsistent.
  • Some AAs (adenine-adenine, the lowest-risk group) also reported digestive issues with dairy, though none were as severe as some of the GGs.
AG or CT?

We came upon something confusing while writing up our results for the rs4988235 SNP of the LCT gene and checking both 23andMe and Nutrigenomix’s reports.

  • The A/G SNP variations were listed by 23andMe. In other words, the three choices are AA, AG, or GG.
  • They are classified as C/T by Nutrigenomix. In other words, the three choices are CC, CT, or TT.

Which of the two options was correct?

Both of them, it turns out.

The term “reference genomes” is used in genetic analysis.

If you want to know what version a person has, you need to know what they differ from.

The Genome Reference Cooperation, an international consortium of scientists from some of the world’s finest academic institutions, has produced and released a set of reference genomes.

GRCh38.p11 (GRC human genome build 38, patch level 11) is the current human reference genome, which was released in July 2017.

(Use that tiny tidbit to start a lively discussion at a cocktail party!) It’s a hit with the crowd!)

Keep in mind that DNA has two strands that are complimentary.

If you see an A on one strand, you may be sure there’s a T in the same spot on the opposing strand. If one has a C on it, you can bet it has a G pal.

When a reference genome build is released, the opposite strand is sometimes used.

Because SNP identifiers are unique to each genome build, a site may be reported as A in one build because one strand has been sequenced, but T in the next build because the complementary strand has been sequenced.

This is great for determining SNP variation because the location varies and you don’t care.

However, regardless of the reference genome, 23andMe always utilizes the letter on the forward (i.e., transcribed) strand.

This is a unique option. The genotypes defined in the reference genome are used in the majority of scientific and clinical literature.

But it’s easy to see why 23andMe would make this choice: it’s simple to say, “This is the A or T that gets transcribed, so this is the one we’ll use.”

What does this mean to you?

  • It’s possible that your inability to digest lactase is inherited.
    • The rs4988235 SNP of the LCT gene is tested by 23andMe.
  • You have a few options if you still want to eat dairy but it causes you problems.
    • Lactase tablets or lactose-free milk are two options.
    • Fermented dairy (yogurt, kefir, etc.) may be OK because the bacterial fermentation process tends to break down carbohydrates. A probiotic supplement may also be beneficial.
  • Depending on your heritage, you may be able to digest lactase due to one (or more) of a number of distinct gene variants. Congratulations! Thanks to convergent evolution, you can enjoy your lattes.
  • There are a variety of other reasons why you can be lactose intolerant. Your gut bacteria, for example, can play a role, as can your sensitivity to other proteins in dairy.
  • Consider working with a nutrition coach or nutritionist to come up with meal alternatives and techniques to fit your food needs if you’ve been diagnosed with lactose intolerance or other food sensitivities.

Fructose intolerance is a condition that is passed down through the generations.

Hereditary fructose intolerance (HFI) is a genetic disorder in which people are unable to adequately break down fructose. Fruit, as well as many processed meals, contain fructose (such as soda).

People with HFI don’t produce enough aldolase B, a fructose-metabolizing enzyme encoded by the ALDOB gene. Our systems can’t efficiently turn sugar into energy if aldolase B isn’t operating, which can lead to hypoglycemia (low blood sugar).

If left untreated, hypoglycemia can lead to seizures, coma, and death. Furthermore, partially digested fructose molecules accumulate in the tissues, causing toxicity and liver and kidney damage.

People with HFI may have a natural aversion to sweets and fruit, which means they may never be adequately diagnosed. This also implies that researchers are unsure of the true prevalence of HFI.

HFI is an autosomal recessive disorder, meaning that a person must inherit two copies of the ALDOB gene mutation that causes the problem in order to develop it. While it can be fatal if not managed appropriately, persons who avoid fructose can live a healthy and symptom-free life.

At least 40 mutations in the ALDOB gene have been related to HFI.

In people of European descent, 23andMe looked at four of the most prevalent ALDOB mutations:

  • rs1800546, also known as A149P (which accounts for about 65 percent of all HFI-causing mutations in this population)
  • rs76917243, also known as A174D (accounting for about 11-14 percent of mutations)
  • rs78340951, also known as N334K (about 5-8 percent )
  • delta4E4 (rs387906225) (about 3 percent )

These mutations account for almost 75% of the HFI-causing mutations in this group.

What we discovered in our research

Fortunately for our PN team, no one has tested for two of the ALDOB HFI mutations: rs1800546 and rs76917243.

What does this mean to you?

  • Consult your doctor if you’re concerned about HFI. Even if your genetic tests for these variations are negative, you could still have an ALDOB mutation or HFI.
  • Even if you don’t have HFI, eating certain types of carbohydrates known as FODMAPs (fermentable oligo-, di-, mono-, and polyols) might cause digestive problems. Fructose is a member of this category.
  • Consider working with a nutrition coach or nutritionist to come up with menu alternatives and techniques to meet your food needs if you’ve been diagnosed with HFI or if you’re noticing other food sensitivities.

What’s next?

We’ll look at how hereditary variables other than dietary intolerances or sensitivities can influence how we absorb and use nutrients in the future chapter.

Food intolerances are real. And they can have drastic consequences on your health. If you’re someone who can’t quite stomach certain foods, you may find it hard to eat healthily. But don’t despair, science has some answers – and there is hope. Using your genetics to make healthier food choices is the best way to beat food allergies and intolerances.. Read more about what happens to dna in food when you eat it and let us know what you think.

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Frequently Asked Questions

Do your genes influence what you eat?

Yes, your genes can influence what you eat.

How do you deal with food intolerances?

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How our genes can shape our response to nutrition?

The genes that are responsible for our response to nutrition can be found in the DNA. Genes are the building blocks of life and they code for proteins, which are the molecules that make up a cells structure.

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