Nutrition and Brain, Baumgartner Explain the role of macro and micronutrients in the brain Give examples of some important micronutrients Vulnerability to nutrient deficiency: what do studies need to consider? how are microbiome and brain development related to one another?

Overall metabolism brain highly metabolically active --> 60% of O2 consumption of child vs 20% adult relies on many different nutrients for growth, repair, function overall, brain's dry matter made up of 60% fat 20% CHO 10% proteins Vulnerability to nutrient deficiency depends on timing and duration of deficiency --> short-term folate deficiency during conception much more dangerous than short-term folate deficiency postnatal brains requirements, which change depending on developmental stage --> omega-3 FA necessary during breastfeeding period study investigating the behavioral changes due to deficiencies must be designed properly: what area is affected by the deficiency --> what function altered when does the specific area develop --> when did deficiency occur or when is supplementation likely to show positive effects eg: assing problem-solving skills in toddlers makes no sense, because area not fully developed at that time dose/degree of deficiency --> may only cause harm at severe deficiencies --> pregnant mother can maintain normal TH despite mild iodine deficiencies, but severe deficiency causes cretinism Folate essential for proper formation of neural tube important before and during conception, because neural tube formed at day 22 Iodine Thyroid hormones important for neuronal migration, proliferation, and myelination --> fetus relies on maternal TH transfer up to 3rd TM severe iodine deficiency results in cretinism --> important that fetus can stock up iodine Omega-3 LCPUFA make up largest part of fats found in brain (50-60%) mostly DHA --> EPA can affect brain via peripheral mechanisms: modulation of sysntemic inflammation and vascular health proportions and accrual of n-3 FA switch in n-6/3 content in brain: up to 10y, ARA content > DHA --> stabilizes in adulthood increase in DHA 35x from 30wk to 18 motnhs --> importance of mother's milk Microbiome development in offrping's microbiome coincides with brain development --> in line with brain-gut-axis-hypothesis early life nutrition may affect microbiota and brain directly and indirectly due to the existing interactions between them

Nutrition and Brain, Baumgartner fundamental questions & key concepts which concepts need to be clear in regards to timing and the relation between nutrients & brain development? what key concepts need to be considered: study design, timing of intervention, tools used...

Fundamental questions Matching: does nutrient affect cognition/behavior beyond sheer brain development? how strong is the relationship? for nutrient(s) --> additive or interactive effects with other nutrients/environment? for given timeframe, e.g. first trimester Are the consequences of a deficiency long-term or short-term? short-term: acute dysfunction long-term: cognitive development delayed/hampered Key concepts Matching (see above) proper tools to assess deciciency per se as well as impact it has on cognitive domains child age: early testing possible, but more reliable as child ages study design rct vs interventional sample size

Nutrition and Brain, Baumgartner What are the 3 types of tools used to study nutrition and brain development in children? what are the strength and limitations?

Approaches to measuring cognition in humans Cognition: involves many different factors, such as language/psychomotor/perception/attention/memory/executive functions (vgl Bild) Global measures: IQ, usually paper-based, otherwise PC-based motor and language based tests for infants limitations widley applied but limited sensitivity due to global assessment of cognitive function --> score difficult to relate to nutrient deficiency timing must be timed properly --> difficulty of test must be appropriate to child's developmental stage may overlook long-term effects when short-term effects are not present high intra and interindividual variability child can be distracted in room or by assessor Domain specific testing test battery that assesses a given cognitive domain that is hypothesized to be affected by a nutrient deficiency at a given time point of development must be sensitive enough for intervention duration has replaced global testing because of higher specificity cultural differences may turn questions more difficult to certain child group --> cultural fairness requires validation does the test depict cognitive domain of interest + does nutrient intervention affect domain of interest? Neurophysiological tools MRI and fMRI measure brain anatomy and function, repsectively EEG: evoked potential of different stimuli can be assessed NIRS, non-invasive and suitable for field strengths & limitations (-): expensive, not suitable for field, expertise required (+): can be used during sleep, very sensitive thereby useful to clarify discrepant findings, potentially smaller sample sizes than with traditional assessment tools

Nutrition and Brain, Baumgartner Iron how distributed in brain? what functions does it take on on brain? what if deciciencies occur? what evidence available? hint: Nepal

Iron and brain development Iron distribution in brain age specific: accumulates over time up to age 40 highly present in areas undergoing myelinisation during development area-, cell-specific: involved in neurotransmission of dopmainergic areas Iron function in brain oxygen transport to brain --> high O2 needs energy production in cytochormes in mitochondria NT synthesis: dopamine synthesis is Fe-dependent myelinisation: Fe used as co-factor of enzymes reponsible for myelinisation as well as FAs deficiency: myelin content and quality (via FA) affected --> transition speed affected in children Iron deficiency crucial for myelination in 3 TM as well as up to age 3 --> deficiencies irriversible long-term damage slow speed of processing and synaptic efficiency spatial memory and learning affected poor school achievement, attention, memory, language development, motor skills and socioemotional development --> child prone to health and psychological chalenges in later life on large scale, poor development results in poverty of a nation Evidence Nepal study: Fe & B9 during pregnancy until 12 months postpartum results in better cognitive outcomes and motorcontrol than placebo group prolonging supplementation from 12 to 36 motnhs shows no additional benefit --> time-window pre/perinatal deficiency as well as anemia can lead to short and long-term consequences on congitive, motor and socioemotional domains short term: O2 supply to brain insufficient? long term: neurological deficits due to hampered myelination anemic school children benefit from supplementation --> example of short term negative consequence

Nutrition and Brain, Baumgartner Omega-3 what effects do n-3 FA have on brain development & structure brain function how do different LCPUFAs contribute to brian health? what are known consequences of LCPUFAs deficiencies? what is the evidence on LCPUFAs intake during pregnancy and childhood?

Omega-3 LCPUFA make up largest part of fats found in brain (50-60%) mostly DHA --> EPA can affect brain via peripheral mechanisms: modulation of sysntemic inflammation and vascular health proportions and accrual of n-3 FA switch in n-6/3 content in brain: up to 10y, ARA content > DHA --> stabilizes in adulthood increase in DHA 35x from 30wk to 18 motnhs --> importance of mother's milk affect brain function via membrane fluidity --> receptor affinity in synapses increased some n-3 FA used as fuel source --> brain requires lots of E indirectly: attenuate inflammation and modulate IS via gene expression LCPUFA deficiency altered FA profile processing speed of visual cues affected during perinatal period, animal model myelinisation, synaptogenesis and neural membran FA composition affected reductions inf brain glucose uptake and metabolism Evidence oberservational studies of seafood intake: beneficial effect when consumed during pregnancy as well as childhood cannot establish causal relation due to nature of study intervention studies of omega-3 supplementation: no effects and inconclusive results

Intro lecture Baumgartner Prevention and treatment what factors are important to prioritize treatment and prevention? wat are modifiable risk factors? how is health captured, name two important factors reflecting health of a population

Prevention and treatmentent Prioritizing of efforts necessary, but this requires knowledge about risk factors, stats and evidence (modifiable) risk factors smoking phyical inactivity alcohol abuse unhelthy diet statistics and evidence help to identifiy most important health problems as well as solutions to it Global Burden of Disease study: ongoing study in entire world since 1990 captures data on incidence, prevalence and mortality of different conditions causing premature death or disability incidence: number of new cases prevalence: number of existing cases at/during a given timepoint/period mortality and morbidity can be extrapolated published in the LANCET: continuous epidemiological data on development of many NCDs population health summary measures --> not applicable to single individuals! HALE: healthy life expectancy compares healthspan with lifespan --> number of years to be lived in full health increases if risk factors are reduced healtcare quality improves decreases if (e.g. gap between HALE and lifespan increase) with age --> usually #1 risk factor for NCDs DALY: disability adjusted life years sums life years lived with disability & non-fatal disease and compares to standard, normative mean of expecte life years --> basically how many years of theoretical maximum are cut short due to illness time-based uses factor to adjust for severity of different diseases experienced not always clear where to draw line betwen healthy and unhealthy death always more impactful on daly than disability/disease metabolic factors make up large part of DALYs DALY and HALEs allow to assess burden of disease as well as efficacy of health system performance target investments

Intro Baumgartner NCDs definition trend worldwide costs

Non-communicable diseases global trend for NCDs is increasing while communicable, neonatal and maternal diseases decrease injuries remain indifferent affect men and women to same degree costs: high because ncds are chronic diseases usually remain for a lifetime or difficult to reverse (obesity, cancer) expensive medication and treatment (antibiotics or other medication against communicable diseases less expensive)

Intro lecture Baumgartner Explain epidemiological transition

Epidemiological shift improvement in hygene, reduction in childhood mortality and healthcare improve --> mosrtality decreases --> demographics: more aged individuals --> higher NCD risk shift from traditional foods to Westernized diet --> obesity and chronic diseases as well as chronic burden of malnutrition increase

Intro lecture Baumgartner explain Fetal Origins of Adult Disease

discovery of increase prevalence of NCDs in men stemming from areas where childhood mortality was higher low birth weight = proxy for poor prenatal nutrition --> associated with T2D, CVD & high bp first 1000d as key timeperiod for health high plasticity --> can backfire in case of maternal malnutrition due to (epigenetic) imprinting evidence on humans almost impossible to obtain due to duration, but evidence from animals available

Costs of chronic diet-related diseases in Siwtzerland, Wieser explain three main dimensions of disease cost how do these dimensions look in CH, how have they changed and which ones are the most important ones how are these dimensions assessed/established?

