The document summarizes a presentation on the gut-brain axis and probiotics. It provides an overview of the gut-brain axis as an integrative bidirectional system involving the brain, gut microbiota, neuroanatomical pathways, the neuroendocrine HPA axis, the gut immune system, gut microbiota and metabolism, and intestinal and blood-brain barriers. It discusses evidence from preclinical studies using germ-free mice models and human studies such as those linking gut microbiota to HPA axis response and evidence from fMRI studies showing probiotic consumption can decrease brain reactivity to negative stimuli.
From Nutrigenomics to Systems Nutrition - The role of nutrition in metabolic...Norwich Research Park
1) The document discusses moving beyond traditional nutrition science to a systems approach to understand the complex interactions between diet, genes, microbiome, and health.
2) A healthy gut microbiome is essential for overall health, and nutrition plays a key role in shaping the microbiome.
3) While no single "superfood" exists, eating a variety of plants foods along with minimizing highly processed foods can help maintain a flexible system and optimal health.
The document discusses how genetic testing and nutrigenetics can be used to personalize nutrition by adapting diets based on individuals' genetic profiles. It provides examples of how polymorphisms in various genes like LCT, AMY1, PPARG, APOC3, CYP1A2, GSTM1, SOD2, IL6 and TNF can influence dietary needs and recommendations. The goal of nutrigenetics is to develop personalized diets and nutrition advice tailored to people's unique genetic makeup.
This document provides recommendations from Cynthia Belew, CNM, WHNP-C on strategies to support the microbiome in women's healthcare. Key recommendations include educating patients on fiber and fermented foods, using probiotics judiciously based on evidence, decreasing antibiotic use by only prescribing when clinically indicated, and engaging in shared decision-making for GBS prophylaxis. The document emphasizes viewing the gut microbiome as integral to human health and considers ways to minimize disruptions during pregnancy and childbirth.
This document provides an overview of nutrigenomics and molecular nutrition research. It discusses:
1) The objectives of the Nutrition, Metabolism and Genomics group, which are to understand how nutrition influences metabolic health at the molecular level and to characterize the role of nutrition and lifestyle factors on translating genotype to phenotype.
2) The research lines of the group, which include metabolic health, the role of epigenetics in aging, and developing infrastructure like databases and omics technologies.
3) The challenges of aging healthily, determining what is healthy, dealing with the rise in diet-related diseases, and how our modern diets interact with our ancient genetics.
4) The concept that
Genetics of Obesity: The thrifty gene hypothesisStephen Magness
Early humans faced regular cycles of feast and famine that promoted the evolution and selection of "thrifty genes" that increased the body's ability to efficiently store and utilize fuels like fat and glucose. While these genes provided an evolutionary advantage in the past by helping humans survive periods of starvation, they predispose modern humans to obesity and related diseases due to our current environment of abundant food and low physical activity levels. The "thrifty genotype" hypothesis has been expanded to include the concept of a "thrifty epigenome," where environmental factors like famine experienced by pregnant mothers can epigenetically influence gene expression and metabolic function in offspring in ways that increase disease risk in a modern context of plentiful food.
Summary
Neurodevelopment is a complex process governed by both intrinsic and extrinsic signals. While historically studied by researching the brain, inputs from the periphery impact many neurological conditions. Indeed, emerging data suggests communication between the gut and the brain in anxiety,
depression, cognition and autism spectrum disorder (ASD). The development of a healthy, functional brain depends on key pre- and post-natal events that integrate environmental cues, such as molecular signals from the gut. These cues largely originate from the microbiome, the consortium of symbiotic bacteria that reside within all animals. Research over the past few years reveals that the gut microbiome plays a role in basic neurogenerative processes such as the formation of the blood-brainbarrier, myelination, neurogenesis, and microglia maturation, and also modulates many aspects of animal behavior. Herein, we discuss the biological intersection of neurodevelopment and the microbiome, and explore the hypothesis that gut bacteria are integral contributors to development and function of the nervous system, and the balance between mental health and disease.
This article challenges the hypothesis that the modern genetic predisposition to obesity has arisen through random genetic drift following predation release. The authors present evidence to support the hypothesis that famines and seasonal food shortages in the post-agricultural era have exerted natural selection favoring fat storage, mediated through fertility selection. The authors conclude that genetic and bioinformatic methods will soon provide a definitive resolution to the long-standing debate over the "thrifty gene" theory of obesity.
The document summarizes a presentation on the gut-brain axis and probiotics. It provides an overview of the gut-brain axis as an integrative bidirectional system involving the brain, gut microbiota, neuroanatomical pathways, the neuroendocrine HPA axis, the gut immune system, gut microbiota and metabolism, and intestinal and blood-brain barriers. It discusses evidence from preclinical studies using germ-free mice models and human studies such as those linking gut microbiota to HPA axis response and evidence from fMRI studies showing probiotic consumption can decrease brain reactivity to negative stimuli.
From Nutrigenomics to Systems Nutrition - The role of nutrition in metabolic...Norwich Research Park
1) The document discusses moving beyond traditional nutrition science to a systems approach to understand the complex interactions between diet, genes, microbiome, and health.
2) A healthy gut microbiome is essential for overall health, and nutrition plays a key role in shaping the microbiome.
3) While no single "superfood" exists, eating a variety of plants foods along with minimizing highly processed foods can help maintain a flexible system and optimal health.
The document discusses how genetic testing and nutrigenetics can be used to personalize nutrition by adapting diets based on individuals' genetic profiles. It provides examples of how polymorphisms in various genes like LCT, AMY1, PPARG, APOC3, CYP1A2, GSTM1, SOD2, IL6 and TNF can influence dietary needs and recommendations. The goal of nutrigenetics is to develop personalized diets and nutrition advice tailored to people's unique genetic makeup.
This document provides recommendations from Cynthia Belew, CNM, WHNP-C on strategies to support the microbiome in women's healthcare. Key recommendations include educating patients on fiber and fermented foods, using probiotics judiciously based on evidence, decreasing antibiotic use by only prescribing when clinically indicated, and engaging in shared decision-making for GBS prophylaxis. The document emphasizes viewing the gut microbiome as integral to human health and considers ways to minimize disruptions during pregnancy and childbirth.
This document provides an overview of nutrigenomics and molecular nutrition research. It discusses:
1) The objectives of the Nutrition, Metabolism and Genomics group, which are to understand how nutrition influences metabolic health at the molecular level and to characterize the role of nutrition and lifestyle factors on translating genotype to phenotype.
2) The research lines of the group, which include metabolic health, the role of epigenetics in aging, and developing infrastructure like databases and omics technologies.
3) The challenges of aging healthily, determining what is healthy, dealing with the rise in diet-related diseases, and how our modern diets interact with our ancient genetics.
