Nutritional Psychology PDF

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lectures on nutritional psychology. Including flavonoids, and nutrition from childhood into ageing. ...

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Nutritional Psychology lecture 1 reading Choi SW & Friso S (2010). Epigenetics: a new bridge between nutrition and health. Abstract - Nutrients can reverse or change epigenetic phenomena such as DNA methylation and histone modifications, thereby modifying the expression of critical genes associated with physiologic and pathologic processes, including embryonic development, aging, and carcinogenesis. It appears that nutrients and bioactive food components can influence epigenetic phenomena either by directly inhibiting enzymes that catalyze DNA methylation or histone modifications, or by altering the availability of substrates necessary for those enzymatic reactions. In this regard, nutritional epigenetics has been viewed as an attractive tool to prevent paediatric developmental diseases and cancer as well as to delay aging-associated processes. In recent years, epigenetics has become an emerging issue in a broad range of diseases such as type 2 diabetes mellitus, obesity, inflammation, and neurocognitive disorders. Although the possibility of developing a treatment or discovering preventative measures of these diseases is exciting, current knowledge in nutritional epigenetics is limited, and further studies are needed to expand the available resources and better understand the use of nutrients or bioactive food components for maintaining our health and preventing diseases through modifiable epigenetic mechanisms. Conclusion-Epigenetics is an inheritable phenomenon that affects gene expression without base pair changes. Epigenetic phenomena include DNA methylation, histone modifications, and chromatin remodeling. Chromatin is quite dynamic and is much more than a neutral system for packaging and condensing genomic DNA. It is a critical player in controlling the accessibility of DNA for transcription. Modifications of chromatin structure can give rise to a variety of epigenetic effects. Due to its reversible character, epigenetics is now considered an attractive field of nutritional intervention. During our lifetime, nutrients can modify physiologic and pathologic processes through epigenetic mechanisms that are critical for gene expression. Modulation of these processes through diet or specific nutrients may prevent diseases and maintain health. However, it is very hard to define the precise effect of nutrients or bioactive food components on each epigenetic modulation and their associations with physiologic and pathologic processes in our body, because the nutrients also interact with genes, other nutrients, and other lifestyle factors. Furthermore, each epigenetic phenomenon also interacts with the others, adding to the complexity of the system. Our knowledge regarding nutritional epigenetics is still limited. In particular, the effects of nutrients or bioactive food components on histone methylation or chromatin remodeling complexes are largely unknown. In the future, we need to investigate more nutrients or bioactive food compounds to find better ones for our health. Understanding the role of nutrients or bioactive food components in altering epigenetic patterns will aid our ability to find a better way to maintain our health through nutritional modulation Jang H & Serro C (2014). Nutrition, Epigenetics and Diseases. Abstract - Increasing epidemiological (=relating to the branch of medicine which deals with the incidence, distribution, and control of diseases) evidence suggests that maternal nutrition and environmental exposure early in development play an important role in susceptibility to disease in later life. In addition, these disease outcomes seem to pass through subsequent generations. Epigenetic modifications provide a potential link between the nutrition status during critical periods in development and changes in gene expression that may lead to disease phenotypes. An increasing body of evidence from experimental animal studies supports the role of epigenetics in disease susceptibility during critical developmental periods, including periconceptional period, gestation, and early postnatal period. The rapid improvements in genetic and epigenetic technologies will allow comprehensive investigations of the relevance of these epigenetic phenomena in human diseases. Conclusion- Developing organisms seem to have a wide range of susceptibility to epigenetic changes. Appropriate dynamics in epigenetic modifications are essential for embryogenesis (= process by which the embryo forms and develops), early fetal development and early postnatal growth. Consequently, the inadequate establishment of epigenetic modifications during critical developmental periods due to changes in the maternal diet or other environmental factors may induce paediatric developmental diseases and even affect health in adulthood. Since much of the reprogramming that occurs during early life may go unrecognized until adulthood, a better understanding of the interplay between genetic and epigenetic interaction in critical time windows of development would improve our ability to determine individual susceptibility to a wide range of diseases.