Direct medical costs monetary value ressources others have to invest in order to cure/take care of diseased person can extend to family and non-professionals/non-medical persons in CH: healthcare about 1/3 of of illness-related expenses amount to healtcare in CH 9730.- Fr/y per capita in CH costs are high but when adjusted for purchasing power, expenses become 20% higher (and more realistic) as opposed to 50% difference in absolute means Production losses of the person affected also measured in monetary fashion --> usually based on salary of individual x time different types of production loss partial loss: absenteeism (some weeks/months) or presneteeism (reduced workload/pensum) total loss: permanent disability or death potential loss: suboptimal development and cognitive weknesses, e.g. LMIC with stunting/nutrient deficiencies how to measure production losses questionnaires to capture how often/long employers absent/reduced workload administrative data to assess partial or total disability epidemiological data for premature mortality additionally impared physical and cognitive development in LMIC production losses in CH mental and musculoskeletal disorders have greatest impact --> chronic and very low mortality cause long absence more "deadly" NCDs have comparable low impact, but also because mortality higher DALYs disability and loss in quality of life measured in DALYs, not monetary DALY two components: time and weight of disease YLD: years lived with disability --> non lethal but disabling condition YLL: years of life lost severity reflect by DALY weight and must be defined --> worldwide questionnaires chornic diseases realtively low weight mental diseases and pain high weight good correlation between different cultures shows agreement on severity of different conditions In CH neoplass responsible for large part of YLL musculoskeletal diseases for YLD --> larger impact than YLL, typical for country with good healthcare system DALY burden has declined by about 30% in last 30 years --> big progress

Costs of chronic diet-related diseases in Siwtzerland, Wieser Give an overview of the current knowledge on costs in CH by what categories can the data be visualized? what are the major causes of disease burden for these categories? what costs are not included how was GBD study used in this particular case?

Dimensions of healthcare costs in CH by service by type of service provider by type of financing instance by illness and disease defined using the GBD study costs for pregnancy, aesthetics and similar not included co-morbidities separated

Enteral and Parenteral Nutrition Meier Malnutrition what is the importance of oral nutrition therapy in regards to malnutrition? how's the situation in hospitals? prevalence WW & CH who's most commonly affected? procedures to identify malnutrition what are signs

Malnutrition Importance of oral nutritional therapy prevalence of malnutrition increases during hospital stay (vgl Bild: nutritiona lstatus deteriorates...) 55% of served food returned --> flight attendant experiment affects therapy outcome and mortality improving nutrition during hospital stay is economic daily requirements of many nutrients not met, depending on which requirements chosen, 53-70% --> nutrition in hospital setting is highly insufficient Reasons for malnutrition (kennste) Clinical: Nausea, Cancer, infections, low BMI --> can affect hunger and appetite hormones Non-clinical mastication problems monotonous food food temperature & serving times Identification of patients at risk of malnutritoin or suffering from malnutrition high risk patients: low BMI, disease-related weight loss geriatric and oncology most commonly affected procedure of malnutritoin identification Risk screening using screening tools: NRS 2002 Diagnostic assessment phenotypic: low FFM measured via DXA/BIA, unintentional weight-loss etiologic: low food intake, disase-related difficulties eating Diagnosis at least one phenotypical and one etiological criterion Severity Grading moderate --> vgl Bild severe --> BMI = 3, >10% weight loss in past 6m, serum albumin < 30g/l prevalence worldwide about 25%, same for CH

Enteral and Parenteral Nutrition Meier ONS Evidence: top or flop? what types exist and when are they do be used?

Oral Nutritional Supplements first line adjuvant nutritional therapy different types polymeric: entire foods, commercially available --> usually better tolerated and used most often oligomeric: broken down macros --> peptides & micro's disease specific: diabetes, CKD... isolated macros Forticifaction of foods first step of malnutrition treatment, further step taken with sip feeds if fotification insufficient concinving evidence for the effectiveness of ONS in the clinical setting (multiple meta-analyses)

Infant and young child feeding, Baumgartner Breastfeeing practices what is the rationale for breastfeeding what are short and long-term effects on breastfeeding on child --> name 3 main domains, then exemplify on mother possible mechanisms mediating the above effects

Breastfeeding practices Timing within one hour of birth until up to age 2 or even beyond, on-demand exclusive breastfeeding for first 6 months HIC: introduction of complemetary foods as of fifth month recommended rationale no adverse outcomes on growth & natural (mother’s milk much more complex and rich in diverse nutrients/bioactives than formulas) short-term (infancy) decreased newborn mortality --> protects against diarrheal and pneumonic infections sudden-infant-death syndrome (SIDS)--> two months reduce risk by 50%, longer breastfeeding further reduces risk of SIDS compared to non/partially breastfed children: not breastfeeding increases infection-realted mortality 2x beneficial effect on gut health --> necrotisation of enterocolitis prevented in pre-term infants long-term (later life) protective against neurodevelopmental delays potential enhancement of motor development protective against metabolic diseases (hypertension, diabetes, obesity) protective against immune-related diseases (allergies, coeliac, IBS) WHO meta-analysis: non or sporadically breastfed children prone to develop obesity whereas breastfeeding for at least 6 months protects children Protective effect possibly mediated but gut microbiome modulation during first 1000d Microbiota of breastfed infants differs from formula fed à more commensal, less pathogenic strains Protective effects also for mother à diabetes, obesity, breast/ovarian cancer

Infant and young child feeding, Baumgartner Complementary feeding practices what importance of complementary feeding, what is the goal? what if complementary feeding fails? what foods shoould be consumed amounts rythm type foods to avoid how many children get appropriate complementary feeding worldwide? important aspects of compl. feeding during illness explain: responsive feeding early protein hypothesis

Complementary feeding practices necessary to cover increased needs as of 6 motnhs that cannot be covered by mother's milk anymore sub-oprtimal complementary feeding à stunting complementary foods (= first foods) semi-solid and soft complement mother's milk --> closes the gap between requirements covered by milk and requirements milk cannot cover but that the growing infant has from month 6 to 23 --> some children ready earlier, around 4 months 70% children WW are introduced to first foods, but only 20% with minimum diversity and frequency à breastfeeding from 12-23 months persists in 65% of cases WW weaning: stopping breastfeeding and switching over to semi-solid foods complemenary feeding practices & recommendations quality of foods important: ensure food variety by feeding at least 5/8 food groups animal foods incl. mother’s milk fruits & veggies avoid empty calories --> high nutrient density foods important Portion sizes: start with small portions, soft and little variety and 2-3 meals per day Variety increase variety, volume and frequency of feeding other important aspects & special situations hygiene & proper food handling use fortified foods if necessary in case of illness --> increase drinking volume and offer favorite foods to ensure proper food intake responsive feeding: watch out for and respect child’s reaction to feeding à foundation of (good) eating habits early protein hypothesis: protein intake > protein requirements primes metabolism to become obese

Infant and young child feeding, Baumgartner DOHaD explain framework --> draw! hints environment early nutrition adult health & disease

DOHaD Framework environmental stressors prime organism à organism becomes prone to diseases if environment changes / is not-well prepared to environment genetic epigenetics DNA Histone Chromatin structure miRNA trajectories in early life more modulable/plastic, relatively low effort and pronounced impact on later life little known on how breastfeeding and complementary feeding affect epigenetics and microbiota obesity incidence more strongly correlated with microbiome at 3 months than at 12 months partial breastfeeding with additional formula à microbiota more similar to formula-fed infants breastfeeding/mother’s milk has epigenetic effects epigenome and microbiome interact with phenotype and early nutrition à 1000d for microbiota modulation

Eating disorders, Milos Definitions General characteristics of eating diorders three types of eating disorders prevalence common co-morbidities mortality

Risks and complications of eating disorders Types Anorexia nervosa (AN) typical symptoms: worry about body shape, self-esteem linked to weight/appearance, fear of gaining weight 1.2% women weight 15% below expectation BMI self-esteem related to weight high food intake due to food attacks --> 1/week vomiting to compensate for food attacks Binge eating food intake >>> during at least 3 months characteristic behavior: fast and abnormally bulky food intake despite absence of hunger followed by disgust and guilt Characteristics often slowly and gradually developing bnormal eating behavior with tendency of becoming chronic eating disorder is hidden from family/friends and third parties profound impact on life: physical, psychological, professional, and social Co-morbidities mostly psychatric nature high rates of suicidal tendencies amongst eating disorders difficulties to assess own and other's emotions difficulties to see big picture, obsessive with details mortality in anorexic people ~6% hormonal foundation: leptin-like effect observed in AN increased activation of HPA and HPG (gonads) axes --> reduced BMD, increased physical activity but also reduced reproductive activity organ specific --> vgl Bild gastric emptying osteoporosis --> 40% of patients have low BMD amenorrhea --> fertility affected cortical brain atrophy

Eating disorders, Milos Etiology & Therapy name three main areas of etiology and exemplify each give an overview of therapy who is involved? who is targeted? what are the main goals of therapy?