4) The concept that
Genetics of Obesity: The thrifty gene hypothesisStephen Magness
Early humans faced regular cycles of feast and famine that promoted the evolution and selection of "thrifty genes" that increased the body's ability to efficiently store and utilize fuels like fat and glucose. While these genes provided an evolutionary advantage in the past by helping humans survive periods of starvation, they predispose modern humans to obesity and related diseases due to our current environment of abundant food and low physical activity levels. The "thrifty genotype" hypothesis has been expanded to include the concept of a "thrifty epigenome," where environmental factors like famine experienced by pregnant mothers can epigenetically influence gene expression and metabolic function in offspring in ways that increase disease risk in a modern context of plentiful food.
Summary
Neurodevelopment is a complex process governed by both intrinsic and extrinsic signals. While historically studied by researching the brain, inputs from the periphery impact many neurological conditions. Indeed, emerging data suggests communication between the gut and the brain in anxiety,
depression, cognition and autism spectrum disorder (ASD). The development of a healthy, functional brain depends on key pre- and post-natal events that integrate environmental cues, such as molecular signals from the gut. These cues largely originate from the microbiome, the consortium of symbiotic bacteria that reside within all animals. Research over the past few years reveals that the gut microbiome plays a role in basic neurogenerative processes such as the formation of the blood-brainbarrier, myelination, neurogenesis, and microglia maturation, and also modulates many aspects of animal behavior. Herein, we discuss the biological intersection of neurodevelopment and the microbiome, and explore the hypothesis that gut bacteria are integral contributors to development and function of the nervous system, and the balance between mental health and disease.
This article challenges the hypothesis that the modern genetic predisposition to obesity has arisen through random genetic drift following predation release. The authors present evidence to support the hypothesis that famines and seasonal food shortages in the post-agricultural era have exerted natural selection favoring fat storage, mediated through fertility selection. The authors conclude that genetic and bioinformatic methods will soon provide a definitive resolution to the long-standing debate over the "thrifty gene" theory of obesity.
This document summarizes a lecture on nutrigenomics given by Michael Müller. It discusses how nutrigenomics allows quantification of the interplay between genetics, lifestyle, nutrition, and the environment in determining phenotypes. Specifically, it highlights how genome-wide transcriptome analysis can identify target genes of nutrients and biomarkers of organ health and resilience. It also provides examples of human nutrigenomics studies examining how diets high in saturated fat or polyunsaturated fat alter gene expression and inflammation. The summary concludes that nutrigenomics is enabling a transition to nutritional science 2.0 through comprehensive, integrated applications and system biology analyses.
Nutrigenomics is the study of how nutrients and bioactive food components influence gene expression and how genetic variations affect individual responses to specific foods or nutrients. It seeks to understand how diet influences health and disease risk based on a person's genetic makeup. Key concepts include that specific diets can modulate health by influencing gene expression, genetic polymorphisms affect disease risk and response to diet, and personalized diets based on genetics may lower disease risk. Nutrigenomics research is providing insights into relationships between nutrition, genes, and chronic diseases like obesity, cardiovascular disease, and cancer.
Costa rica Lecture 3. on 4 Oct 2012 Nutrigenomics: We are what we eat - why?Norwich Research Park
Nutrigenomics is the study of how nutrients and foods impact gene expression and phenotype. A high protein diet was shown to prevent non-alcoholic fatty liver disease in mice by enhancing lipid secretion and reducing energy utilization from food. High protein diets modulate lipid handling in the small intestine and alter the gut microbiota. Deeper genomic profiling and systems biology approaches are needed to better understand metabolic flexibility and personalize nutrition recommendations.
Recovery from developmental nonylphenol exposure is possible i. maleAlexander Decker
This study examined whether the effects of developmental exposure to the endocrine disrupting chemical nonylphenol (NP) could be reversed in subsequent unexposed generations of rats. Female rats were exposed to NP during pregnancy and lactation, and their offspring (F1 generation) showed increased body weight and hyperadrenalism at adulthood. The F1 females were bred to produce the F2 generation without further NP exposure. The F2 offspring did not show increased body weight or hyperadrenalism, indicating the developmental effects of NP exposure were reversed. This suggests that the "default state" can be recovered after a generation that experiences the health impacts and costs of developmental NP exposure.
The study of how genes and gene products interact with dietary chemicals to alter phenotype and, conversely, how genes and their products metabolize nutrients is called nutritional genomics or “Nutrigenomics”.
This document discusses the potential for developing localized probiotic formulations tailored to specific geographic regions and populations. It notes key differences in gut microbiota composition and dietary habits between regions that could impact probiotic efficacy. Specific needs in developing nations like vitamin production and diarrhea prevention are also addressed. The document advocates considering how probiotics might survive locally consumed foods and addresses technological advances that could aid rational probiotic selection based on regional diets and health issues.
Nanjing 2 2013 Lecture "Nutrigenomics part 2" From healthy to too much: The r...Norwich Research Park
1. The lecture discusses the role of the small intestine in metabolic flexibility and how its function is affected by dietary factors like saturated and unsaturated fats. Microarray analysis showed high-fat diets significantly impact gene expression in the small intestine, especially related to lipid metabolism.
2. Unsaturated fats are more efficiently taken up in the small intestine by activating nutrient sensing pathways like PPARs, helping prevent early pathology from a high-fat diet. Saturated fats stimulate obesity, hepatic steatosis, and affect the gut microbiota composition.
3. A systems genetics study of mouse strains found a genetically determined set point for obesity. Certain strains showed robust, strain-specific changes in obesity traits from a
This document discusses nutrition and genomics. It begins with an introduction to nutrigenomics, which examines how foods affect genetic expression and how an individual's genetics influence nutrient metabolism and response. It then covers nutrigenetics, nutrigenomics, and nutritional epigenomics, and how bioactive food components can influence genetic and epigenetic events. Problems in the field include food variability and the complex relationship between genes and disease. However, future potential includes developing personalized dietary interventions to prevent disease and validating product claims.
From Nutrigenomics to nutritional systems biology of fatty acid sensingNorwich Research Park
- The document discusses research into understanding the cellular responses to dietary lipids and fatty acids through nutrigenomics approaches such as transcriptomics.
- Key findings include identifying transcription factors like PPARs that sense fatty acids and regulate gene expression, as well as species-specific and tissue-specific differences in these responses.
- Models are being developed to better understand how nutrients regulate genes and pathways involved in lipid metabolism and energy homeostasis in different metabolic organs like the liver and intestine.
This document provides an overview of nutritional genomics, which combines molecular biology, genetics, and nutrition. Nutritional genomics examines how diet, nutrients, and food components interact with an individual's genetic makeup to influence health and disease. It discusses key concepts like nutrigenomics, which focuses on how nutrients affect genes and metabolic processes, and nutrigenetics, which examines how genetic variations influence interactions between diet and health. The document also outlines some tools and techniques used in nutritional genomics, such as analyzing single nucleotide polymorphisms to understand individual responses to nutrients.
