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So That's Why · Yesterday · 24 min

Why Do We Get Allergies?

obody has ever been born with an allergy, so why do so many of us get them? Jen, Chris and Matt explain the moment it happens. In this episode of So That’s Why, the team tackles a question that sounds simple but hides a lot of clever biology. Not reacting to pollen, dust mites or cat dander turns out to be an active decision your immune system makes thousands of times a day. Allergies happen when that decision goes the other way. The team looks at what twin studies reveal about how much of allergy risk is inherited, why the gut bacteria a baby has at one month old can matter years later, and why the famous “we’re too clean” hygiene hypothesis is roughly right but not for the reason most people think. They also explain sensitisation, the silent first encounter that sets an allergy up, how food allergies can start on the skin, and what treatments like oral immunotherapy can and can’t do. Episode timestamps 00:00 Nobody is born with an allergy 01:40 Immune tolerance and why most of us don’t react 03:48 Is it in your genes? 07:41 Gut bacteria and the first few months of life 11:27 The hygiene hypothesis 14:17 Sensitisation, the allergy “first date” 16:49 How food allergies can start on the skin 18:54 Can allergies be outgrown or treated? Why Not Reacting Is the Real Achievement Starts at 01:40 Every day you breathe in foreign protein from pollen, dust mite droppings and cat dander. The impressive thing isn’t that some people react. It’s that most of the time, nobody does. This is called immune tolerance, and it’s active rather than passive Regulatory T cells step in and hold the rest of the immune system back In someone with an allergy, the same encounter triggers a Type 2 response instead Chris: “Your immune system isn’t just kind of ignoring pollen, it’s making decisions about it.” So an allergy isn’t a weak immune system. It’s an immune system doing a full-on job on something harmless. How Much of Your Allergy Risk Is Genetic? Starts at 03:48 Allergic disease has been climbing globally for decades, and our genes haven’t changed in that time. Genetics still set the starting point, though. What’s inherited isn’t the allergy itself but a tendency towards a TH2 response, the branch of immunity involved in allergic reactions. A study from the Netherlands Twin Register involving more than 14,000 people estimated inheritance at about 75% for asthma and 66% for allergy overall A cohort of about 25,000 Swedish twins found 82% for childhood asthma and 60 to 80% for hay fever, eczema and food allergy Specific genes have been linked to risk, including gasdermin B, IL1RL1 and TLR4 Chris: “So the genes set you up, but they don’t settle it, which I think is the hopeful bit.” How Gut Bacteria Teach the Immune System Tolerance Starts at 07:41 The gut microbiome is established in the first weeks and months of life, and it shapes how the immune system behaves for years. Babies whose gut is dominated by Bifidobacterium at one month old show lower rates of food sensitisation years later Less diverse microbiomes, or dominance by Bacteroides or Klebsiella, are linked to higher risk by the first birthday The mechanism: gut bacteria make short-chain fatty acids (propionate and butyrate), which boost regulatory T cells, which act as a brake on the allergic response The team is clear that factors like birth mode and antibiotic use are associations, not causes, and that antibiotics in infancy are given for very important reasons. The First Date That Creates an Allergy Starts at 14:17 There’s a specific moment when an allergy starts. It’s called sensitisation, and Matt compares it to a first date. Nothing seems to happen, but a memory is made. On first contact, TH2 cells produce IgE antibodies tuned to that allergen The IgE sits on mast cells and basophils, the cells that hold histamine On the second encounter, the mast cells release histamine in a fast, coordinated burst Jen: “Well, he wasn’t fine. He was being sensitised.” The team also explains how food allergies can begin through broken skin, which helps explain the link between eczema and later food allergy, and why introducing allergenic foods early now seems to help. About So That’s Why So That’s Why is a weekly podcast where Jen, Chris and Matt unpack the science behind everyday health questions. No jargon, no judgement. Just genuine curiosity and proper research. Website:

0:00 · Nobody is born with an allergy-24:57

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show notes

obody has ever been born with an allergy, so why do so many of us get them? Jen, Chris and Matt explain the moment it happens.