Multifactorial etiology Biological and genetic factors genome-wide association found 8 loci involved in AN pre- and perinatal factors: infections during pregnancy SGA birth complications feeding disorders in infant childhood: obsessive, perfectionistic behavior Neuro alteratino in the dopaminergic system leads to self-starvation becoming a trigger of motivation --> viscous cicle Personality and individual experiences Character traits low self-esteem obsessiveness anxiety emotional inhibition trauma sexual abuse or other trauma strict diets in family critical experiences towards appearance/weight/eating Socio-cultural factors beauty standards fashion standard overabundance of food unhealthy role models Therapy interdisciplinary --> communication is key! medical entities (family physician, specialists, gynecologists, dentists, internal medicine) employer social services psychiatry target patients as well as patient's surrounding get insight and enhance trust, and motivate change family, relationship work major goals reach at least BMI = 18.5 or stabilize weight if normal BMI normalize eating habits --> 3 meals/d with 2-3 snacks treat comorbidities (somatic/psychiatric)

Musculoskeletal diseases and nutrition, Andersson Bone basics bone homeostasis renewal duration BMD pattern throughout life --> draw same for all?

Bone homeostasis Bone basics trabecular: 15.25% calcified cortical bone: 80-90% calcified, cells osteoblasts & osteoclasts: build/resorb bone osteocytes: derive form osteoblasts and represent mature cell, 80-90% of bone renewal every 10 years peak bone mass between age 30 and 40 gender differences: women have lower BMD to begin with --> 60-80% genetically inherited, rest modulated by environment menopause-caused fall in estrogen results in greater bone resorbtion and therefore lower BMD in females

Musculoskeletal diseases and nutrition, Andersson Osteoporosis prevalence --> how many falls burden of fractures risk of fracture depending on first/seonc fracture and gender how measured/proxy reatment and preventive strategies

Osteoporosis loss of bone mass (quantity) and deterioration of bone archtecture (quality) consequences greater fracture risk most commonly spine, hip or wrist fractured 5-6% of falls actually result in fracture collapsed vertebra --> tooped posture prevalence gender differences --> 20% females, but also 5% males affected worldwide variance in prevalence assumed to have genetic reason, not nutritional 75% of osteoporotic fractures in >70 year-olds risk for first fracture differs between gender (50% or more for females vs 20% males), but not for second fracture: 20% both gender risk for second fracture highest in the year following the first fracture cost & disease burden 13'000€/hospitalization --> greater than cancer, heart, and stroke combined due to greater prevalence of osteoporosis fractures than other link to sarkopenia fear of falling reduces mobility and thereby muscle mass --> ultimately increases fall risks muscle strength correlates with BMD

Musculoskeletal diseases and nutrition, Andersson Sarkopenia prevalence consequences etiology risk factors

Sarcopenia prevalence: 20-75%, depending on population and source of information consequences poor hospital outcomes, risk of falls, loss of independence definition and diagnosis not always clear --> muscle mass measurements, handgrip strength muscle strength via handgrip peak in early adulthood bi-phasic decline --> gradual as of age 40, substantial as of age 50 etiology systemic inflammation ageing-associated processes reduced autophagy loss of mitochondria with additional decline in mitochondrial function impared stem cell regeneration los protein intake and negative protein turnover --> decrease in MyoPS and MitoPS Risk factors sarcopenic obesity extreme weight loss drugs & pharmacological therapy --> ACE inhibitors smoking & alcohol sedentariness genetic/intrsinsic factors: gender, sex hormone deficiency, comorbidities Prevention sarcopenia considered to be a nutritional disorder lifestyle interventions effective exercise: less conclusive evidence nutrition: evidence more equivocal and in favor of greater protein intakes pharmacological treatments use hormone replacement --> testo / SARMs

Musculoskeletal diseases and nutrition, Andersson Osteoporosis Risk factors what clinical RF exist? Screening typical tool used cut-off values how do informatics play a role in risk assessment? Exemplify! What typical areas of body fractured?

Risk assessment Risk factors clinical --> vgl Bild BMT-D score --> assessed using DXA recommended treatment if: FRAX risk > treshold (country specific) fracture of hip, vertebrae, proximal humerus, pelvis, distal arm who to screen essentially, screening is recommended to postmenopausal women, especially >65y men >70 recommended to screen depending on Consensus/Foundation

Musculoskeletal diseases and nutrition, Andersson Vitamin D & risk of fractures and falls what is the recommended dosing deficiency what is special about cut-off values? compare different regions: Northern EU vs rest of EU vs middle east evidence inconsitsent findings: why? what is still recommended who is liekly to benefit?

Vitamin D deficiency serum 25(OH)-D best marker for Vit D status disagreement regarding cut-off values but unanimity that more sun not necessarily more Vit D Evidence link to muscle function mechanistic muscle has vit-D-receptor (VDR) and converts it to 25OH-D --> supplementation increases VDR expression deficiency affects mostly type 2 fibers lower strength & functional decline in vit D deficient individuals observed in observational studies supplementation shows reduced fall incidence Lancet meta-analysis suggests no benefit of vit D supplementation to decrease fall incidence negligable effect on vit D vs control as well as high vs low dose small effect on selected populations (es = 0.83) critiqued by mani experts in the field biased study selection: no studies of vit D an calcium --> 40% of high quality data not included in meta-analysis deffectiveness of daily dose of 800-1000 IU well established Dosing 2000 IU no effect on fall and fracture incidence DO-HEALTH doses of 20'000 IU/d for prolonged period may increase risk of falls 800 IU usual recommendation to at-risk population (elderly and little exposure to sunlight) >4000 IU not recommended, unless malabsorbtion Supplementation & approach in case of deficiency, supplementation is required and likely to reduce risk of falls replete individuals are unlikely to benefit from supplementation

Musculoskeletal diseases and nutrition, Andersson Protein intake recommendations evidence on protein intakes and bone health (not muscle!) how do types differ? what are the advantages and disadvantages of greater protein intakes?

Protein 1.2-1.5 g/kg/d to overcome anabolic resistance --> often unfeasible due to lack of appetite, too much food, mastication problems... 25-30g protein per meal required Evidence for protein & bone health moderate evidence: protein with Ca and vit D might improve BMD and amount: higher protein intakes are generally better than low in terms of bone health --> no effects on bone biomarkers meta-analysis across life-course shows different result depending on data used non-adjusted: greater protein intake associated with better bone health covariate adjusted: no association between amount or type of protein and fractures higher protein intakes have at least no deleterious effects type: soy and animal-based protein seem indifferent in terms of how they affect bone health

Food and Nutrition for Disease Prevention

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This flashcard set delves into the intricate relationship between food, nutrition, and disease prevention at a university level, focusing on key factors like protein intake, vitamin D, calcium, and their effects on musculoskeletal health. It explores how different nutrients influence disease risk, particularly in conditions like osteoporosis and sarcopenia, and discusses preventive strategies. This set is invaluable for students and healthcare professionals aiming to understand how dietary choices impact long-term health and disease management.

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Englisch

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Biologie

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Universität

Erstellt / Aktualisiert

07.03.2021 / 11.06.2021

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Intro lecture Baumgartner

explain Fetal Origins of Adult Disease

discovery of increase prevalence of NCDs in men stemming from areas where childhood mortality was higher
low birth weight = proxy for poor prenatal nutrition --> associated with T2D, CVD & high bp
first 1000d as key timeperiod for health
- high plasticity --> can backfire in case of maternal malnutrition due to (epigenetic) imprinting
- evidence on humans almost impossible to obtain due to duration, but evidence from animals available

Costs of chronic diet-related diseases in Siwtzerland, Wieser

explain three main dimensions of disease cost
- how do these dimensions look in CH, how have they changed and which ones are the most important ones
- how are these dimensions assessed/established?

Direct medical costs

monetary value
ressources others have to invest in order to cure/take care of diseased person
- can extend to family and non-professionals/non-medical persons
in CH: healthcare
- about 1/3 of of illness-related expenses amount to healtcare in CH
  - 9730.- Fr/y per capita
  - in CH costs are high but when adjusted for purchasing power, expenses become 20% higher (and more realistic) as opposed to 50% difference in absolute means

Production losses

of the person affected
also measured in monetary fashion --> usually based on salary of individual x time
different types of production loss
- partial loss: absenteeism (some weeks/months) or presneteeism (reduced workload/pensum)
- total loss: permanent disability or death
- potential loss: suboptimal development and cognitive weknesses, e.g. LMIC with stunting/nutrient deficiencies
how to measure production losses
- questionnaires to capture how often/long employers absent/reduced workload
- administrative data to assess partial or total disability
- epidemiological data for premature mortality
  - additionally impared physical and cognitive development in LMIC
production losses in CH
- mental and musculoskeletal disorders have greatest impact --> chronic and very low mortality cause long absence
  - more "deadly" NCDs have comparable low impact, but also because mortality higher

DALYs

disability and loss in quality of life measured in DALYs, not monetary
DALY two components: time and weight of disease
- YLD: years lived with disability --> non lethal but disabling condition
- YLL: years of life lost
severity reflect by DALY weight and must be defined --> worldwide questionnaires
- chornic diseases realtively low weight
- mental diseases and pain high weight
- good correlation between different cultures shows agreement on severity of different conditions
In CH
- neoplass responsible for large part of YLL
- musculoskeletal diseases for YLD --> larger impact than YLL, typical for country with good healthcare system
- DALY burden has declined by about 30% in last 30 years --> big progress

Costs of chronic diet-related diseases in Siwtzerland, Wieser

Give an overview of the current knowledge on costs in CH

by what categories can the data be visualized?
- what are the major causes of disease burden for these categories?
- what costs are not included
- how was GBD study used in this particular case?