1) The study examined the effect of probiotics in preventing necrotizing enterocolitis (NEC) in preterm neonates compared to a control group.
2) 115 preterm infants weighing 750-1500g or less than 32 weeks gestation received probiotics or did not (control). The probiotic group had significantly lower incidence of NEC and fewer cases of elevated C-reactive protein.
3) However, there were no significant differences between the groups in duration of oxygen therapy, total parenteral nutrition, time to full feeding, or length of hospital stay. The study results suggest probiotics have a protective effect against NEC in preterm infants.
Genetic considerations in obesity developmenthelix1661
The document summarizes genetic research on human obesity from the Pennington Biomedical Research Center. It details that over 600 genes have been associated with obesity. Specific genetic disorders are described that can cause obesity like Cushing's syndrome. Mouse models are used to study obesity genes and their role in food intake and metabolism. Genome-wide studies have linked obesity phenotypes to particular chromosomes. The research aims to identify gene combinations and mutations that influence obesity risk and how they interact with environment.
Probiotics have been shown in meta-analyses to reduce rates of necrotizing enterocolitis (NEC) and mortality in preterm infants. However, there is still resistance to implementing their use due to concerns about the variability of probiotic strains and regimes used across studies, lack of data specifically in extremely low birth weight infants, and unproven long-term safety. The author argues that these objections are not valid given the consistent beneficial effects seen across probiotic types, the biological plausibility of the effects, and the lack of documented safety issues in the thousands of infants exposed to probiotics in clinical trials. Widespread adoption of probiotic supplementation could significantly reduce NEC rates and mortality in preterm infants.
An extensive literature review on Nutrigenetics -A new trajectory in obesity...nutritionistrepublic
Obesity is a multifactorial disease influenced by genes and environment. Various genes involved in appetite, metabolism, and fat storage have been identified that can cause differential responses to diet. Nutrigenetics examines how genetic variations affect the interaction between diet and disease, with the goal of developing personalized diets. One study found that patients who received nutrigenetic testing and were given a personalized diet based on their genetic profile lost more weight and better maintained reductions in BMI and blood glucose levels over time compared to a control group without genetic testing. While nutrigenetics shows promise for developing targeted weight loss strategies, challenges remain in fully characterizing gene-diet interactions and implementing testing in clinical practice.
What is health? NUGO International nutrigenomics Conference Wageningen Sept 9...Norwich Research Park
What is health? Can Nutrigenomics allow to quantify metabolic health? (YES)
My very personal conclusions of a wonderful conference (NUGO Week 2011) in Wageningen (The Netherlands) that we organized.
Stress can disrupt the body's homeostasis and lead to psycho-spiritual awakening as the body seeks balance. The human gut microbiome, which outnumbers human cells 10 to 1, plays a key role in this process. Chronic stress and an unhealthy lifestyle can cause chronic inflammation and disease by disrupting the diversity of the gut microbiota. Adopting a diet low in refined carbs and sugar, fasting, probiotic supplementation, spiritual practice, and exercise can help reduce stress, inflammation, and bring the microbiome back into balance.
Recent research suggests that a variety of lifestyle - especially dietary - changes influencing the integrity of gastrointestinal function may be driving at least some portion of the increased prevalence of illnesses of civilization, including neuropsychiatric problems, such as autism, attention-deficit-hyperactivity disorder, major depression, obsessive-compulsive disorder and Alzheimer disease. One area of interest involves the relationship between the gut's microbiome (as well as the related functional integrity of the gastrointestinal tract) and mental health.
This presentation is an overview of our recent publication in the Appetite Journal. "Preclinical Evidence for the Addiction Potential of Highly Palatable Foods: Current Developments Related to Maternal Influence" by David Wiss, Kristin, Criscitelli, Mark Gold, and Nicole Avena.
1. Nutritional programming theories suggest that the prenatal and early life nutritional environment can influence long-term health by permanently programming physiological functions and disease risk.
2. Animal studies demonstrate a direct link between nutrient imbalance during fetal development and later diseases like hypertension, diabetes, and heart disease, independent of growth rates.
3. Exposure to glucocorticoids and alterations in gene expression from nutrient imbalance in early life are thought to be important mechanisms influencing tissue development and function long-term.
The document discusses nutrigenomics and nutrigenetics. It begins with important terms related to omics fields like genomics, nutrigenomics, and epigenetics. It then provides a basic understanding of nutrigenomics and nutrigenetics, including how genetic diversity and environmental factors affect nutrient metabolism and health outcomes. The goals of nutrigenomics are discussed, including customizing nutrition based on an individual's genetics. Experimental approaches like genomics, transcriptomics and metabolomics are used to study these fields. Examples are provided on how nutrigenomics has clarified roles of specific dietary factors and potential applications in disease prevention.
This document summarizes a lecture on nutrigenomics given by Michael Müller. It discusses how nutrigenomics allows quantification of the interplay between genetics, lifestyle, nutrition, and the environment in determining phenotypes. Specifically, it highlights how genome-wide transcriptome analysis can identify target genes of nutrients and biomarkers of organ health and resilience. It also provides examples of human nutrigenomics studies examining how diets high in saturated fat or polyunsaturated fat alter gene expression and inflammation. The summary concludes that nutrigenomics is enabling a transition to nutritional science 2.0 through comprehensive, integrated applications and system biology analyses.
Nutrigenomics is the study of how nutrients and bioactive food components influence gene expression and how genetic variations affect individual responses to specific foods or nutrients. It seeks to understand how diet influences health and disease risk based on a person's genetic makeup. Key concepts include that specific diets can modulate health by influencing gene expression, genetic polymorphisms affect disease risk and response to diet, and personalized diets based on genetics may lower disease risk. Nutrigenomics research is providing insights into relationships between nutrition, genes, and chronic diseases like obesity, cardiovascular disease, and cancer.
Costa rica Lecture 3. on 4 Oct 2012 Nutrigenomics: We are what we eat - why?Norwich Research Park
Nutrigenomics is the study of how nutrients and foods impact gene expression and phenotype. A high protein diet was shown to prevent non-alcoholic fatty liver disease in mice by enhancing lipid secretion and reducing energy utilization from food. High protein diets modulate lipid handling in the small intestine and alter the gut microbiota. Deeper genomic profiling and systems biology approaches are needed to better understand metabolic flexibility and personalize nutrition recommendations.
