Th1, Th2 and Immune Modulation

Th1 and Th2 dominance is an example of one very significant difference in people, and it affects much of the supplement, lifestyle, and diet recommendations for an individual.

Th cells are short for T helper cells. T helper cells are kind of like a symphony conductor. The conductor sends signals to the band and the musicians play the music. T helper cells send signals or more technically release cytokines that guide other immune cells that do the attacking.

It’s important to know if you’re Th1 or Th2 dominant because that will allow you to figure out which course of action to take.

Trying to figure it out based on symptoms or reactions to supplements isn’t always accurate.


Th1 Dominance

Th1 cells are part of what’s called cell-mediated immunity, which is an immune response that does not involve antibodies, but does involve the release of various cytokines in response to foreign proteins.

People with Th1 dominance have what’s called a delayed-type hypersensitivity

It’s caused by the overstimulation of immune cells, commonly lymphocytes(Natural killer cells, T cells) and macrophages, resulting in chronic inflammation.

Interferon gamma (IFNy) is the main cytokine in Th1 dominance. It inhibits the production of most IgG’s and IgE and increases the secretion of IgM [R, R].

Food processing may matter here since cooking may alter proteins/antigens. For example, there are less IgM antibodies to raw peanuts than cooked peanuts [R].

There are also more IgM antibodies to fried chicken, canned tuna and fried salmon [R].

This may be a reason why I get a lot of inflammation from canned tuna, much more so than fresh tuna.

I’m Th1 dominant, which I cured with the lectin avoidance diet.

Th1 dominance is evidenced by:

  • Delayed food sensitivities: This is evidenced by getting inflammation from food, yet the effects aren’t necessarily immediate [R].
  • Brain fog: This is also a symptom of Th2 dominance.
  • Fatigue: After meals and acute exercise or fatigue, in general, is usually more severe in Th1 dominance because Th1 cells increase the cytokine interferon gamma, which increases other cytokines like IL-1b and TNF-alpha, both of which cause fatigue via suppression of orexin neurons. TNF-alpha can also be elevated in Th2 dominance because it can be released by IL-1and mast cells, but it’s likely more elevated in Th1 dominance [RRR].
  • IBS: People with IBS are more likely to be Th1 dominant (elevated IL-12). Interferon reduces serotonin in the gut and also increases oxidative stress(by activating IDO). However, people with Th2 can also have IBS. [RR].
  • Rheumatoid arthritis [R]
  • Hashimoto’s thyroiditis (IL-18) [RR]
  • Low T3 Syndrome: When levels of T3 and/or T4 are at unusual levels, but the thyroid gland does not appear to be dysfunctional. I had this and I’ve seen this in many Th1 dominant clients of mine, who are also relatively thin (likely because of hyperleptinemia). It comes from elevations in IL-6, Interferon gamma,TNF-alpha, and IL-1b [RRRR].
  • More likely to be thin: This is a very noticeable observation of mine. The vast majority of Th1 dominant people are relatively thin. It can be explained by 2 mechanisms:
    • 1) TNF-alpha and IL-1beta inhibit orexin, which decreases appetite. TNF-alpha is also a direct fat buster, which leads to insulin resistance in fat cells. Anti-TNF-alpha therapy results in weight gain – an average of 5.5 kg or 11 pounds in only 12 weeks [RR].
    • 2) Interferon gamma, like TNF-alpha, also creates insulin resistance in fat cells and differentiation of fat cells, which means that it prevents you from getting fat. There are many aspects to hunger and weight gain, so it’s obviously not a perfect correlation [RR].
  • IBD: Characterized by a different cellular subset: Th17 cells and IL-18. This pattern is connected with Th1 dominance [RR].
  • Psoriasis and rosacea [R, R]
  • Celiac disease [R]
  • Crohn’s disease [R]
  • Type 1 diabetes [R]
  • PCOS (IL-18) [R]
  • Alzheimer’s (IL-18) [RR]
  • Lupus (also Th2) [R]
  • Multiple sclerosis (also Th2) [R]
  • Guillain-Barré syndrome [R]
  • Post-infection IBS [R]
  • Behcet’s [R]
  • Vitiligo (Th1 chemokine) [R]
  • Inflammation after Lyme infection – Lyme disease can elevate the Th1 system initially (but eventually becomes th2 dominant) [R],
  • Inflammation after the following: Strep, mono (EBV), HPV, herpes, pneumonia, H. pylori or Cytomegalovirus. These are common infections that also invoke the Th1 system; in some people with a genetic predisposition like myself, the immune system remains active after these infections. In some environments, this may have been a survival advantage since you’d be more likely to survive into adulthood and bear offspring [RRRRRR].
  • Chemotherapy-induced neuropathy has increased CCL2 and IFNy, and lower levels of IL-10 [R, R].
  • Low pregnenolone levels – my observations. Every client who was Th1 dominant had low pregnenolone levels. (People with Th2 dominance also likely have low pregnenolone levels).