Leonard WR (2002). Food for thought: dietary change was a driving force in human evolution. Summary points -why are we evolutionarily more successful than other primates? -many aspects of humans are largely the result of natural selection acting to maximize dietary quality and foraging efficiency. Changes in food availability over time strongly influenced our hominid ancestors. What we eat differentiates us from our primate kin. Contemporary human populations the world over have diets richer in calories and nutrients than those of apes. Humans are flexible eaters (don’t have restricted diets). Diet is used for biological processes are all critical aspects of an organism's ecology. -The energy dynamic between organisms and their environments (energy expended in relation to energy acquired) has adaptive consequences for survival and reproduction. Maintenance energy is what keeps an animal alive on a day-to-day basis. Productive energy is associated with producing and raising offspring for the next generation. For mammals like ourselves, this must cover the increased costs that mothers incur during pregnancy and lactation. Becoming Bipeds – living nonhuman primates habitually move around on all fours, or quadrupedally, when they are on the ground. Theories of why● Two-legged locomotion freed the arms to carry children and foraged goods. ● Bipedalism emerged as a feeding posture that enabled access to foods that had previously been out of reach. ● Moving upright allowed early humans to better regulate their body temperature by exposing less surface area to the blazing African sun. ● Bipedalism evolved in our ancestors at least in part because it is less energetically expensive than quadrupedalism. - bipedalism can be viewed as one of the first strategies in human nutritional evolution, a pattern of movement that would have substantially reduced the number of calories spent in collecting increasingly dispersed food resources. Big Brains and Hungry Hominids- dramatic enlargement of the brain - big brains use up a lot of energy roughly 16 times as much as muscle tissue per unit weight. Humans have bigger brains than primates but energy use is the same. We therefore use a much greater share of our daily energy budget to feed our brains - bipedalism enabled hominids to cool their cranial blood, thereby freeing the heat-sensitive brain of the temperature constraints that had kept its size in check. Brain expansion almost certainly could not have occurred until hominids adopted a diet sufficiently rich in calories and nutrients to meet the associated costs. Species with bigger brains dine on richer foods, and humans are the extreme example. - Contemporary hunter-gatherers derive, on average, 40 to 60 percent of their dietary energy from animal foods (meat, milk and other products). Modern chimps, in comparison, obtain only 5 to 7 percent of their calories from these comestibles. Animal foods are far denser in calories and nutrients than most plant foods. For early Homo, acquiring more gray matter meant seeking out more of the energy-dense fare. The continued desiccation of the African landscape limited the amount and variety of edible plant foods available to hominids. Those on the line leading to the robust australopithecines coped with this problem morphologically, evolving anatomical specializations that enabled them to subsist on more widely available, difficult-to-chew foods. Homo took a different path. As it turns out, the spread of grasslands also led to an increase in the relative abundance of grazing mammals such as antelope and gazelle, creating opportunities for hominids capable of exploiting them. H. erectus did just that, developing the first hunting-and-gathering economy in which game animals became a significant part of the diet and resources were shared among members of the foraging groups.These changes in diet and foraging behaviour did not turn our ancestors into strict carnivores; however, the addition of modest amounts of animal foods to the menu, combined with the sharing of resources that is typical of huntergatherer groups, would have significantly increased the quality and stability of hominid diets. Improved dietary quality alone cannot explain why hominid brains grew, but it appears to have played a critical role in enabling that change. After the initial spurt in brain growth, diet and brain expansion probably interacted synergistically: bigger brains produced more complex social behaviour, which led to further shifts in foraging tactics and improved diet, which in turn fostered additional brain evolution.