Recovery from developmental nonylphenol exposure is possible i. maleAlexander Decker
This study examined whether the effects of developmental exposure to the endocrine disrupting chemical nonylphenol (NP) could be reversed in subsequent unexposed generations of rats. Female rats were exposed to NP during pregnancy and lactation, and their offspring (F1 generation) showed increased body weight and hyperadrenalism at adulthood. The F1 females were bred to produce the F2 generation without further NP exposure. The F2 offspring did not show increased body weight or hyperadrenalism, indicating the developmental effects of NP exposure were reversed. This suggests that the "default state" can be recovered after a generation that experiences the health impacts and costs of developmental NP exposure.
The study of how genes and gene products interact with dietary chemicals to alter phenotype and, conversely, how genes and their products metabolize nutrients is called nutritional genomics or “Nutrigenomics”.
This document discusses the potential for developing localized probiotic formulations tailored to specific geographic regions and populations. It notes key differences in gut microbiota composition and dietary habits between regions that could impact probiotic efficacy. Specific needs in developing nations like vitamin production and diarrhea prevention are also addressed. The document advocates considering how probiotics might survive locally consumed foods and addresses technological advances that could aid rational probiotic selection based on regional diets and health issues.
Nanjing 2 2013 Lecture "Nutrigenomics part 2" From healthy to too much: The r...Norwich Research Park
1. The lecture discusses the role of the small intestine in metabolic flexibility and how its function is affected by dietary factors like saturated and unsaturated fats. Microarray analysis showed high-fat diets significantly impact gene expression in the small intestine, especially related to lipid metabolism.
2. Unsaturated fats are more efficiently taken up in the small intestine by activating nutrient sensing pathways like PPARs, helping prevent early pathology from a high-fat diet. Saturated fats stimulate obesity, hepatic steatosis, and affect the gut microbiota composition.
3. A systems genetics study of mouse strains found a genetically determined set point for obesity. Certain strains showed robust, strain-specific changes in obesity traits from a
This document discusses nutrition and genomics. It begins with an introduction to nutrigenomics, which examines how foods affect genetic expression and how an individual's genetics influence nutrient metabolism and response. It then covers nutrigenetics, nutrigenomics, and nutritional epigenomics, and how bioactive food components can influence genetic and epigenetic events. Problems in the field include food variability and the complex relationship between genes and disease. However, future potential includes developing personalized dietary interventions to prevent disease and validating product claims.
From Nutrigenomics to nutritional systems biology of fatty acid sensingNorwich Research Park
- The document discusses research into understanding the cellular responses to dietary lipids and fatty acids through nutrigenomics approaches such as transcriptomics.
- Key findings include identifying transcription factors like PPARs that sense fatty acids and regulate gene expression, as well as species-specific and tissue-specific differences in these responses.
- Models are being developed to better understand how nutrients regulate genes and pathways involved in lipid metabolism and energy homeostasis in different metabolic organs like the liver and intestine.
This document provides an overview of nutritional genomics, which combines molecular biology, genetics, and nutrition. Nutritional genomics examines how diet, nutrients, and food components interact with an individual's genetic makeup to influence health and disease. It discusses key concepts like nutrigenomics, which focuses on how nutrients affect genes and metabolic processes, and nutrigenetics, which examines how genetic variations influence interactions between diet and health. The document also outlines some tools and techniques used in nutritional genomics, such as analyzing single nucleotide polymorphisms to understand individual responses to nutrients.
1) The study examined the effect of probiotics in preventing necrotizing enterocolitis (NEC) in preterm neonates compared to a control group.
2) 115 preterm infants weighing 750-1500g or less than 32 weeks gestation received probiotics or did not (control). The probiotic group had significantly lower incidence of NEC and fewer cases of elevated C-reactive protein.
3) However, there were no significant differences between the groups in duration of oxygen therapy, total parenteral nutrition, time to full feeding, or length of hospital stay. The study results suggest probiotics have a protective effect against NEC in preterm infants.
Genetic considerations in obesity developmenthelix1661
The document summarizes genetic research on human obesity from the Pennington Biomedical Research Center. It details that over 600 genes have been associated with obesity. Specific genetic disorders are described that can cause obesity like Cushing's syndrome. Mouse models are used to study obesity genes and their role in food intake and metabolism. Genome-wide studies have linked obesity phenotypes to particular chromosomes. The research aims to identify gene combinations and mutations that influence obesity risk and how they interact with environment.
Probiotics have been shown in meta-analyses to reduce rates of necrotizing enterocolitis (NEC) and mortality in preterm infants. However, there is still resistance to implementing their use due to concerns about the variability of probiotic strains and regimes used across studies, lack of data specifically in extremely low birth weight infants, and unproven long-term safety. The author argues that these objections are not valid given the consistent beneficial effects seen across probiotic types, the biological plausibility of the effects, and the lack of documented safety issues in the thousands of infants exposed to probiotics in clinical trials. Widespread adoption of probiotic supplementation could significantly reduce NEC rates and mortality in preterm infants.
An extensive literature review on Nutrigenetics -A new trajectory in obesity...nutritionistrepublic
Obesity is a multifactorial disease influenced by genes and environment. Various genes involved in appetite, metabolism, and fat storage have been identified that can cause differential responses to diet. Nutrigenetics examines how genetic variations affect the interaction between diet and disease, with the goal of developing personalized diets. One study found that patients who received nutrigenetic testing and were given a personalized diet based on their genetic profile lost more weight and better maintained reductions in BMI and blood glucose levels over time compared to a control group without genetic testing. While nutrigenetics shows promise for developing targeted weight loss strategies, challenges remain in fully characterizing gene-diet interactions and implementing testing in clinical practice.
What is health? NUGO International nutrigenomics Conference Wageningen Sept 9...Norwich Research Park
What is health? Can Nutrigenomics allow to quantify metabolic health? (YES)
My very personal conclusions of a wonderful conference (NUGO Week 2011) in Wageningen (The Netherlands) that we organized.
Stress can disrupt the body's homeostasis and lead to psycho-spiritual awakening as the body seeks balance. The human gut microbiome, which outnumbers human cells 10 to 1, plays a key role in this process. Chronic stress and an unhealthy lifestyle can cause chronic inflammation and disease by disrupting the diversity of the gut microbiota. Adopting a diet low in refined carbs and sugar, fasting, probiotic supplementation, spiritual practice, and exercise can help reduce stress, inflammation, and bring the microbiome back into balance.
Recent research suggests that a variety of lifestyle - especially dietary - changes influencing the integrity of gastrointestinal function may be driving at least some portion of the increased prevalence of illnesses of civilization, including neuropsychiatric problems, such as autism, attention-deficit-hyperactivity disorder, major depression, obsessive-compulsive disorder and Alzheimer disease. One area of interest involves the relationship between the gut's microbiome (as well as the related functional integrity of the gastrointestinal tract) and mental health.