Dimensions of healthcare costs in CH

by service
by type of service provider
by type of financing instance
by illness and disease
- defined using the GBD study
  - costs for pregnancy, aesthetics and similar not included
  - co-morbidities separated

Enteral and Parenteral Nutrition Meier

Malnutrition
- what is the importance of oral nutrition therapy in regards to malnutrition?
  - how's the situation in hospitals?
- prevalence
  - WW & CH
  - who's most commonly affected?
- procedures to identify malnutrition
  - what are signs

Malnutrition

Importance of oral nutritional therapy
- prevalence of malnutrition increases during hospital stay (vgl Bild: nutritiona lstatus deteriorates...)
  - 55% of served food returned --> flight attendant experiment
- affects therapy outcome and mortality
  - improving nutrition during hospital stay is economic
  - daily requirements of many nutrients not met, depending on which requirements chosen, 53-70% --> nutrition in hospital setting is highly insufficient
Reasons for malnutrition (kennste)
- Clinical: Nausea, Cancer, infections, low BMI --> can affect hunger and appetite hormones
- Non-clinical
  - mastication problems
  - monotonous food
  - food temperature & serving times
Identification of patients at risk of malnutritoin or suffering from malnutrition
- high risk patients: low BMI, disease-related weight loss
- geriatric and oncology most commonly affected
procedure of malnutritoin identification
- Risk screening
  - using screening tools: NRS 2002
- Diagnostic assessment
  - phenotypic: low FFM measured via DXA/BIA, unintentional weight-loss
  - etiologic: low food intake, disase-related difficulties eating
- Diagnosis
  - at least one phenotypical and one etiological criterion
- Severity Grading
  - moderate --> vgl Bild
  - severe --> BMI<18.5, NRS >= 3, >10% weight loss in past 6m, serum albumin < 30g/l
prevalence
- worldwide about 25%, same for CH

Enteral and Parenteral Nutrition Meier

Parenteral Nutrition

indications
- access to stomach blocked
  - anatomical reasons: cancer
  - gut dysfunctional: perforation, obstruction...
- tube feeding unsafe
  - excessive vomiting: pregnant women
- patients who require bowel rest
  - acute gastroenteritis, radiation etheropathy, high output fistulas
- major clinical indications
  - Acute and critically ill patients
  - Post acute patients (eg after surgery)
  - Pre operative malnutrition
  - Home parenteral nutrition (eg short bowel)
contraindications
- gastrointestinal tract fully operational
- no access to veins (vena subclavia most common)
Delivery systems
- bags/containers with different nutrients that can easily be mixed
  - All in one options also available
- Home parenteral nutrition
  - for chronic intestinal failure
  - short bowel syndrome or Crohn's
  - cancer patients with intestinal failure --> most common
must take present and future into account: assure safety and nutritional balance for existing benign condition (ex short bowel) + prevent future complications related to nutrition
will affect QoL and may become unsuited in an unpredictable time span due to laignant comorbidities
complications often occur in PN and can be reduced via monitoring
- metabolic
  - Refeeding syndrome
  - Hyperglycaemia and hypoglycaemia
  - Hypertriglyceridaemia
  - Hepato biliary complications (HPN)
  - PN induced bone disease (HPN)
- technical
  - early: pneumothorax, bleeding
  - late: vein thrombosis
- infections --> local can develop to systemic
- monitoring
  - anthropos: monitor weight, arm cicrumferences, BIA --> indicator for muscle mass
  - funtion: check hand grip strength
    - lab results of bioechical, haematological, microbiological values

Enteral and Parenteral Nutrition Meier

Enteral Nutrition

Nasogastric/enteral tube (enteral nutrition, EN)

main goal: treat malnutrition and improve outcome
performed if foods intake in coming 7 days anticipated to be insufficient or if malnutrition diagnosed
- ethical consideration: EN must improve QoL --> if it prolongs suffering of a dying patient, it is unethical
- prior to insertion of tube, expected benefit must be considered
contraindications
- gastrointestinal issues: obstruction of intestines + others (vgl Bild)
- circulatory: schock, cardiac insufficiency
- metabolic: coma, ketoacidosis (diabetes)
Different accesses types for different durations
- nasogastric & nasojejunal
  - short term less than 30d --> longer periods via parenteral or special types of enteral
- percutaneous endoscopic gastrostomy: PEG, PEG-J, D-PEG
  - access to stomach via inserted tube --> food injected into stomach with seringe (Dave having lunch)
Complications
- reflux
- infections
- malpositioning of tube in brain or lung
- refeeding syndrome: reintroduction of food results in ATP generation, yet micronutrient deficiencies limit many biochemical processed so that organism is overtaxed putting the individual in a life threatening situation

Enteral and Parenteral Nutrition Meier

ONS

Evidence: top or flop?
what types exist and when are they do be used?

Oral Nutritional Supplements

first line adjuvant nutritional therapy
different types
- polymeric: entire foods, commercially available --> usually better tolerated and used most often
- oligomeric: broken down macros --> peptides & micro's
- disease specific: diabetes, CKD...
- isolated macros
Forticifaction of foods first step of malnutrition treatment, further step taken with sip feeds if fotification insufficient
concinving evidence for the effectiveness of ONS in the clinical setting (multiple meta-analyses)

Enteral and Parenteral Nutrition Meier

Oral Nutrition Hospital

special types of criteria to adapt nutrition to patient
- protein requirements can differ between patient groups
  - restricted: e.g. renal insufficiency
  - elevated: e.g. dialysis patients
- Energy
  - elevated: malnutrition
  - restricted: obesity
- medical indications
  - gastroenterogical: gluten free, lactose free...
  - speicial conditions: frc free, germ reduced, phenyl-alanine free
Protected Mealtime Policy
- assistance for people who need help (paralysis, e.g.)
- give patients enough time to consume meal -->no doctors or nurses present
- in between snacks to increase kcal intake
Monitoring of food intake via supervisisoin of tray collection

Infant and young child feeding, Baumgartner

Breastfeeing practices

what is the rationale for breastfeeding
what are short and long-term effects on breastfeeding
- on child --> name 3 main domains, then exemplify
- on mother
possible mechanisms mediating the above effects

Breastfeeding practices

Timing
- within one hour of birth
- until up to age 2 or even beyond, on-demand
exclusive breastfeeding for first 6 months
- HIC: introduction of complemetary foods as of fifth month recommended
rationale
- no adverse outcomes on growth & natural (mother’s milk much more complex and rich in diverse nutrients/bioactives than formulas)
- short-term (infancy)
  - decreased newborn mortality --> protects against diarrheal and pneumonic infections
    - sudden-infant-death syndrome (SIDS)--> two months reduce risk by 50%, longer breastfeeding further reduces risk of SIDS
    - compared to non/partially breastfed children: not breastfeeding increases infection-realted mortality 2x
  - beneficial effect on gut health --> necrotisation of enterocolitis prevented in pre-term infants
- long-term (later life)
  - protective against neurodevelopmental delays
    - potential enhancement of motor development
  - protective against metabolic diseases (hypertension, diabetes, obesity)
  - protective against immune-related diseases (allergies, coeliac, IBS)
    - WHO meta-analysis: non or sporadically breastfed children prone to develop obesity whereas breastfeeding for at least 6 months protects children
  - Protective effect possibly mediated but gut microbiome modulation during first 1000d
    - Microbiota of breastfed infants differs from formula fed à more commensal, less pathogenic strains
  - Protective effects also for mother à diabetes, obesity, breast/ovarian cancer

Infant and young child feeding, Baumgartner

Complementary feeding practices

what importance of complementary feeding, what is the goal?
- what if complementary feeding fails?
what foods shoould be consumed
- amounts
- rythm
- type
- foods to avoid
how many children get appropriate complementary feeding worldwide?
important aspects of compl. feeding during illness
explain:
- responsive feeding
- early protein hypothesis

Complementary feeding practices

necessary to cover increased needs as of 6 motnhs that cannot be covered by mother's milk anymore
- sub-oprtimal complementary feeding à stunting
complementary foods (= first foods)
- semi-solid and soft
- complement mother's milk --> closes the gap between requirements covered by milk and requirements milk cannot cover but that the growing infant has
- from month 6 to 23 --> some children ready earlier, around 4 months
- 70% children WW are introduced to first foods, but only 20% with minimum diversity and frequency à breastfeeding from 12-23 months persists in 65% of cases WW
weaning: stopping breastfeeding and switching over to semi-solid foods
complemenary feeding practices & recommendations
- quality of foods important:
  - ensure food variety by feeding at least 5/8 food groups
    - animal foods incl. mother’s milk
    - fruits & veggies
  - avoid empty calories --> high nutrient density foods important
  - Portion sizes: start with small portions, soft and little variety and 2-3 meals per day
  - Variety increase variety, volume and frequency of feeding
- other important aspects & special situations
  - hygiene & proper food handling
  - use fortified foods if necessary
  - in case of illness --> increase drinking volume and offer favorite foods to ensure proper food intake
- responsive feeding: watch out for and respect child’s reaction to feeding à foundation of (good) eating habits
- early protein hypothesis: protein intake > protein requirements primes metabolism to become obese

