This document discusses how our genes and health are influenced by what we eat. It argues that current research and healthcare is still too focused on treatment rather than prevention of non-communicable diseases like diabetes and heart disease. A new dynamic health concept is needed that is based on metabolic plasticity and resilience, viewing health as our ability to adapt to challenges. Nutrigenomics research allows us to understand how nutrients regulate our genes and phenotype through sensing molecular switches and changing gene expression. Phenotypic plasticity means our phenotype can change in response to our environment like nutrition, and that "we are what we eat and have eaten" in receiving, recording, remembering and revealing foods through our metabolome, proteome, transcriptome, epigen
We are what we eat - a path towards personal health
1. We are what we eat
The path from public health to personal health
Michael Müller
Netherlands Nutrigenomics Centre
& Nutrition, Metabolism and Genomics Group
Division of Human Nutrition, Wageningen University
4. 2013 – our health (care) reality
• The next health tsunami => non-communicable diseases (NCDs) >
communicable diseases (CDs).
• Our research is often still focused on treatment instead of prevention of NCDs.
• Research is largely fragmented with the ambition to find “magic bullets”: gene X
is responsible for the disease & could be drug target.
• We have no efficient strategies to treat or cure complex NCDs (Diabetes, CVD,
cancer, mental disorders) => chronic diseases that require life-long treatment.
• Mono-target approaches (“one drug fits all” bestsellers) fail in the efficient
treatment of NCD => increasing health care costs & decreasing quality of life.
• A “creative deconstruction of medicine (Eric Topol) and health care” is needed.
We need a new dynamic health concept based
on metabolic plasticity and resilience =>
“Health as the capacity to adapt to challenges!”
5. Nutrigenomics & molecular nutrition allows
us to define the mechanistic framework
Blood
triglycerides
6. “2 hits” in Metabolic Syndrome
“Too much metabolic & inflammatory stress”
Complex NC diseases are caused by dysregulation
Nature Medicine 2012
11. Understanding Nutrition
How nutrients regulate our genes: via sensing molecular switches
Changed
organ
metabolic
capacity
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12. Phenotype plasticity
Phenotypic plasticity is the ability of an organism to
change its phenotype in response to changes in the
environment (e.g. nutrition or exercise).
CYP4A10
14
12
10
FC vs WT ctrl
8
6
4
2
0
WT KO WT KO WT KO WT KO WT KO WT KO WT KO WT KO WT KO
ctrl WY feno C10:0TG C18:1TG C18:2TG C18:3TG C20:5TG C22:6TG
13. Your are what you eat
Healthy food (pattern)s have large impact on our gene expression & phenotype
• (Micro & Macro) Nutrients
– Mono & polyunsaturated fatty acids
– Vitamines (e.g. vitamine A & D) , minerals (e.g. Zn)
• Microbiota (from foods)
– Vegetarians / omni- /carnivores => different microbiota
– “Raw” (e.g. “Sushi”) or fermented food consumption => food-
specific microbiota
• Food components (bitter, toxic, “healthy”)
– Secondary plant metabolites (e.g. resveratrol, glucosinolates,
cafestol....)
– MicroRNA (e.g. rice) => “nutrient”?
• Less foods/calories (caloric restriction) => “chromatin”
exercise
15. “We are what we eat and have eaten”
Received, Recorded, Remembered & Revealed
16. Nutrigenomics
Quantification of the nutritional genotype-phenotype
Phenotype
Metabolome
Lifestyle
Proteome
Nutrition
Microbiota
Transcriptome
Environment
Epigenome
Genotype
17. chronically
Examples: Do not overload organs
40 cm
4 cm
C1 C2 C3 C4 C5 C6 C7 C8 C9 C10
10% FAT
45% FAT
18. „Obese-linked‟ pro-inflammatory
gene expression profile by SFAs
SFA diet MUFA diet
• The SFA-rich diet:
• Induces a pro-
inflammatory obese-linked
gene expression profile
• Decreases expression and
plasma level of the anti-
inflammatory cytokine
adiponectin
• “Personal Transcriptomes”
Van Dijk et al. AJCN 2009