This presentation is an overview of our recent publication in the Appetite Journal. "Preclinical Evidence for the Addiction Potential of Highly Palatable Foods: Current Developments Related to Maternal Influence" by David Wiss, Kristin, Criscitelli, Mark Gold, and Nicole Avena.
1. Nutritional programming theories suggest that the prenatal and early life nutritional environment can influence long-term health by permanently programming physiological functions and disease risk.
2. Animal studies demonstrate a direct link between nutrient imbalance during fetal development and later diseases like hypertension, diabetes, and heart disease, independent of growth rates.
3. Exposure to glucocorticoids and alterations in gene expression from nutrient imbalance in early life are thought to be important mechanisms influencing tissue development and function long-term.
The document discusses nutrigenomics and nutrigenetics. It begins with important terms related to omics fields like genomics, nutrigenomics, and epigenetics. It then provides a basic understanding of nutrigenomics and nutrigenetics, including how genetic diversity and environmental factors affect nutrient metabolism and health outcomes. The goals of nutrigenomics are discussed, including customizing nutrition based on an individual's genetics. Experimental approaches like genomics, transcriptomics and metabolomics are used to study these fields. Examples are provided on how nutrigenomics has clarified roles of specific dietary factors and potential applications in disease prevention.
Nutrigenomics is the science that examines the response of individuals to food compounds using post-genomic and related technologies (e.g. genomics, transcriptomics, proteomics, metabol/nomic etc.). The long-term aim of nutrigenomics is to understand how the whole body responds to real foods using an integrated approach termed 'systems biology'. The huge advantage in this approach is that the studies can examine people (i.e. populations, sub-populations - based on genes or disease - and individuals), food, life-stage and life-style without preconceived ideas.
'Lo último en obesidad'. Este es el título del Simposio Internacional que organizamos en la Fundación Ramón Areces los días 1 y 2 de diciembre de 2015. En colaboración con la Fundación General CSIC, reunió a algunos de los mayores expertos en la materia para analizar cómo reducir este grave problema de salud pública.
the new emerging field of science that is nutrigenomics can deal with the issues of health and improve out health with the simple tools by understanding the risk and the baic genome of a person
We are what we eat - The role of diets in the gut-microbiota-health interactionNorwich Research Park
Lecture at Summer School Nutrigenomics in Camerino Italy Sept. 2016.
The (small) intestine has increasingly been recognized to play a key role in the early phase of pro-inflammatory disturbances e.g. by enhanced overflow of dietary components to the distal intestine (ileum, colon) and affecting the gut microbiota & their metabolites (e.g. bile acids, short chain fatty acids). Transcription factors e.g. PPARγ, FXR, AHR or NRF2 are involved in host sensing mechanisms of microbial metabolites. Strong impact of dietary composition on small and large intestinal microbiota and their metabolic functions.
Targeting the (small) intestine and its microbiota with (plant) foods, bioactives, probiotics and drugs will improve gut and liver functions with strong implications for human health during life.
This document discusses the use of probiotics in the neonatal intensive care unit (NICU) to help prevent diseases like necrotizing enterocolitis (NEC). It provides background on the development of the infant gut microbiome and how probiotics may benefit preterm infants by competing with pathogens, producing antimicrobial substances, and modulating the immune system. Several studies cited found probiotic supplementation significantly reduced the risk of NEC and mortality in very low birth weight infants. Meta-analyses support the routine use of probiotics in the NICU.
What is gut microbiota? What is the influence of diet on the proper functioning of our gut microbiota? How does the gut-brain axis (GBA) influence the emotional and cognitive centers of the brain? Tune into this webinar to find out more about this timely topic.
Learning Objectives:
List the neurological and physiological connections that enable the bidirectional communication between the gut and the brain
Identify lifestyle, dietary, and microbial influences on the flow and function of signaling molecules along the gut-microbiota-brain axis
Implement dietary regimens that target the gut and gastrointestinal microbiota to improve or maintain optimal physical and mental health
RDNs earn 1.0 CEU
We Are More Than What We Eat Dietary Interventions Depend on Sex and Genetic ...InsideScientific
To learn more visit: https://insidescientific.com/webinar/we-are-more-than-what-we-eat-dietary-interventions-depend-on-sex-and-genetic-background/
Despite evidence that sex and genetic background are key factors in the response to diet, most studies of how diet regulates metabolic health and even longevity in mice examine only a single strain and sex.
Using multiple strains and both male and female mice, Dr Lamming's team has found that improvements in metabolic health and in longevity in response to reduced levels of protein or specific amino acids strongly depend on sex and strain. While some phenotypes were conserved across strains and sexes, including increased glucose tolerance and energy expenditure, they observed high variability in adiposity, insulin sensitivity, and circulating hormones. Using a multi-omics approach, they identified mega-clusters of differentially expressed hepatic genes, metabolites, and lipids associated with each phenotype, gaining new insight into role of the energy balance hormone FG21 in the response to protein restriction.
My recent introduction talk for the Nutrigenomics Masterclass 2011in Wageningen (The Netherlands):
How to use Nutrigenomics & molecular nutrition? From challenges to solutions
Gastrointestinal motility disorders in critically ill patientsUbaidur Rahaman
1) Gastrointestinal motility disorders are common in critically ill patients, affecting 60% with intolerance to enteral feeding.
2) Motility is impaired throughout the GI tract in critical illness, with absent gastric migrating motor complexes, delayed gastric emptying, reduced antral contractions, and disorganized small bowel and colonic motility.
3) Risk factors for GI dysmotility in the ICU include surgery, sepsis, medications like opioids and sedatives, fluid imbalances, and underlying comorbidities.
Nutrigenomics is the study of how foods and their components affect gene expression. It explores how an individual's genetic makeup influences their nutritional requirements and response to foods. Single nucleotide polymorphisms, which are small genetic differences between individuals, can change how one metabolizes and responds to diet, and influence disease risk patterns. Understanding nutrigenomics may help prevent diseases by developing personalized diets and promoting healthy lifestyle choices based on one's genetics.
Short intro epigenetics & nutrigenomics& the early impact of nutrition Norwich Research Park
Our “genes” are not fixed: “Plasticity” of the genotype by epigenetic mechanisms => important for the phenotypic impact of nutrition.
• Histone and DNA modifications have impact on gene transcription efficiency. Methylation (more stable) and acetylation (more flexible) have impact on chromatin
structures.
• Epigenetic modifications have impact on offspring, embryo development, ageing and disease development or prevention => example: Dutch Hunger Winter.
Health status of future parents are very important for the future health of children.
Early healthy nutrition & lifestyle essential for successful healthy life & “ageing”.
Nutrigenomics is the application of genomics to nutritional research to understand how foods and dietary components influence gene expression. It studies the interactions between nutrition, genes, and health on a genome-wide scale. The goals of nutrigenomics are to identify dietary signals, understand how they interact with genes and signaling pathways, characterize target genes, and use this information to develop personalized diets that can help prevent diseases. Future applications include using nutrigenomics approaches to better understand polygenic diseases and create customized diets based on an individual's genetic profile.