Infant and young child feeding, Baumgartner

DOHaD

explain framework --> draw!
hints
- environment
- early nutrition
- adult health & disease

DOHaD Framework

environmental stressors prime organism à organism becomes prone to diseases if environment changes / is not-well prepared to environment
- genetic
- epigenetics
  - DNA
  - Histone
  - Chromatin structure
  - miRNA
trajectories in early life more modulable/plastic, relatively low effort and pronounced impact on later life
- little known on how breastfeeding and complementary feeding affect epigenetics and microbiota
  - obesity incidence more strongly correlated with microbiome at 3 months than at 12 months
- partial breastfeeding with additional formula à microbiota more similar to formula-fed infants
- breastfeeding/mother’s milk has epigenetic effects
epigenome and microbiome interact with phenotype and early nutrition à 1000d for microbiota modulation

Eating disorders, Milos

Definitions

General characteristics of eating diorders
three types of eating disorders
- prevalence
common co-morbidities
- mortality

Risks and complications of eating disorders

Types
- Anorexia nervosa (AN)
  - typical symptoms: worry about body shape, self-esteem linked to weight/appearance, fear of gaining weight
  - 1.2% women
  - weight 15% below expectation
  - BMI < 17.5 kg/m2
  - weight loss caused by active or non-active measures
    - active: vomiting, laxatives
    - non-active. eating-restriction
  - always a behavioral and psychologic features
- Bulimia nervosa (BN)
  - typical symptoms (same as AN): worry about body shape, self-esteem linked to weight/appearance, fear of gaining weight
  - normal weight, but preoccupation with weight --> self-esteem related to weight
  - high food intake due to food attacks --> 1/week
  - vomiting to compensate for food attacks
- Binge eating
  - food intake >>> during at least 3 months
  - characteristic behavior: fast and abnormally bulky food intake despite absence of hunger followed by disgust and guilt
Characteristics
- often slowly and gradually developing bnormal eating behavior with tendency of becoming chronic
- eating disorder is hidden from family/friends and third parties
- profound impact on life: physical, psychological, professional, and social
Co-morbidities
- mostly psychatric nature
  - high rates of suicidal tendencies amongst eating disorders
  - difficulties to assess own and other's emotions
  - difficulties to see big picture, obsessive with details
- mortality in anorexic people ~6%
- hormonal foundation: leptin-like effect observed in AN
  - increased activation of HPA and HPG (gonads) axes --> reduced BMD, increased physical activity but also reduced reproductive activity
- organ specific --> vgl Bild
  - gastric emptying
  - osteoporosis --> 40% of patients have low BMD
  - amenorrhea --> fertility affected
  - cortical brain atrophy

Eating disorders, Milos

Etiology & Therapy

name three main areas of etiology and exemplify each
give an overview of therapy
- who is involved?
- who is targeted?
- what are the main goals of therapy?

Multifactorial etiology

Biological and genetic factors
- genome-wide association found 8 loci involved in AN
- pre- and perinatal factors:
  - infections during pregnancy
  - SGA
  - birth complications
  - feeding disorders in infant
  - childhood: obsessive, perfectionistic behavior
- Neuro
  - alteratino in the dopaminergic system leads to self-starvation becoming a trigger of motivation --> viscous cicle
Personality and individual experiences
- Character traits
  - low self-esteem
  - obsessiveness
  - anxiety
  - emotional inhibition
- trauma
  - sexual abuse or other trauma
  - strict diets in family
  - critical experiences towards appearance/weight/eating
Socio-cultural factors
- beauty standards
  - fashion standard
- overabundance of food
- unhealthy role models

Therapy

interdisciplinary --> communication is key!
- medical entities (family physician, specialists, gynecologists, dentists, internal medicine)
- employer
- social services
- psychiatry
target patients as well as patient's surrounding
- get insight and enhance trust, and motivate change
- family, relationship
- work
major goals
- reach at least BMI = 18.5 or stabilize weight if normal BMI
- normalize eating habits --> 3 meals/d with 2-3 snacks
- treat comorbidities (somatic/psychiatric)

Musculoskeletal diseases and nutrition, Andersson

Bone basics

bone homeostasis
- renewal duration
- BMD pattern throughout life --> draw
  - same for all?

Bone homeostasis

Bone basics
- trabecular: 15.25% calcified
- cortical bone: 80-90% calcified,
- cells
  - osteoblasts & osteoclasts: build/resorb bone
  - osteocytes: derive form osteoblasts and represent mature cell, 80-90% of bone
renewal every 10 years
peak bone mass between age 30 and 40
- gender differences:
  - women have lower BMD to begin with --> 60-80% genetically inherited, rest modulated by environment
  - menopause-caused fall in estrogen results in greater bone resorbtion and therefore lower BMD in females

Musculoskeletal diseases and nutrition, Andersson

Osteoporosis
- prevalence --> how many falls
- burden of fractures
- risk of fracture depending on first/seonc fracture and gender
- how measured/proxy
- reatment and preventive strategies

Osteoporosis

loss of bone mass (quantity) and deterioration of bone archtecture (quality)
consequences
- greater fracture risk
  - most commonly spine, hip or wrist fractured
  - 5-6% of falls actually result in fracture
- collapsed vertebra --> tooped posture
prevalence
- gender differences --> 20% females, but also 5% males affected
- worldwide variance in prevalence assumed to have genetic reason, not nutritional
- 75% of osteoporotic fractures in >70 year-olds
- risk for first fracture differs between gender (50% or more for females vs 20% males), but not for second fracture: 20% both gender
  - risk for second fracture highest in the year following the first fracture
cost & disease burden
- 13'000€/hospitalization --> greater than cancer, heart, and stroke combined due to greater prevalence of osteoporosis fractures than other
link to sarkopenia
- fear of falling reduces mobility and thereby muscle mass --> ultimately increases fall risks
- muscle strength correlates with BMD

Musculoskeletal diseases and nutrition, Andersson

Sarkopenia

prevalence
consequences
etiology
risk factors

Sarcopenia

prevalence: 20-75%, depending on population and source of information
consequences
- poor hospital outcomes, risk of falls, loss of independence
definition and diagnosis not always clear --> muscle mass measurements, handgrip strength
muscle strength via handgrip
- peak in early adulthood
- bi-phasic decline --> gradual as of age 40, substantial as of age 50
etiology
- systemic inflammation
- ageing-associated processes
  - reduced autophagy
  - loss of mitochondria with additional decline in mitochondrial function
  - impared stem cell regeneration
- los protein intake and negative protein turnover --> decrease in MyoPS and MitoPS
Risk factors
- sarcopenic obesity
- extreme weight loss
- drugs & pharmacological therapy --> ACE inhibitors
- smoking & alcohol
- sedentariness
- genetic/intrsinsic factors: gender, sex hormone deficiency, comorbidities
Prevention
- sarcopenia considered to be a nutritional disorder
- lifestyle interventions effective
  - exercise: less conclusive evidence
  - nutrition: evidence more equivocal and in favor of greater protein intakes
- pharmacological treatments use hormone replacement --> testo / SARMs

Musculoskeletal diseases and nutrition, Andersson

Osteoporosis

Risk factors
- what clinical RF exist?
Screening
- typical tool used
- cut-off values
- how do informatics play a role in risk assessment? Exemplify!
What typical areas of body fractured?

Risk assessment

Risk factors
- clinical --> vgl Bild
- BMT-D score --> assessed using DXA
  - < -1 SD: osteopenia
  - <= -2.5 SD: osteoporosis
  - <= -3 SD: severe osteoporosis
- BMD is integrated into the FRAX algorithm (fracture risk assessment tool) with clinical risk factors to predict 10-y risk for certain fractures
- sometimes no BMD assessemtn available (e.g. men or subsequent to typical fracture) --> recommended treatment if:
  - FRAX risk > treshold (country specific)
  - fracture of hip, vertebrae, proximal humerus, pelvis, distal arm
who to screen
- essentially, screening is recommended to postmenopausal women, especially >65y
- men >70 recommended to screen depending on Consensus/Foundation

Musculoskeletal diseases and nutrition, Andersson

Calcium

requirements increase slightly after 50y from 800 to 1000 mg/d
recommendations
- 800-1200 mg/d
- foods preferred source
- addition of vitamin D in institutionalized individuals
calcium rich foods: mostly dairy and animal-based, although present in many fruits and vegetables too
- average intake in Western 700-900 mg/d
- dairy product effective in preventing the decline of BMD, but not in its restauration
  - under debate: evidence for persisting bone loss in postmenopausal women despite intakes of Ca of 300 - 2000 mg/d
supplements
- supplements sometimes necessary to meet recommendations --> 30-50% of older women in western countries prescribed supplements
- uptake kinetics between dairy and supplemental Ca differs
  - supplements peak vs dairy plateaus --> potential mechanism for vascular complications, but not yet clearly identified
Evidence
- may increase risk of vascular diseases
- inconsistent results on fracture reduction (meta-analysis)
  - reduction total fractures and vertebral fractures but not forearm or hip
  - often supplementes combined with vitamin D --> no additional effect
  - overall: no convincing evidence and, if any beneficial effects of Ca on BMD, then only minor
- increased BMD by 1% after 1y --> not cost-effective

Musculoskeletal diseases and nutrition, Andersson

Vitamin D & risk of fractures and falls

what is the recommended dosing
deficiency
- what is special about cut-off values?
- compare different regions: Northern EU vs rest of EU vs middle east
evidence
- inconsitsent findings: why?
- what is still recommended
- who is liekly to benefit?