In this episode of So That’s Why, the team tackles a question that sounds simple but hides a lot of clever biology. Not reacting to pollen, dust mites or cat dander turns out to be an active decision your immune system makes thousands of times a day. Allergies happen when that decision goes the other way.

The team looks at what twin studies reveal about how much of allergy risk is inherited, why the gut bacteria a baby has at one month old can matter years later, and why the famous “we’re too clean” hygiene hypothesis is roughly right but not for the reason most people think. They also explain sensitisation, the silent first encounter that sets an allergy up, how food allergies can start on the skin, and what treatments like oral immunotherapy can and can’t do.

Episode timestamps

  • 00:00 Nobody is born with an allergy
  • 01:40 Immune tolerance and why most of us don’t react
  • 03:48 Is it in your genes?
  • 07:41 Gut bacteria and the first few months of life
  • 11:27 The hygiene hypothesis
  • 14:17 Sensitisation, the allergy “first date”
  • 16:49 How food allergies can start on the skin
  • 18:54 Can allergies be outgrown or treated?

Why Not Reacting Is the Real Achievement

Starts at 01:40

Every day you breathe in foreign protein from pollen, dust mite droppings and cat dander. The impressive thing isn’t that some people react. It’s that most of the time, nobody does.

  • This is called immune tolerance, and it’s active rather than passive
  • Regulatory T cells step in and hold the rest of the immune system back
  • In someone with an allergy, the same encounter triggers a Type 2 response instead

Chris: “Your immune system isn’t just kind of ignoring pollen, it’s making decisions about it.”

So an allergy isn’t a weak immune system. It’s an immune system doing a full-on job on something harmless.

How Much of Your Allergy Risk Is Genetic?

Starts at 03:48

Allergic disease has been climbing globally for decades, and our genes haven’t changed in that time. Genetics still set the starting point, though. What’s inherited isn’t the allergy itself but a tendency towards a TH2 response, the branch of immunity involved in allergic reactions.

  • A study from the Netherlands Twin Register involving more than 14,000 people estimated inheritance at about 75% for asthma and 66% for allergy overall
  • A cohort of about 25,000 Swedish twins found 82% for childhood asthma and 60 to 80% for hay fever, eczema and food allergy
  • Specific genes have been linked to risk, including gasdermin B, IL1RL1 and TLR4

Chris: “So the genes set you up, but they don’t settle it, which I think is the hopeful bit.”

How Gut Bacteria Teach the Immune System Tolerance

Starts at 07:41

The gut microbiome is established in the first weeks and months of life, and it shapes how the immune system behaves for years.

  • Babies whose gut is dominated by Bifidobacterium at one month old show lower rates of food sensitisation years later
  • Less diverse microbiomes, or dominance by Bacteroides or Klebsiella, are linked to higher risk by the first birthday
  • The mechanism: gut bacteria make short-chain fatty acids (propionate and butyrate), which boost regulatory T cells, which act as a brake on the allergic response

The team is clear that factors like birth mode and antibiotic use are associations, not causes, and that antibiotics in infancy are given for very important reasons.

The First Date That Creates an Allergy

Starts at 14:17

There’s a specific moment when an allergy starts. It’s called sensitisation, and Matt compares it to a first date. Nothing seems to happen, but a memory is made.

  1. On first contact, TH2 cells produce IgE antibodies tuned to that allergen
  2. The IgE sits on mast cells and basophils, the cells that hold histamine
  3. On the second encounter, the mast cells release histamine in a fast, coordinated burst

Jen: “Well, he wasn’t fine. He was being sensitised.”

The team also explains how food allergies can begin through broken skin, which helps explain the link between eczema and later food allergy, and why introducing allergenic foods early now seems to help.

About So That’s Why

So That’s Why is a weekly podcast where Jen, Chris and Matt unpack the science behind everyday health questions. No jargon, no judgement. Just genuine curiosity and proper research.

Website:

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