This is the presentation of my systems theory of autistogenesis made at the Western Psychological Association, the Autism Society, and the American Psychological Association. Since that time, new information has continued to support this theoretical perspective and I am now moving into experimental studies to confirm.
The document discusses insights from nutrigenomics research on how diet shapes our health. It makes three key points:
1) Our "paleolithic" hunter-gatherer genes interact with modern diets high in processed foods and lack of challenges from varied whole foods. This mismatch may contribute to disease.
2) Components in plant foods like fibers can have anti-inflammatory effects and influence the gut microbiome in ways that promote health. Dietary challenges from varied whole foods that activate genes like PPARg are more beneficial than safe but nutritionally "empty" processed foods.
3) The gut microbiome plays an important role in mediating the effects of diet on health and disease. For example
Richard Frye, MD, PhD, FAAP, FAAN, CPI, will discuss:
*The enteric (gut) microbiome has an important influence on health and disease states in humans.
* The enteric microbiome influences the human host using chemical mediators, some of which can directly affect mitochondrial function
* Short chain fatty acids produced by gut bacteria not only modulate mitochondrial function and cellular regulatory pathways, but can also be used as mitochondrial fuels.
NUTRIGENETICS AND PERSONALZIED NUTRITION DUBAI 2020.pptxMARIA VRANCEANU
This document discusses personalized nutrition using nutrigenetics and nutrigenomics in clinical practice. It describes how genetic testing can be used to understand an individual's nutritional needs and disease risks based on their genetic variations and single nucleotide polymorphisms (SNPs). SNPs may help predict disease susceptibility, dietary requirements, and drug responses. Understanding a person's genomic background through genetic testing can help design personalized diets and supplement plans tailored to their individual genetics.
The gut-brain axis (GBA) consists of bidirectional communication between the central and the enteric nervous system, linking emotional and cognitive centers of the brain with peripheral intestinal functions. Recent advances in research have described the importance of gut microbiota in influencing these interactions.
Similar to Perinatal Nutrition, Appetite And Food Preferences (20)
Perinatal Nutrition, Appetite And Food Preferences
1. Perinatal Nutrition, Nutrigenomics
Appetite and Food and
Personalized
Preferences Nutrition
Alejandra Ponce Garza
Itxaso Vázquez Varona
2. DEFINITIONS
Appetite:
The natural instinctive desire for food.
It should be distinguished from hunger (need for food)
Food Preferences :
Prefer one food to another.
Perinatal nutrition :
Nutrition that happens pertaining to the period immediately before and after birth
Starts: 20 th -28 th week of gestation
Ends: 1-4 weeks after birth.
Itxaso Vázquez Varona * Alejandra Ponce Garza
2
MSc. Nutrigenomics and Personalized Nutrition
3. BACKGROUND
1.Bellinger, Leanne, and Simon C. Langley -
Evans. "Fetal Programming of Appetite by
Exposure to Maternal Low-protein Diet in the
Rat." Clinical Science 109 (2005): 413 -20. Print.
2. Brion, M.-J. A., A. R. Ness, I. Rogers, P.
Emmett, V. Cribb, G. Davey Smith, and D. A.
Lawlor. "Maternal Macronutrient and Energy
Intakes in Pregnancy and Offspring Intake at 10
Y: Exploring Parental Comparisons and Prenatal
Effects." American Journal of Clinical Nutrition
91.3 (2010): 748-56. Print.
Itxaso Vázquez Varona * Alejandra Ponce Garza
3
MSc. Nutrigenomics and Personalized Nutrition
4. BACKGROUND (1)
Epidemiological observations of associations
between early life nutrition and long-term
disease risk have prompted detailed
experimental investigation of the biological
basis of programming.
Animal experiments
Human interventions:
Global food restriction determine a consistent
Protein restriction cluster of disorders
in the resulting offspring
Micronutrient restriction
Excess fat feeding
Itxaso Vázquez Varona * Alejandra Ponce Garza
4
MSc. Nutrigenomics and Personalized Nutrition
5. BACKGROUND (2)
Maternal macronutrient (carbohydrate, fat, and protein) and
energy intakes potentially influence fetal growth and
program future appetite
Encouraging pregnant women to engage in healthy dietary
behaviors may be of benefit to the development of the fetus
and to later dietary habits of their children.
Itxaso Vázquez Varona * Alejandra Ponce Garza
5
MSc. Nutrigenomics and Personalized Nutrition
6. MECHANISMS
1. Langley-Evans, Simon C., Leanne Bellinger, and
Sarah McMullen. "Animal Models of Programming:
Early Life Influences on Appetite and Feeding
Behaviour." Maternal and Child Nutrition 1 (2005):
142-48
2. Vucetic, Z., J. Kimmel, K. Totoki, E. Hollenbeck, and T.
M. Reyes. "Maternal High-Fat Diet Alters Methylation
and Gene Expression of Dopamine and Opioid-
Related Genes." Endocrinology 151.10 (2010): 4756-
764. Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
6
MSc. Nutrigenomics and Personalized Nutrition
7. APPETITE: MOLECULAR BASIS (1)
Persistent hyperphagic state in animals
exposed to:
Fetal undernutrition
Early postnatal overfeeding
Non-optimal nutrition at critical phases of
development may promote
1. Adaptive responses
2. Modification of the structures of key
hypothalamic nuclei responsible for appetite
control.
Itxaso Vázquez Varona * Alejandra Ponce Garza
7
MSc. Nutrigenomics and Personalized Nutrition
8. APPETITE: MOLECULAR BASIS (1)
Exposure of the rat fetus to
a low protein diet modifies
vascularization of the
cerebral cortex.
Bennis-Taleb et al (1999) Offsrping of rats fed with
low protein diet: Increased
Rats fed low protein diets neural density in the PVN
throughout gestation and and VMN, with fewer NPY
lactation showed differences and CCK neurons.
in whole brain volume and Langley-Evans et al (2005)
volume of the
paraventricular and
ventromedial nuclei of the
hypothalamus.
Plagemann et al., (2000)
Itxaso Vázquez Varona * Alejandra Ponce Garza
8
MSc. Nutrigenomics and Personalized Nutrition
9. APPETITE.: MOLECULAR BASIS (1)
Structural adaptations
Permanently predispose
the animal to increased
appetite
Gene microarray
studies indicate that
the expression of a
relatively narrow
profile of genes in the
hypothalamus is
programmed by fetal
exposure to a maternal
low protein diet Langley-Evans, Simon C., Leanne Bellinger, and Sarah McMullen. "Animal
Models of Programming: Early Life Influences on Appetite and Feeding
Behaviour." Maternal and Child Nutrition 1 (2005): 142-48
Itxaso Vázquez Varona * Alejandra Ponce Garza
9
MSc. Nutrigenomics and Personalized Nutrition
10. MECHANISMS AND DNA (2)
Human study: n=4000
Hypothesis:
Molecules that participate in regulating consumption of
palatable foods (dopamine and opioids) maybe altered in
offspring from mothers fed a HF diet.
