International Academy of Medical Innovation and Science

Diana Molander, MD

Lecture Title: Personalized nutrition based on genes and gut health as part of any therapeutic approach.

Conference program.

1. Core Thesis

There is no perfect diet.
Effective nutrition must be personalized, integrating genetic potential (DNA) with current physiological reality (gut microbiome).

Universal dietary advice fails because it ignores biological diversitygene–nutrient interactions, and microbial context. Personalized nutrition is positioned not as a lifestyle trend, but as a clinical necessity.

2. Why Universal Dietary Advice Fails

Standard recommendations such as “eat less, move more” oversimplify health and shift responsibility onto willpower, while overlooking:

  • Genetic variability

  • Metabolic differences

  • Microbiome-mediated responses

  • Environmental stressors

Consequence

Patients often experience:

  • Repeated diet failure

  • Confusion from contradictory advice

  • Harm from influencer-driven, non–biology-matched diets

This reframes diet failure as physiological mismatch, not lack of discipline.

3. Modern Context: Nutrition in 2025

Citing contemporary thought (e.g. Justin Harris), the presentation describes today’s environment as:

  • Excess calories, mostly ultra-processed

  • Extreme information noise, amplified by social media

  • Choice paralysis caused by too many mutually exclusive dietary models

Key Reframe

Food is presented as an epigenetic signal:

Every meal sends instructions to the body with lasting biological effects.

Implication:
Personalization is no longer optional—it is a survival strategy in an overprocessed, over-informed food landscape.

4. Nutrigenetics & Nutrigenomics: The Scientific Foundation

Nutrigenetics

Genetic variants (SNPs) influence how individuals:

  • Absorb nutrients

  • Convert nutrients

  • Metabolize macronutrients and micronutrients

Example:

  • BCMO1 gene: Some individuals poorly convert beta-carotene → vitamin A

  • These individuals require preformed retinol, not plant carotenoids

Nutrigenomics

Nutrients themselves influence:

  • Gene expression

  • Inflammatory pathways

  • Long-term health outcomes

Key Principle

The gene–nutrition relationship is bidirectional:

  • Genes shape nutritional needs

  • Nutrition reshapes gene expression

This directly challenges dietary dogma and justifies a precision-based approach.

5. DNA in Personalized Nutrition

DNA testing provides insight into:

  • Carbohydrate, fat, and vitamin metabolism

  • Risk predispositions (e.g. insulin resistance, lactose intolerance, inflammatory tendencies)

  • Nutritional strategies aligned with genetic ability rather than ideology

DNA defines potential and constraints, not destiny.

6. The Gut Microbiome: The Dynamic Half of the Equation

Unlike DNA, the microbiome is modifiable and responsive.

Role of the Microbiome

  • Nutrient breakdown & absorption

  • Vitamin synthesis

  • Immune modulation

  • Metabolic and even neurobehavioral influence

Dysbiosis Consequences

  • Malabsorption

  • Chronic inflammation

  • Poor dietary response despite “correct” nutrition

Clinical Case Logic

Microbiome testing → targeted probiotics/prebiotics/dietary changes → symptom reversal within ~6 weeks.

Key distinction:
DNA is static. The microbiome is adaptive.

7. From Knowledge to Clinical Application

Foundational Clinical Rules

  • Interpret patterns, not individual organisms

  • Marker levels must be contextualized with:

    • Symptoms

    • Stool chemistry

    • Diet

    • Inflammatory markers

  • Avoid treating single microbes in isolation

This prevents reductionist errors and unnecessary interventions.

8. Case Example: Microbial Pattern Interpretation (Table Overview)

The referenced table illustrates pattern-based decision-making, not organism eradication.

Examples:

  • Faecalibacterium prausnitzii

    • Low: inflammatory risk, barrier weakness

    • High: carb overload or maldigestion

    • Intervention focuses on cross-feeding and anti-inflammatory substrates, not suppression

  • Akkermansia muciniphila

    • Low: metabolic dysfunction

    • High: possible neuro-inflammatory associations

    • Strategy differs based on context and functionality

  • Methanogens

    • High: IBS-C, slowed motility

    • Low: inflammatory vulnerability

    • Interventions adjust fermentation and energy flux

  • Fusobacterium spp.

    • High: systemic inflammatory associations

    • Strategy emphasizes oral–gut axis and polyphenol modulation

The emphasis remains consistent: context > presence.

9. Reframing Diet Failure

A central psychological and clinical insight:

Diet failure is rarely about willpower.

DNA and microbiome data reveal:

  • Neurochemical drivers of appetite

  • Microbial influences on cravings and tolerance

  • Structural reasons certain diets predictably fail for specific individuals

This shift reduces patient blame and increases clinical precision.

10. Final Takeaway

The presentation advances a clear hierarchy:

  1. Universal diets fail

  2. Genes define capacity

  3. Microbiome defines current response

  4. Functional testing bridges science and application

  5. Clinical personalization replaces dietary ideology

Personalized nutrition is framed as evidence-based, clinically grounded, and biologically respectful—not trendy, not permissive, and not motivational rhetoric.


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