Vitamin D

deficiency
- serum 25(OH)-D best marker for Vit D status
- disagreement regarding cut-off values but unanimity that <25 nmol/l severe deficiency
- values <50 nmol/l increase from Northern Europe to Western/Southern/Eastern Eruope and up to 80% of individuals deficient in Middle East --> more sun not necessarily more Vit D
Evidence
- link to muscle function
  - mechanistic
    - muscle has vit-D-receptor (VDR) and converts it to 25OH-D --> supplementation increases VDR expression
    - deficiency affects mostly type 2 fibers
  - lower strength & functional decline in vit D deficient individuals observed in observational studies
  - supplementation shows reduced fall incidence
- Lancet meta-analysis suggests no benefit of vit D supplementation to decrease fall incidence
  - negligable effect on vit D vs control as well as high vs low dose
  - small effect on selected populations (es = 0.83)
  - critiqued by mani experts in the field
    - biased study selection: no studies of vit D an calcium --> 40% of high quality data not included in meta-analysis
    - deffectiveness of daily dose of 800-1000 IU well established
- Dosing
  - 2000 IU no effect on fall and fracture incidence
    - DO-HEALTH
    - doses of 20'000 IU/d for prolonged period may increase risk of falls
  - 800 IU usual recommendation to at-risk population (elderly and little exposure to sunlight)
  - >4000 IU not recommended, unless malabsorbtion
Supplementation & approach
- in case of deficiency, supplementation is required and likely to reduce risk of falls
- replete individuals are unlikely to benefit from supplementation

Musculoskeletal diseases and nutrition, Andersson

Protein

intake recommendations
evidence on protein intakes and bone health (not muscle!)
- how do types differ?
- what are the advantages and disadvantages of greater protein intakes?

Protein

1.2-1.5 g/kg/d to overcome anabolic resistance --> often unfeasible due to lack of appetite, too much food, mastication problems...
- 25-30g protein per meal required
Evidence for protein & bone health
- moderate evidence: protein with Ca and vit D might improve BMD and
- amount: higher protein intakes are generally better than low in terms of bone health --> no effects on bone biomarkers
  - meta-analysis across life-course shows different result depending on data used
    - non-adjusted: greater protein intake associated with better bone health
    - covariate adjusted: no association between amount or type of protein and fractures
- higher protein intakes have at least no deleterious effects
- type: soy and animal-based protein seem indifferent in terms of how they affect bone health

Cancer and Nutrition, Andersson

Cancer development

how does cancer develop?
- phases
- reasons/mechanisms
- relation to age
- what types of cancer are there?

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Cancer development

can be somatic or inherited --> 90% somatic
- functional gene on one of both chromosome pairs can compensate for mutation on other, e.g.: inherited mutation from mother can be compensated via euivalent gene inherited from father --> loss of function of both genes that will result in cancer
3 phases: initiation, promotion and progression
cancer risk accumulates over time and is therefore higher in aged individuals
- may affect all ages though
Cancer types
- benign: slow cell multiplication
- maligng: invades and destroys surrounding tissues, rapid cell growth
- metastasis: affects multiple organs as cancerigenous cells spread throughout body
process requiring lots of time: cell's repair mechanisms (p53) are defect --> mutation is not corrected and persists in daughter-cells --> becomes cancer / malignant as soon as cells multiply and invade other tissues
- bad-luck-theroy: cells with high turnover are more susceptible to DNA errors
- p53: guardian of the genome
  - mutated in >50% of cancers --> precancerous cells esacape apoptosis pathways (=quality control)
  - induces apoptosis if DNA errorr is detected

Cancer and Nutrition, Andersson

Cancer epidemiology

what are the most frquenent types of cancer?
- How do demographics and socioeconomics affect this?
how do mortality and incidence behave now and in the future?

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Cancer prevalence

most frequent cancers vgl Bild
- cancer patterns--> cancer type and total prevalences differ between countries
  - suboptimal food storage (curing --> high salt ; no fridge --> mold (aflatoxin)
  - LMIC affected by cancers related to poverty and infections --> digestive tract affected
  - high income countries: lung (smoking?), breast prostate (hormonal imbalances)
  - lifestyle factors: much higher cancer prevalences overall --> many-fold or less many-fold increase depending on cancer type (vgl. slide 36)
mortality lower in high income countries because of treatment options
Trend predicts stabilization of prevalence but increase in total numbers because of increase of world population
comparison between countries only possible with proper age-standarization --> higher aged associated with greater risk, so age needs to be accounted for

Cancer and Nutrition, Andersson

Cancer assessment tools

what kind of studies to assess cancer risk factors?

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Lifestyle factors

migrants studies: people with same genetic background living in different environment, on population level
twin studies: as migrant studies but on an individual or lower scale level
correlational studies: e.g. meat intake vs cancer prevalence or cancer deaths
- will inly show trends, not highest quality data
- national and international levels possible --> std for age imporant for comparison
Time-trend studies: ??
case-control: ??
intervention studies: ??
Cohort studies
- current state of the art in cancer research
- FFQ + biomarkers used
- long-term, prospective studies

Tools

questionnaires: food, lifestyle and risk factors such as e.g. smoking
- carcinogens usually found in toxicology and mechanistic studies --> informs questionnaires (and vice versa)
biomarkers: b-carotene

Cancer and Nutrition, Andersson

Nutrition and Cancer: how are both linked to one another?
What other modifiable risk factors exist and how to they affect cancer risk?

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Nutrition

body / cell require nutrients for cell cycle and proper functioning
Hormonal imbalances drive cancer development
- overfeeding, diabetes --> fats and sugars
- obesity second largest known risk factor for cancer
  - waist circumference correlates with breast cancer
  - weight loss reduces risk of cancer
  - often accompanied by other cancer promoting states --> inflammation, lack of fibre ==> obese cancer patients are more likely to die of cancer due to obesity (or other way around?)
- menopause: increase in risk due to changes in hormones --> lower pre-menopausal risk for same cancer type (breast)
- pregnancy: hormonal changes during/after pregnancy protect women
hallmarks activated via obesity
- insulin resistance as key driver of cancer
  - increase in estrogen due to reduced SHBG --> estrogen-dependent tumors
  - higher IGF1 levels
  - hyperglycemia --> anaerobic oxidation = cancerigenous
  - inflammation
importance of exercise
- reduces inflammation, improves insulin sensitivity, stabilizes weight
- convincing evidence for reduces colon cancer

Cancer and Nutrition, Andersson

Give an overview of which factors increase or decrease cancer risk

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Multiple nutritional factors influence cancer risk

Increase risk
- Red and processed meats: 1.2% increase
  - Red and processed meats increase risk for colorectal cancer, white meat and fish decrease it marginally
  - Nitrosamines, saturated fats and ROS stress due to heme as potential drivers
- Alcohol
  - Genotoxicity of acetaldehyde + other à vgl Bild
  - Increases risk for many cancers
  - Decreases risk for kindey cancer
Decrease risk
- Dairy and fish decrease certain cancer risks à vgl Bild
- Fibre
  - Overall chance of contact between carcinogens & enterocytes is reduced
    - Faster transit times
    - Binding of carcinogens
    - Greater bulk à lower likelihood of contact
  - Reduce insulin resistance
  - Bioactive compounds of wholegrains
- Fruit
  - Decrease in cancer risk limited

Cancer and Nutrition, Andersson

What strategies exist to prevent cancer?
- How do they work?
- On what levels?

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Cancer prevention

Individual level
- Healthy weight and physically active
- Diet rich in fruits, vegetabes and beans
- Limit intake of SSB, red meat, fast food, alcohol
- Do not use supplements for cancer prevention
- Breast feed
Government
- Incentives to fruit and vegetable consumption
- Clear nutritional labels
- Nutritional education and personalized advice
- Healthy meals for the masses à schools, workplaces, institutions

Cancer and Nutrition, Andersson

Which micronutrients affect cancer risk, and how?

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Micronutrients

B-carotene
- Plasma levels have sotrnger correlation with cancer prevention than dietary intake à shows that plasma markers are more reliable
- Supplementation increased cancer incidence in asbestos workers and smokers
  - B-carotene not recommended for cancer prevention, backed up by meta-analysis
  - Doses of 20-30mg/d
  - study had to be stopped
  - no deleterious effects observed with vit A and E
Folate
- Double edged sword: due to methylation, folate can promote cancer growth once tumorous cells have developed
- Higher intake not found to increase cancer risk in 5.5y RCTs yet
- Epidemiological studies show inverse relation between intake and development of colorectal cancer

Nutrition & CVD, Faeh

CVD epidemiology

how situation in CH
how do Swiss CVD trends compare to international CVD trends?
- what are strengths and weaknesses of CH treatment and screening strategies?