Mechanisms: Maternal consumption of HF diet would alter
DNA methylation either globally or within the promoter
regions of dopamine- and opioid-related genes.
The study examines the potential underlying
mechanisms linking maternal consumption of HF
diet to adverse offspring development.
Itxaso Vázquez Varona * Alejandra Ponce Garza
10
MSc. Nutrigenomics and Personalized Nutrition
11. MECHANISMS AND DNA (2)
HF diet during pregnancy and
lactation associated with
altered expression:
Opioid receptor
The opiate ligand preproenkephalin,
Genes specifically linked to the intake
of palatable foods.
Epigenetic modification
(promoter region
hypomethylation) as a
potential mechanism for
increased long-term
expression of dopamine and
opioid-related genes (DAT,
MOR, and PENK) Vucetic, Z., J. Kimmel, K. Totoki, E. Hollenbeck, and T. M. Reyes. "Maternal High-
Fat Diet Alters Methylation and Gene Expression of Dopamine and Opioid-
Related Genes." Endocrinology 151.10 (2010): 4756-764. Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
11
MSc. Nutrigenomics and Personalized Nutrition
12. MECHANISMS AND DNA (2)
Decreased methylation of the promoter region of
GH secretagogue receptor.
Effect persisting into at least the second generation
suggesting the possibility that our observed epigenetic
effects on dopamine and opioid gene expression may extend
beyond the F1 generation.
Itxaso Vázquez Varona * Alejandra Ponce Garza
12
MSc. Nutrigenomics and Personalized Nutrition
13. SALTY
1. Prenatal imprinting of postnatal specific appetites and
feeding behavior. Stylianos Nicolaïdis. Metabolism Clinical
and Experimental 57 (Suppl 2) (2008) S22–S26
2. Crystal SR, Bernstein IL. Morning sickness: impact on
offspring salt preference. Appetite 1995;25:231-40.
Itxaso Vázquez Varona * Alejandra Ponce Garza
13
MSc. Nutrigenomics and Personalized Nutrition
14. APPETITE FOR SALTY (1,2)
Sodium appetite increases in response to
hypovolemic and hypoosmotic deficits.
When these deficits recur, hypernatriophilia
develops.
Hypernatriophilia:
Hypothesis that extracellular dehydration imposed
on a pregnant rat could bring about
hypernatriophilia in its offspring when they reach
adulthood.
Itxaso Vázquez Varona * Alejandra Ponce Garza
14
MSc. Nutrigenomics and Personalized Nutrition
15. APPETITE FOR SALTY (1,2)
Hypothesis was successfully verified by
Crystal and Bernstein
cohort of 169 students: reported higher salt use were
precisely the ones whose mothers had experienced
vomiting during pregnancy.
Kochli and coworkers.
Curtis and associates have shown in the rat that
manipulations of dietary NaCl levels during
gestation and the early postnatal period lead to
persistent changes both in “need-free” and
stimulated NaCl intake by adult rats.
Itxaso Vázquez Varona * Alejandra Ponce Garza
15
MSc. Nutrigenomics and Personalized Nutrition
16. FLAVORS
1. Trout, K. K., and L. Wetzel -Effinger. "Flavor
Learning in Utero and Its Implicat ions for Future
Obesity and Diabetes." Current Diabetes Reports 12.1
(2012): 60+. Print.
2. Mennella, J. A., C. P. Jagnow, and G. K. Beauchamp.
"Prenatal and Postnatal Flavor Learning by Human
Infants." Pediatrics 107.6 (2001): E88
3. Mannella, J. A., C. E. Griffi n, and G. K. Beauchamp.
"Flavor Programming During Infanc y." Pediatrics 113.4
(2004): 840 -45. Print.
Itxaso Vázquez Varona * Alejandra Ponce Garza
16
MSc. Nutrigenomics and Personalized Nutrition
17. FLAVORS (1,3)
Flavors in the mother diet Amniotic fluid.
Amniotic fluid swallowed by the fetus.
PREFERENCES.
Persisten during infancy Childhood Adulthood
Early exposure to different flavors can lead
to increased acceptance of and preferences
for these flavors in later life.
Itxaso Vázquez Varona * Alejandra Ponce Garza
17
MSc. Nutrigenomics and Personalized Nutrition
18. FLAVORS (3)
Hydrolyzed
protein formulas.
Mannella, J. A., C. E. Griffin, and G. K. Beauchamp. "Flavor Programming During
Infancy." Pediatrics 113.4 (2004): 840-45. Print.
Itxaso Vázquez Varona * Alejandra Ponce Garza
18
MSc. Nutrigenomics and Personalized Nutrition
19. FLAVORS (2)
First experimental study that demonstrates that
prenatal flavor experiences enhances the
acceptances and enjoyment of similarly flavored
foods during weaning.
Groups: 46 women. Drank 300ml
Pregnancy Lactation
1 - CW Carrot Juice Water
2 - WC Water Carrot Juice
3 - WW Water Water
Babies: CW weaning period enjoyment of
carrot-flavored cereal.
Itxaso Vázquez Varona * Alejandra Ponce Garza
19
MSc. Nutrigenomics and Personalized Nutrition
20. JUNK FOOD
1. Bayol, Stéphanie A., Samantha J. Farrington, and
Neil C. Stickland. "A Maternal ‘junk Food’ Diet in
Pregnancy and Lactation Promotes an Exacerbated
Taste for ‘junk Food’ and a Greater Propensity for
Obesity in Rat Offspring." British Journal of Nutrition
98.04 (2007). Print.
Itxaso Vázquez Varona * Alejandra Ponce Garza
20
MSc. Nutrigenomics and Personalized Nutrition
21. JUNK FOOD (1)
Bayol, Stéphanie A., Samantha J. Farrington, and Neil C. Stickland. "A Maternal ‘junk Food’ Diet in Pregnancy
and Lactation Promotes an Exacerbated Taste for ‘junk Food’ and a Greater Propensity for Obesity in Rat
Offspring." British Journal of Nutrition 98.04 (2007). Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
21
MSc. Nutrigenomics and Personalized Nutrition
22. A maternal junk food diet before weaning
promotes an exacerbated preference for junk
food and leads to a greater propensity for
obesity in the offspring.
Palatability
Protection against hyperphagia when mother
was fed –at some point- with a control diet.