Most people with a balanced immune system just need to eat less, sleep more, be less stressed, exercise, and eat a balanced diet with fish and animal foods and lots of fruits and veggies to be healthy. Sun or supplementing with vitamin D is a good idea, too.

In my consulting practice, I get a lot of people who mention their health issues started after an infection. This is because many common infections increase the Th1 system.

The best way to know if you’re Th1 dominant is to discern if you have trouble with inflammation and food intolerances, yet you don’t display the classical Th2 dominant symptoms. I like to check this by seeing if people are Th2 dominant.

If people don’t display any signs of Th2 dominance and they have an inflammatory condition, Th1 dominance is to be suspected.

Th1 dominance comes from a combination of genetics and environment. The environment is heavily influenced by infections.

Bacterial and most viral infections increase your Th1 system and if you have the wrong genetic cards, it will increase it too much.

People with a Th1 system out of control tend to release more cortisol than the average person because cortisol decreases Th1-related inflammation, so the body activates your HPA system every time you get a Th1 spike to keep things in balance.

Interferon gamma is the major cytokine involved with Th1 dominant people. Chronic, low-grade interferon gamma (Th-1 type inflammation) accelerates aging and could contribute to the onset of major age-related psychiatric conditions (such as depression, anxiety, insomnia, and cognitive impairment) and medical diseases (such as cardiovascular diseases, neurodegeneration, osteoarthritis and osteoporosis, and diabetes). Some research shows that it may also be involved in the development of aggressive tumors [R].

The Benefits of an Elevated Th1 System

There are some benefits of having an elevated Th1 immune system.

For one, people with Th1 dominance tend to get sick much less than others because their immune system is on guard. But if these people are chronically stressed, they will get sick sometimes because cortisol decreases Th1-related inflammation and makes these people more susceptible to infections.

Another benefit is a decreased likelihood of cancer [R].

Th1 cells and cytokines like interferon gamma and TNF scour your body for tumor cells and destroy them. There is a trade-off with cancer and autoimmunity. This is a generalization, as some cancers like multiple myelomas are Th1 dominant [R].

Cancer is relatively rare in my family, but autoimmunity is common. This is because the more active your immune system is the more likely it will destroy cancer cells before they start multiplying out of control. But it’s also the case that it’s more likely to mistake your own tissue as a foreign invader and attack it.

The key is to balance your immune system. Know what kind of dominance you have – if any – and supplement and diet accordingly. Most people have one dominance or another.

Some people have been gifted to have a system that’s in balance and these people don’t have inflammation issues or have cancer, but age usually is the time bomb that messes everything up. As people get older their immune system starts to malfunction and autoimmunity and cancer start to occur.

Regarding the initial occurrence of my own issues, I used to get lots of strep and other infections as a kid. This probably made my Th1 system spiral out of control.

As an adult, I rarely got sick because of this elevation, but as I bring it down I notice I’m getting sick more often.

I had a close call a couple of months ago but dodged the bullet with a bunch of supplements. This time around, I haven’t been as fortunate and got some infection yesterday (not serious).

Keep in mind that you don’t actually have to have an active infection to have elevated Th1 inflammation.

Th2 Dominance

Th2 cells mediate the activation and maintenance of the “humoral,” or antibody-mediated, immune response.

Actually, Th2 dominance is considered an anti-inflammatory profile because people with this profile have lower levels of systemic inflammation. The negative effects of Th2 dominance are probably more benign than people with Th1 dominance.

People with Th2 dominance produce a lot of antibodies and instant food allergies are more likely to occur.

People with Th2 dominance, in general, have a weaker immune system, but they are better at fighting infections that take hold outside of cells (extracellular infections).

The dominant cytokine in Th2 dominance is IL-4, which produces IgG1 and IgE but markedly inhibits IgM, IgG3, IgG2a, and IgG2b [R].

People with Th2 dominance should do a skin scratch test and check blood IgE levels to check for what they’re allergic to.

It’s interesting that one study found food processing has an effect on IgE levels. Raw eggs, raw peanuts, and raw pecans show a lower level of IgE antibodies than cooked eggs, indicating that Th2 dominant people would do better with raw eggs, raw peanuts, and raw pecans, at least in one respect [R].