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CVD epidemiology

CH
- CVD: increasing rates ever since population infectious diseases could be prevented/reduced --> opulations ages and becomes prone to CVD
  - Since 1980 and current trend: declining CVD mortality --> CH one of the highest ranking countries in terms of ortality because time to reach hospital after event is short and treatment excellent
  - cancer: trend remains stable
- mortality vs. incidence values available for CVD
  - changes in mortality are due to treatment or screening --> decrease in mortality due to improvements in treatment
  - changes in incidence reflect efficacy of preventive measures
  - CH: decreasing mortality but increase in incidence, especially for males --> treatment has improved, preventive measures seem ineffective
- Age as an important factor for CVD: mortality increases as of 65, at 85+ becomes most common cause of death
  - individuals <65 can still suffer from CVD
- death remain stable while hospitalization is increasing --> screening improved? (slide 8)
  - healthcare and socioeconomic burden big, despite decreasing mortality
- Regional and societal differences
  - higher class less prone to CVD --> also less smokers
  - Romandie less affected than Deutschschweiz
International
- trends also declining
- similar trends in US, DE, FR, and CH
- Switzerland ranks amongst lowest CVD mortality countries --> treatment and screening efficacous

Nutrition & CVD, Faeh

Diet and CVD evidence
- What problems do nutritional sciences have ingeneral?
- what problems are specific to RCTs?

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Diet and CVD evidence

Bradford-Hill Criteria --> vgl Bild
- most nutritional sciences studies do not fulfil criteria sufficiently, so causality remains weak
  - Coffeexception: fulfils many criteria, incl linearity
Problems of evidence in nutritional sciences
- intermediate risk factors & soft vs hard outcomes
  - do not necessarily correlate with actual CVD mortality, although increase risk factors --> use of hard facts as more reliable information
    - coffe affects risk factors negatively but has positive outcome on CVD risk
    - n-3 improves blood TAG but not CVD mortality
  - CVD deaths more convincing than increased TAGs or intermediate risk factors
- residual confounding: confounding factors that cannot be adjusted for / controlled
  - age/smoking/gender can be adjusted for, but impossible to adjust for behavior/mindset --> fish consumers likely to behave differently than non fish consumers
- sponsoring
  - margarine industry sponsored some studies on saturated fats to increase fear of butter
- causality difficult/impossible to find/relate to certain food
  - relating one nutrient to certain outcome never possible because diet comprises many foods
  - diet affects hormones --> E storage and metabolism modulated
  - meal will affect thermogenic effect
  - microbiota as intermediate player
Problems specific to RCTs --> vlg Bild
- control of exposures difficult in long run --> yet CVD needs time to develop
- behaviour adapted when aware of control --> not realistic behaviour
- forcing people to artificially follow a protocol that would never been adhered to in real life
  - low salt intake --> hard to adhere to and unrealistic, additionally only marginal benefits
- time-dependent results --> diseases only show up late, difficult to maintain RCT for so long
- vulnerable populations (with hypertension or with case of CVD) usually used --> not translatable to general population

Nutrition & CVD, Faeh

Illustrate how dietary risk and protective factors may impact on CVD risk
- give example of specific/controverse foods

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Foods and CVD

food groups: all-cause mortality rarely linear --> U-shaped relations
many prospective cohort studies with very limited causality
Some RCTS available but still with limitations
examples
- meat: inconsistency and low point estimates (Waht does that mean?), but more consitent when looked at meat preservatives, many animal studies
- dairy: weak scientific evidence with conflicting results, some beneficial except for prostate cancer
  - strong evidence for preventive effects on diabetes → impact on gut microbiome/fermetation (less sugar)
- fish: effect overstimated and dependent on region (preparation, freshness), maybe real advantage is replacement of red meat with fish
  - protein swap (slide 33): fish, milk and poultry protein comparable impact on CVD risk, plant protein might lower while eggs and processed meats might increase CVD risk
- SSB
  - moderate increase for CVD --> meta-analysis found no effect on stroke, but CHD and hypertension
  - effect mediated via IR, obesity, hypertension ? --> unknown
  - substantial residual confounding: food choices of aware/unaware person not adjustable
  - swaping sugar for artificial sweeteners --> may decrease weight but might increase risk of CVD
- Coffee (& tea)
  - negative impact on risk factors but associations show decrease in mortality
    - acrylamide, increase in LDL cholesterol and blood pressure
    - maximal benefit @ 4 cups/d
expert consens as most reliable source of information --> vgl table
- high agreement:
  - beneficial: DASH, high potassium intake, fibre, fruits and vegetables, seeds, yoghurt
  - harmful: artificial fats (partilly hdrogenated vegetable oils), high sodium, SSB, refined sugar
- medium agreement
  - beneficial: seafood, n-3, olive oil, phenolic compounds
  - harmful: moderate Na, high GI foods
- low agreement
  - beneficial: cheese, low fat-milk
  - harmful: dietary cholesterol, eggs, butter, unprocessed red meats

Nutrition and CVD, Faeh

How do these nutrients relate to CVD risk?
- Trans-fats
- SFA
- CHO
- Supplements

Fats

trans-fats
- most problematic of fats in regards to CVD mortality and total
- industrial trans fats consistently show to increase CHD risk & mortality
- ruminant trans-fats less conclusive data --> some even beneficial on T2DM (perhaps reason for protective effects of dairy on T2DM)
saturated fats
- saturated fats less conclusive data than trans-fats
- some studies sponsored by margarine industry
- replacement of kcal from SFA by other E sources affects CVD risk --> vlg Bild
  - AHA concludes that MUFA and especially PUFA should replace SFA for CVD risk reduction

Carbohydrate

low-carb diets: not protective in the long run --> U-shaped relation with CVD risk
- CHO source not taken into account
all cause mortality U-shaped with optimal intake at 50-60 %En
Whole grain: curve flattens out --> benefit up to ~60g/d

Supplements

High dose of D3, A, b-carotene all shown to increase mortality (in specific populations)
primary or secondary prevention with supplements is not evidence-based
Ca supplements can even increase risk of CVD at higher doses
main message: not suitable for primary prevention because of lack of evidence
- drugs may not be adequate either in primary prevention, e.g. statins

Nutrition & CVD, Faeh

Ethanol

what does new evidence suggest?
- give two reasons for flawed studies
changes in protective and risk factors: which ones ocurr and what dominaztes in the end?

Ethanol

improves intermediate risk factors
- fibrinogen: prevent clotting
- increases HDL levels
- adiponectin: promotes b-ox & increases insulin sensitivity --> lowered in metabolic syndrome
worsen other intermediate risk factors
- combined with beneficial influences, Lausanne study showed that despite increase in HDL, the increase in syst BP outweighs the benefit and leads to increased CAD risk
- study in heavy drinkers
- wine increases HDL, beer increase TAG
Protective effect of alcohol likely to be biased finding
- many studies suggesting beneficial effects of moderate alcohol consumption may be biased due to overestimation + residual confounding of moderate drinkers vs abstainers
  - moderate drinkers vs abstainers have different behaviors and the beneficial effect of mderate drinking might be overestimated
- Selection biases in observational studies:
  - moderate drinkers not only adopt drinking but also particular lifestyle and have survived until study recruitment + are congintively fit enough to be enrolled --> selection bias
- Risk thresholds for alcohol consumption:
  - Shows dose-dependent risk for different CVD-related disease depending on alcohol intake. Recent data, suggests no benefit of moderate alcohol intake on overall CVD mortality

Nutrition & CVD, Faeh

Nutrients and CVD: Salt

What is evidence for CVD and dietary salt ?
- type of studies
- type of CVD
Na intake in a broader spectrum
- nutrition
- hormones
Who might benefit from reduced salt intake?

Sodium an CVD risk

fact: higher Na intake increases blood pressure in hyper- and normotensive individuals --> intermediary risk factor, so not necessarily increased CVD risk
- question to ask: does reduction in salt intake result in lowered disease risk? (it does undeniably lower BP)
- BP can be reduced without lowering Na intake --> normal salt DASH diet ==> further improvement with low Na DASH diet
- target population who may benefit from salt reduction
  - very high salt intake population: >12g/d
  - hypertensive population
  - elderly
Normotensive and hypertensive individual's risk for CVD depending on salt intake is different
- U-shaped for hypertensive
- flattened out for high intake
TOHP (trials of hypertension prevention): Na reduction with mortality assessed --> minimal risk but big effort --> not worth it
- Evidence on Na intake mostly from obeservations studies --> questionable
Sodium intake vs potassium intake on different CVD-related risks
- stroke: <5g safe zone --> increased risk with higher intake
- myocardial infarction: not associated with Na intake
- potassium intake:
  - linear, negative association with all CVD related risks
K/Na excretion
- greater K excretion generally associated with lower CVD risk
- risk will depend on ratio, not absolute Na intake --> low Na intake with low K intake worse than higher Na intake with higher K intake --> high fruit and vegetable intake
RAAS system
- could explain small reduction (if any) in CVD risk of Ny intake --> hormonal counter regulation of Bp increasing hormones
- lowered Na intake result in increase of, amongst other, stress hormones --> damages other tissues

Nutrition & CVD, Faeh

Dietary patterns to reduce CVD risk

What nutritional strategies exist to reduce CVD risk?
- describe one strategy in detail
- what is the evidence?
- what have in common?

