Short and Medium Chain Fatty Acids Study

(Requires the General Profile Study to be conducted)

What do we analyze?

Acetic acid, butyric acid, capric acid, caprylic acid, hydrochloric acid, lauric acid, propionic acid, ammonia, methane.

Study of Hormones and Neurotransmitters

(Requires the General Profile Study to be conducted)

What do we analyze?

Acetylcholine, adrenaline, adrenochrome, alpha-N-acetylgalactosaminidase, BH2, BH4, cortisol, DHPPA, DMT, dopamine, GABA, glycine, histamine, lactoferrin, melatonin, methylation, noradrenaline, serotonin, zonulin.

Study of 417 Food Intolerances

It is recommended if the patient has suffered inflammatory, dermal, or digestive reactions after consuming certain foods or being exposed to some types of environmental pollen.

What do we analyze?

Beverage intolerances, condiments, sweeteners, cooked fruits, raw fruits, fats and oils, seafood and fish, nuts, dairy, cereals and starches, meat and eggs, cooked vegetables, raw vegetables, animal dander, as well as various types of pollen: cereal pollen, shrub pollen, and tree pollen

Study of Genes Associated with Seizures and Epilepsy

When a child has seizures or epilepsy, one of the most difficult parts for the family is living a path of trial and error: trying medications, adjusting doses, changing treatments, and sometimes without a clear explanation of why one thing works and another does not.

The Study of Genes Associated with Seizures and Epilepsy seeks a deeper answer: to identify if there is a genetic predisposition that is influencing the seizures. This can help make the medical plan more targeted and personalized, instead of making decisions “blindly.”

What can this study reveal?

1. What type of “switch” in the brain may be involved
   In the brain, there are channels and receptors that regulate electrical activity (for example, sodium, potassium, calcium channels; and receptors like GABA or glutamate). Some genetic variants can alter these “switches,” making the brain more prone to seizures.
   Knowing which system is altered can guide better decisions for therapy.
2. If the problem is due to “excess” or “lack” of function
   Some variants make a channel work more (as if it speeds up), and others make it work less (as if it slows down). This difference helps to understand if the focus should be on slowing down the hyperactivity or supporting a function that is low, always under medical criteria.
3. Medications to avoid in certain cases
   There are genes that can indicate a higher risk of adverse effects with some drugs. With that information, the doctor can avoid options that could be riskier for that particular patient.
4. How the body metabolizes some medications (pharmacogenomics)
   Not everyone processes medications the same way. Some variants can make a child a slower or faster metabolizer, which is associated with:

• higher risk of side effects, or
• lack of efficacy due to insufficient dosage.
  This can support finer adjustments to treatment.

1. Clues for diet and metabolic support (when applicable)
   In some cases, certain genes are related to cellular energy/mitochondria or nutrient transport, which can guide whether it is worth considering strategies such as: ketogenic diet, fasting management, or metabolic support (for example, cofactors and antioxidants), always personalized.
2. Comorbidities and early supports
   Several genes associated with epilepsy are also related to areas of development (language, learning, behavior, attention). Having this information can help to anticipate supports and plan early intervention (speech therapy, neuropsychology, school support, etc.).

Encephalopathy Study

This test is recommended if the patient has suffered from recurrent infections, such as strep throat, which can cause the immune system to mistakenly attack areas of the brain — suddenly triggering symptoms like OCD, tics, extreme anxiety, hyperactivity, and behavioral changes. 

What do we analyze?

AMPA R1/R2, anti-dopamine D1 receptor, anti-dopamine D2 receptor, anti-lysoganglioside GM1, anti-tubulin, CaMKII, caspase 3, caspase 7, caspase 8, CASPR2, cyclooxygenase, cytochrome P450 reductase, ROS, GABA B1/B1 receptor, WAS gene, 41% glyphosate, IL-17, LGI1, lipoxygenase, NAD(P)H oxidase, NMDA receptor, NOS, NOX, iNOS, WAS protein, Th17, xanthine oxidase.