Th2 cells are produced by IL-2 and IL-4 and they give off IL-4, IL-5, IL-6, IL-10, and IL-13 (see picture above).

Th2 dominance is evidenced by:

  • IgE-related allergies, which are immediate and measured by skin scratch tests [R]
  • Seasonal allergies
  • Airway constriction
  • Asthma
  • Nasal drip
  • Mucus
  • Eczema (Dermatitis)
  • Hay fever (Allergic rhinitis)
  • Increased stomach acidity or GERD
  • Excess histamine or what some people call “histamine intolerance”
  • Hives (Urticaria)
  • Chronic Fatigue Syndrome [R]
  • Autism [R]
  • Uveitis, Grave’s disease, Sjogren’s, Oral Lichen Planus, SLE (also Th1 dominant) [RRRR]

Types 1, 2, and 3 hypersensitivity are caused by Th2 dominance.

The other effects stem from the main Th2 cytokine, IL-4, and IgE antibodies. They stimulate mast cells to release histamine, serotonin, and leukotriene to cause airway constriction and intestinal peristalsis.

Th2 dominance can be from a parasite or helminth infection, but could also just be genetic.

I had a client with a classic case of Th2-related inflammation that started when he got a parasite in a third-world country. He had no inflammation issues before.

Note that you don’t actually have to have a parasite to have an elevated Th2 related inflammation and it’s likely that most Th2 dominant people don’t have parasites.

It’s fully possible to have both Th1 and Th2 elevations, but usually one or the other is dominant.

Acute bouts of Th2 immune responses can kill cancer, but chronic elevations increase your risk for some cancers like breast cancer, colorectal cancer, and pancreatic cancer, to name a few [R].

The Benefits of an Elevated Th2 System

The Th2 immune system is considered an anti-inflammatory profile. This means that the person experiences low levels of systemic inflammation.

The problem is when the immune system is shifted too much to the Th2 system, as people develop allergies to everything. It’s the allergens that then start causing the problems.

It may seem odd why Th2 dominant people have increased stomach acidity. The reason is because gastric fluid acidification can help expel helminths. So, this response is actually quite adaptive, and serves an important purpose in our evolutionary history.

Th1/Th2 Dominance and Methylation

People who are Th1 dominant have lower methylation of certain genes [RRRRR].

In simple terms, methylation silences a gene. In people with Th1 dominance, since they don’t methylate or silence a certain gene enough (interferon gamma), too much of it is produced and that has a ripple effect throughout the immune system. In MS, another Th1 dominant condition, homocysteine is elevated, indicating hypomethylation [R].

The result is that people with Th1 dominance produce too much interferon gamma, which may result in intolerance to food and a delayed hypersensitivity to these foods.

In Th2 dominance, the opposite is true, and there is too much methylation of the interferon gamma gene, resulting in too little interferon gamma being produced and, therefore, more Th2 cells and their products.

In Th2 dominance, people are under/hypomethylating a different gene (IL-4) [RR].

In both kinds of dominance, some genes are over-methylated and some under-methylated. Even so, upping your methylation with TMG, SAM-e, and B-vitamins should deactivate the immune system to a degree. I have had a positive experience with these supplements.

Inflammatory Diseases That Are Neither Th1 nor Th2 Dominant

  • Autism [R]
  • IBS and ADHD are associated with inflammation, but can have elevations of either Th1 or Th2 systems [RR]
  • Heart disease is from IFN-gamma, VEGF, TGF-beta1. IL-10 has protective effects [RR]
  • Bipolar disorder is associated with elevated TNF-α, IL-6, and IL-8 during manic and depressive phases, and IL-2, IL-4, and IL-6 are elevated during mania
  • Schizophrenia, as some studies show it’s Th1 dominant, while others show elevated TNF-alpha and IL-6 is the culprit [RR]
  • OCD cytokine profiles vary, but a meta-analyses only showed a reduction in IL-1b in people with OCD as a common denominator; my experience has been that my OCD had disappeared after I eliminated my inflammation. This is likely a result of reduced glutamate excitotoxicity that was a result of inflammation [R]
  • Ulcerative colitis has no dominant system, but has increased IL-8 levels [R]
  • Carpal tunnel syndrome has increased IL-2, a Th1 cytokine [R]
  • Diabetic neuropathy has elevated IL-18 and TGF-beta – there’s no dominant profile here. Other inflammatory factors include PDGF AA/BB, RANTES, leptin, osteoprotegerin, G-CSF, sE-Selectin, sICAM, sVCAM, CRP and fibrinogen.. Patients with painful neuropathy had higher sICAM-1 and CRP levels when compared to painless neuropathy [RRR]

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