Lecture one Our diet has shaped the development of our brain and our cognitive capacity Evolution - Our brain size has influenced our nutritional needs ●

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Brain:body mass ratio is high in humans ○ Encephalisation ○ Over 4 million year our brain size has tripled Energy demands of neural tissue is high ○ 16x more energy expensive than skeletal tissue

Changes in encephalisation (brain mass) over time Dietary changes associated with early brain evolution •

Austropithecines –

Seasonally varied diet

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Mainly plant-based (fruits, seeds, grasses & tubers)

– •

Brain size, body weight and post-canine tooth surface areas of hominids

Limited animal foods

Homo erectus Further tool development, hunter-gatherer economy

Homo habilis

Meat is common (hunting &

Tool development aided processing of carcasses

scavenging)

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More animal foods (likely scavenged not hunted)

diet

–

Increases in meat, energy- & nutrient-rich marrow

–

More high quality & stable

Importance of fatty acids in brain development ●

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Consumption of animal food ○ Greater caloric content ○ Increased levels of polyunsaturated fatty acids Long-chain polyunsaturated fatty acids ○ Docosahexaenoic acid (DHA) ○ Arachidonic acid (AA) ○ Critical for brain growth

But where does DHA and AA come from on the African savannah? Broadhurst CL, Cunnane SC, Crawford MA. 1998. Rif Valley lake fish and shellfish provided brain-specific nutrition for early Homo

Limited dietary DHA & AA constrained brain evolution Resolved by greater consumption of animal & fish

Abstract - An abundant, balanced dietary intake of long-chain polyunsaturated fatty acids is an absolute requirement for sustaining the very rapid expansion of the hominid cerebral cortex during the last one to two million years. The brain contains 600 g lipid/kg, with a long-chain polyunsaturated fatty acid profile containing approximately equal proportions of arachidonic acid and docosahexaenoic acid. Long-chain polyunsaturated fatty acid deficiency at any stage of fetal and/or infant development can result in irreversible failure to accomplish specific components of brain growth. For the past fifteen million years, the East African Rift Valley has been a unique geological environment which contains many enormous freshwater lakes. Paleoanthropological evidence clearly indicates that hominids evolved in East Africa, and that early Homo

What are the implications for our current (Western) diet? ● ●

Over the last 10000 years there have been significant changes in our diet (& lifestyle), but not genomes! -Altered nutritional characteristics of Western diets ○ Glycaemic load, fatty acid composition, macronutrient composition, micronutrient density, acid-base balance, sodium-potassium ratio & fibre content

Do these changes underlie the emergence of the typical chronic diseases of Western societies Cordain et al (2005) Origins and evolution of the Western diet: health implications for the 21st century Summary - Major changes in brain size and diet occurred between 2-1.7 million years ago as the genus, Homo, evolved Abstract - There is growing awareness that the profound changes in the environment (eg, in diet and other lifestyle conditions) that began with the introduction of agriculture and animal husbandry ≈10000 y ago occurred too recently on an evolutionary time scale for the human genome to adjust. In conjunction with this discordance between our ancient, genetically determined biology and the nutritional, cultural, and activity patterns of contemporary Western populations, many of the so-called diseases of civilization have emerged. In particular, food staples and food-processing procedures introduced during the Neolithic and Industrial Periods have fundamentally altered 7 crucial nutritional characteristics of ancestral hominin diets: 1) glycemic load, 2) fatty acid composition, 3) macronutrient composition, 4) micronutrient density, 5) acid-base balance, 6) sodium-potassium ratio, and 7) fiber content. The evolutionary collision of our ancient genome with the nutritional qualities of recently introduced foods may underlie many of the chronic diseases of Western civilization.

Summary- In the United States and most Western countries, diet-related chronic diseases represent the single largest cause of morbidity and mortality. These diseases are epidemic in contemporary Westernized populations and typically afflict 50 – 65% of the adult population, yet they are rare or nonexistent in huntergatherers and other less Westernized people. Although both scientists and lay people alike may frequently identify a single dietary element as the cause of chronic disease (eg, saturated fat causes heart disease and salt causes high blood pressure), evidence gleaned overthe past 3 decades nowindicatesthat virtually all so-called diseases of civilization have multifactorial dietary elements that underlie their etiology, along with other environmental agents and genetic susceptibility. Coronary heart disease, for instance, does not arise simply from excessive saturated fat in the diet but rather from a complex interaction of multiple nutritional factors directly linked to the excessive consumption of novel Neolithic and Industrial era foods (dairy products, cereals, refined cereals, refined sugars, refined vegetable oils, fatty meats, salt, and combinations of these foods). These foods, in turn, adversely influence proximate nutritional factors, which