Folate Receptor Genes Study

(Includes MTHFR panel)

This study tells us how your child's body works on the inside, especially the folate and methylation pathways that influence brain, behavior, and energy. With that information, we design a diet and supplementation tailored to their genetics, to better support language, attention, sleep, and emotional regulation, instead of making random diets or supplements.

Includes the following:

1. MTHFR (C677T, A1298C, 3)

2. SOUX (C847T)

3. FOLR1 (T696C, A80C)

4. MTRR (S257T, H595Y, 11, R415T, K350A, A66G)

5. SLC19A1 (A80G)

6. SHMT1 (C1420T)

7. MTR (A2756G)

8. AHCY (G226A)

9. CBS (T833C)

10. BHMT (G716A)

11. FOLR3 (C436T)

12. VDR (T2C)

13. FOLR2 (A647C)

This study evaluates 21 genes related to folate receptors, the methylation cycle, and the metabolism of homocysteine, methionine, and sulfur.

Estudio de Genes Especificos

(Requires the study of Encephalopathy, to be conducted)

At IG LAB, we analyze a panel of encephalopathy biomarkers that together tell a precise story about the neuroinflammatory, oxidative, and immune state of your brain. But more importantly: each of these genes can be modulated from the inside out—through what you eat, breathe, and how you live.

Markers such as ROS, NOX, iNOS, NOS, cyclooxygenase, lipoxygenase, and xanthine oxidase act as the brain's "reverse firefighters": when overexpressed, they generate free radicals and chronic inflammation that silently damage neurons. Nutrigenomics identifies which bioactive molecules—such as polyphenols, omega-3s, or curcumin—can "turn off" these genes without destroying their natural protective function. Epigenomics reveals whether this overactivation is embedded in DNA methylation marks or histone modifications, meaning it can actually be reprogrammed.

The AMPA R1/R2, NMDA, GABA B1/B2, and Dopamine D1/D2 receptors are the brain's electrical gates. When autoimmune antibodies attack them—as seen with CASPR2 and LGI1—the result is brain fog, seizures, sleep disorders, and mood dysregulation. Nutriepigenomics can modulate the expression of these receptors by influencing the methylation of their regulatory genes, restoring the balance between neuronal excitation and inhibition without the need for harsh medications.

Caspases 3, 7, and 8 are the "molecular scissors" that execute programmed cell death (apoptosis). Their overactivation in the context of neuroinflammation is a clear signature of active neuronal damage. The exciting part is that dietary patterns rich in neuroprotective compounds can epigenetically silence these apoptotic pathways, giving the brain a chance to repair itself.

Cytochrome P450 reductase detoxifies the brain, but when it is hypomethylated (as in Parkinson's disease), it becomes overexpressed and generates dopaminergic oxidative stress. CaMKII is a master kinase that regulates synaptic plasticity; its alteration is closely linked to memory and learning deficits. NAD(P)H oxidase fuels microglial inflammation. Personalized nutrigenomics can rewrite these expression patterns by adjusting the cellular redox state directly through diet.

The Th17/IL-17 axis is the immune system's "rebel army": when chronically activated, it crosses the blood-brain barrier and inflames nervous tissue. Anti-lysoganglioside GM1 and anti-tubulin antibodies signal an autoimmune response that can be triggered by environmental and dietary factors. This includes 41% glyphosate—an herbicide that alters the gut microbiome and, through the gut-brain axis, modifies the epigenetic expression of neuroinflammatory genes. Targeted dietary interventions, such as ketogenic diets, probiotics, and diets rich in methyl donors, can rebalance this immune axis at an epigenetic level.

The WAS gene (Wiskott-Aldrich Syndrome protein) regulates the actin cytoskeleton in immune cells. Its dysfunction creates chaotic immune signaling that amplifies neuroinflammation. Its expression is highly sensitive to epigenetic modifications, making it a highly effective target for nutrigenomic intervention in immunomodulation protocols.