JUNK
JJJ
FOOD
CCJ
(1)
JCJ
CCC JJC JCC
Bayol, Stéphanie A., Samantha J. Farrington, and Neil C. Stickland. "A Maternal ‘junk Food’ Diet in Pregnancy and Lactation
Promotes an Exacerbated Taste for ‘junk Food’ and a Greater Propensity for Obesity in Rat Offspring." British Journal of
Nutrition 98.04 (2007). Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
22
MSc. Nutrigenomics and Personalized Nutrition
23. JUNK FOOD (1)
Palatability
Major role in
appetite regulation.
Inhibit the satiety
signal while
promoting hunger
and stimulating the
reward centres.
Bayol, Stéphanie A., Samantha J. Farrington, and Neil C. Stickland. "A Maternal ‘junk
Food’ Diet in Pregnancy and Lactation Promotes an Exacerbated Taste for ‘junk Food’
and a Greater Propensity for Obesity in Rat Offspring." British Journal of Nutrition
98.04 (2007). Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
23
MSc. Nutrigenomics and Personalized Nutrition
24. JUNK FOOD (1)
Lactation: important
period for the
programming of an
exacerbated intake of
junk food.
Key role in influencing
long-term appetite.
Milk intake and
composition might be key
regulators of the
development and
maturation of the central Bayol, Stéphanie A., Samantha J. Farrington, and Neil C. Stickland. "A
Maternal ‘junk Food’ Diet in Pregnancy and Lactation Promotes an
and peripheral control of Exacerbated Taste for ‘junk Food’ and a Greater Propensity for Obesity in
appetite. Rat Offspring." British Journal of Nutrition 98.04 (2007). Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
24
MSc. Nutrigenomics and Personalized Nutrition
25. PALATABILITY
1. Langley-Evans , Simon C., Leanne Bellinger, and
Sarah McMullen . "Animal Models of Programming:
Early Life Influences on Appetite and Feeding
Behaviour." Maternal and Child Nutrition 1 (2005):
142-48
2. Vucetic , Z., J. Kimmel, K. Totoki, E. Hollenbeck, and
T. M. Reyes. "Maternal High -Fat Diet Alters
Methylation and Gene Expression of Dopamine and
Opioid-Related Genes." Endocrinology 151.10
(2010): 4756 -764. Print
3. Teegarden , S.l., A.n. Scott, and T.l. Bale. "Early Life
Exposure to a High Fat Diet Promotes Long -ter m
Changes in Dietary Preferences and Central Reward
Signaling." Neuroscience 162.4 (2009): 924 -32. Print
Itxaso Vázquez Varona * Alejandra Ponce Garza
25
MSc. Nutrigenomics and Personalized Nutrition
26. HIGH-FAT FOOD (1)
First evidence of
perturbation of the
nutritional
environment in utero:
12 week old female
offspring of rats fed with
low-protein diet during
gestation and lactation
preferred a high-fat diet
over a high-protein or a
high-carbohydrate diet. Langley-Evans, Simon C., Leanne Bellinger, and Sarah McMullen. "Animal Models
of Programming: Early Life Influences on Appetite and Feeding Behaviour."
Maternal and Child Nutrition 1 (2005): 142-48
Itxaso Vázquez Varona * Alejandra Ponce Garza
26
MSc. Nutrigenomics and Personalized Nutrition
27. HIGH-FAT AND HIGH-
CARBOHYDRATE FOOD (2)
Effect of HF diet and/or maternal obesity on
hypothalamic neuropeptides that affect food intake
Increased expression of NPY, AgRP, NPY Y1 receptor, and
MC4Rand, more consistently, an increase in POMC.
Increase neurogenesis, specifically neurons that express
galanin, enkephalin, dynorphin, orexin, and MCH
Differential expression of dopamine- related genes in the
nucleus accumbens (NAc).
Little examination of circuitry outside the hypothalamus
Animal studies have shown that maternal
consumption of a palatable diet can increase the
preference for fat and sugar in the offspring
Itxaso Vázquez Varona * Alejandra Ponce Garza
27
MSc. Nutrigenomics and Personalized Nutrition
28. HIGH-FAT AND HIGH-
CARBOHYDRATE FOOD (3)
Examination of the effects of early life exposure to
a high fat diet on adult macronutrient preferences
in mice:
Mice were exposed to a high fat diet for one week, from postnatal days
21-28:
The time during which they begin to consume solid food and are no
longer dependent on the dam for nutrition
Hypothalamic development is complete,
In a 10-day macronutrient choice preference test, high fat diet early -
exposed mice showed
A significantl y greater preferenc e for a high fat diet as adults
No differenc es in total daily caloric intake or weight gain during the
macronutrient choice preference period
Itxaso Vázquez Varona * Alejandra Ponce Garza
28
MSc. Nutrigenomics and Personalized Nutrition
29. HIGH-FAT AND HIGH-
CARBOHYDRATE FOOD (3)
Possible mechanisms:
Reduced dopamine signal transmission in the
ventral striatum in these mice may result in an
increased preference for the high fat diet in an
attempt to normalize dopamine levels.
Exposure to a palatable, high fat diet during early
life may lead to long-term reprogramming of the
reward system,
Risk for maladaptive eating habits
Risk for disorders of the reward system.
Itxaso Vázquez Varona * Alejandra Ponce Garza
29
MSc. Nutrigenomics and Personalized Nutrition
30. CONTRADICTION
1. Bellinger, Leanne, and Simon C. Langley -
Evans. "Fetal Programming of Appetite by
Exposure to Maternal Low -protein Diet in the
Rat." Clinical Science 109 (2005): 413 -20.
Print.
Itxaso Vázquez Varona * Alejandra Ponce Garza
30
MSc. Nutrigenomics and Personalized Nutrition
31. LOW-PROTEIN HIGH-FAT FOOD (1)
Low protein diets:
LP-Early: 0-7 day of gestation
LP-Medium: 8-14 day gestation
LP-Late: 15-22 day of gestation
At 4 weeks of age: offspring
were weaned on to standard
chow diet.
At 12 weeks of age, two
male and two female
offspring from each litter
were self-selection diet
protocol to assess appetite
and food preferences.
Bellinger, Leanne, and Simon C. Langley-Evans. "Fetal Programming of
Appetite by Exposure to Maternal Low-protein Diet in the Rat." Clinical
Science 109 (2005): 413-20. Print.
Itxaso Vázquez Varona * Alejandra Ponce Garza
31
MSc. Nutrigenomics and Personalized Nutrition
32. FUTURE PERSPECTIVES
Guidelines for nutrition during pregnancy and
lactation Flavors.
Infant formulas Flavors
Investigate more about mechanisms.
Itxaso Vázquez Varona * Alejandra Ponce Garza
32
MSc. Nutrigenomics and Personalized Nutrition