Correlates with an important adaptive shift ● ● ● ●

Evolution of first hunter-gatherer economy Greater consumption of animal foods Transport of food resources to homebases Sharing of food within social groups

Consumption of animal food provided key long-chain polyunsaturated fatty acids (DHA & AA) necessary for brain growth. Nutritional epigenetics ● ●

Study of inherited changes in phenotype (appearance) or gene expression caused by mechanisms other than changes in the underlying DNA sequence Epigenetic events alter our phenotype ○ DNA methylation ○ Covalent modifications of histones ○ Chromatin & RNA interference

Our diet can influence epigenetic events: nutritional epigenetics ○ ○ ○

The kind and quantity of food eaten by a parent or infant, can change their constitution at a molecular level, and this may be transmitted across generations This is not a mutation but a change in the potential of genes to be expressed in the body as various protein products Our diet can affect our own long-term health (i.e De Rooij et al, 2006) and that of our future generations (i.e Pembrey et al, 2006)

Roseboom, T., de Rooij, S., & Painter, R. (2006)- Small size at birth is linked with an increased risk of

chronic diseases in later life. Poor maternal nutrition during gestation may contribute to restricted fetal growth, leading to increased disease susceptibility in later life. Animal studies have shown that undernutrition during gestation is associated with reduced life span and increased disease susceptibility. The Dutch famine is a unique counterpart for animal models that study the effects of restricted maternal nutrition during different stages of gestation. This paper describes the findings from a cohort study of 2414 people born around the time of the Dutch famine. Exposure to famine during any stage of gestation was associated with glucose intolerance. We found more coronary heart disease, a more atherogenic lipid profile, disturbed blood coagulation, increased stress responsiveness and more obesity among those exposed to famine in early gestation. Women exposed to famine in early gestation also had an increased risk of breast cancer. People exposed to famine in mid gestation had more microalbuminuria and obstructive airways disease. These findings show that maternal undernutrition during gestation has important effects on health in later life, but that the effects on health depend on its timing during gestation. Especially early gestation seems to be a vulnerable period. Adequate dietary advice to women Pembrey et al. (2006)- Transgenerational effects of maternal nutrition or other environmental ‘exposures’ are well recognised, but the possibility of exposure in the male influencing development and health in the next generation(s) is rarely considered. However, historical associations of longevity with paternal ancestors’ food supply in the slow growth period (SGP) in mid childhood have been reported. Using the Avon Longitudinal Study of Parents and Children (ALSPAC), we identified 166 fathers who reported starting smoking before age 11 years and compared the growth of their offspring with those with a later paternal onset of smoking, after correcting for confounders. We analysed food supply effects on offspring and grandchild mortality risk ratios (RR) using 303 probands and their 1818 parents and grandparents from the 1890, 1905 and 1920 O¨ verkalix cohorts, northern Sweden. After appropriate adjustment, early paternal smoking is associated with greater body mass index (BMI) at 9 years in sons, but not daughters. Sex-specific effects were also shown in the O¨ verkalix data; paternal grandfather’s food supply was only linked to the mortality RR of grandsons, while paternal grandmother’s food supply was only associated with the granddaughters’ mortality RR. These transgenerational effects were observed with exposure during the SGP (both grandparents) or fetal/infant life (grandmothers) but not during either grandparent’s puberty. We conclude that sex-specific, male-line transgenerational responses exist in humans and hypothesise that these transmissions are mediated by the sex chromosomes, X and Y. Such responses add an entirely new dimension to the study of gene–environment interactions in development and health

Dutch famine- Extreme food shortage during the 6 months of WWII = Opportunity to study effects of prenatal undernutrition on health Aim- Evaluation of whether prenatal exposure to famine led to impaired glucose/insulin homeostasis with increasing age. Found- People exposed to famine in utero showed impaired OGTT responses Longitudinal study of 300 Swedish families in an isolated village. Birth, death, health & genealogical records assessed. 100 years, 3 generations. ● ●

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