Mediterranean Diet

characteristics
- no salt limits
- low red (processed) meat
- high unprocessed fruits and vegetable intake
- protein mostly from plants or fish/poultry
- High-quality olive oil as main source of fat
much greater effect than low-fat diets (WHI study vs PREDIMED)
overall, moderate risk reduction observed in prospective and RCT studies

DASH

very similar to MedDiet
version with salt reduction (50mmol/d) --> even more effective at reducing BP (does not mean CVD risk is reduced)

Other diets

Nordic diet, Japanese diet, Harvard Diet...
rely on similar features: high in fruits and vegetables, unprocessed,

Childhood Obesity, Lallemand

Factors influencing normal growth
growth phases
- relate to nutrition
- which factors other than nutrition affect growth?

growth charts: increase in height and weight for boys and girls
- different charts (WHO)
- target height: mean between father and mother
growth phases
- infancy: first year of life mostly dependent on nutrition, less genetics / hormones
- puberty: nutrition required to meet E demands of growing individual
  - Thyroid hormones involved as of 2 years of life
Factors influencing growth
- emotional stability --> especially eraly childhood
- favorable socioeconomic conditions
- absence of significant morbidity --> celiac disease
- genetics: will define height but growth less dependent on it than nutrition

Childhood Obesity, Lallemand

Hormones

what are the hormones associated with
- satiety
- obesity
how does obesity affect these hormones?

hormones

satiety signals:
- PYY, GLP-1 --> catabolic pathways (decrease food intake and increase E expenditure) --> dysfunctional in case of obesity
- Ghrelin --> anabolic effect --> increases food intake and decreases energy expenditure (motivation to exercise)
obesity signals: leptin & insulin

Childhood Obesity, Lallemand

BMI

How is obesity defined using BMI?
- what are common problems to BMI and how can they be adressed?
What methods other than BMI are used to define obesity?

Obesity is defined using either BMI, BIA/DXA/Skinforld, or waist/hight ratio

defined as BMI > 97th percentile (overweight >90)
- WHO classification used for adults and IOTF for children: correlation between fat mass and obesity never been assessed for children, but likely to correlate, similarly to adults
- healthy control children selected based on maother's health status: all continents, non-smoking, godd socioeconomic status
- New Swiss BMI Reference also uses 97th percentile, but perhaps more
definition using waist/hight ratio
- waist circumference > 2 SD
- waist/hight ratio > 0.5
definition using BIA
- >25% (20-25%) fat mass in boys
- >30% fat mass in girls

BMI

problems
- fat and muscle mass not distinguished
  - !! prevalence can decrease but actually decrease in muscle mass and not fat mass, due to low PA
- height strong impact on BMI value --> short statured children will have lower BMI despite being overweight/obese --> respect weight-for-height charts
- weight-for-height charts
  - valid until age of about 5 years
  - preferred over BMI in short or high statured children

BIA to assess fat mass and not muscle mass

skin folds difficult in children beacause fat very compact
obesity >25% fat mass in boys and 30% in girls
DXA also used

Waist circumference

obesity defined as
- waist/height < 0.5 --> individual is used as own reference, therefore useful
- waist CF > 2 SD; based on reference charts that takes age into account, as well as waist/hight ratio
measures abdominal fat which is associated with comorbidities: hypertension, IR in children, CVD
- reflects abdominal fat, around the liver, dangerous!
- <88cm for females; <105cm for males
either waist or hip circumference used, reference table available for both

Childhood Obesity, Lallemand

Pathophysiology

How are hormones and hunger related?
- why can hunger persist, how is this caused?
- relate to neuronal aspects

Pathophysiology

Satiety
- set-point of satiety upregulated if E intake and E expenditure are out of balance for prolonged period --> remains elevated despite fat/weight loss --> yoyo-effect
Energy intake should be adapted to PA of child

Hormones

CNS receives signals via blood and nerves
obesity signals --> dysregulation of set-point between accelerating (anabolic) and decelerating (catabolic) pathways
- leptin (&insulin) activates catabolic pathway --> stops eating, be active!
  - leptin and insulin resistance result in loss of breaking/decelerating signals --> hyperactivation of anabolic pathway
- NPY anabolic pathway --> eat, stop moving!
Reward system & neurological aspects of obesity
- dopaminergic system rewards for eating
  - very active in child's brain
- Ghrelin release from stomach also rewarding
- addictive power of food
  - addiction: amount of food needs to increase to trigger satisfaction (example with mouse)
  - advertisement of fatty/sweet foods to children should be limited
Adipose tissue is homronally highly active
- cytokines --> inflammation and macrophage activation
- induce insulin resistance
- activates thrombogenic messengers
- activation of sympathetic activates adipocyte proliferation (?)
- vagus increases insulin's anabolic effect on adipocytes

Childhood Obesity, Lallemand

Pathophysiology

Microbiome: how affected by diet?
associations between obesity and antibiotics?

Microbiome

many effects (vgl Bild)
- suppress b-ox in muscle tissue
- increase in fermenting enzymes
- monosacch absorbtion
- increase in SCFA, which interact with recpetors --> increase in PYY --> satiety
- inhibit lipolysis
microbiome changes in response to Western diet --> mice become fat
- artificial sweeteners negatively affect microbiome --> tendency to obesity
use of antibiotics in first year of life associated with obesity

Childhood Obesity, Lallemand

Risk factors

what risk factors exist?
- internal and external ones
- other than physical
how can taste-perception affect obesity?

pre-natal: U-shaped risk of under/overnutrition

maternal undernutrition prepares fetus to food scarcity --> hyperinsulinism after birth if food plentiful
maternal, prenatal overweight also increases risk of hyperinsulinusm and obesity as adult (x2.2)
genetics: 25-50% --> environment and lifestyle play greater role
- environment: many factors leading to a toxic surrounding, resulting in increased food intake, lower food density as well as lower PA (vgl Bild)

parental overweight

overall most impactful risk factor (44% compared to ~10% for other common risk factors)
regardless of parental status, overweight is carried over into adulthood more often if obesity develops in adolescence
children of obese parents are more likely to become and remain obese thourghout life

physical activity & screen time

60min/d of PA only met by children up to 12y
associations between number of cars and television viewing in a family more impactful on obesity than fat intake
decrease in performance of recruits reflecting decreased PA and fitness
differences amongst Swiss regions, genders and cultural background --> female expats the least physically active, Swiss Germans the most

nutrition

taste-development in tuero --> sweet foods consumed during pregancy modulate taste preferences of child
breast feeding
nighttime feeding problematic --> important to respect "fasting period" in infants of about 10h

smoking during pregnancy

increases likelihood of obesity by about 14%

socioeconomic factors

education as remedy against toxic environment is difficult to obtain in low socioeconomic classes
chlidren with migrational background more susceptible to obesity --> being fat culturally appraised

sleep duration

less than 10.5h/night
hypothesis: lack of a fasting period or lack of GH and its lipolytic effects, also stress reduction with sleep and relation between stress and IR

psychiatric risk factors

ADHD and increasde impuslivity associated with overweight
depression --> obese children suffer from emotional eating
stress, including pre-school children
strongly reduce QoL and self confidence --> QoL as low as cancer patients

1 / 68

Lernkarten

Nutrition and Brain, Baumgartner

Explain the role of macro and micronutrients in the brain

Give examples of some important micronutrients
Vulnerability to nutrient deficiency: what do studies need to consider?
how are microbiome and brain development related to one another?

Overall metabolism

brain highly metabolically active --> 60% of O2 consumption of child vs 20% adult
relies on many different nutrients for growth, repair, function
overall, brain's dry matter made up of
- 60% fat
- 20% CHO
- 10% proteins

Vulnerability to nutrient deficiency

depends on timing and duration of deficiency --> short-term folate deficiency during conception much more dangerous than short-term folate deficiency postnatal
brains requirements, which change depending on developmental stage --> omega-3 FA necessary during breastfeeding period
study investigating the behavioral changes due to deficiencies must be designed properly:
- what area is affected by the deficiency --> what function altered
- when does the specific area develop --> when did deficiency occur or when is supplementation likely to show positive effects
  - eg: assing problem-solving skills in toddlers makes no sense, because area not fully developed at that time
- dose/degree of deficiency --> may only cause harm at severe deficiencies --> pregnant mother can maintain normal TH despite mild iodine deficiencies, but severe deficiency causes cretinism

Folate

essential for proper formation of neural tube
important before and during conception, because neural tube formed at day 22

Iodine

Thyroid hormones important for neuronal migration, proliferation, and myelination --> fetus relies on maternal TH transfer up to 3rd TM
severe iodine deficiency results in cretinism --> important that fetus can stock up iodine

Omega-3 LCPUFA

make up largest part of fats found in brain (50-60%)
mostly DHA --> EPA can affect brain via peripheral mechanisms: modulation of sysntemic inflammation and vascular health
proportions and accrual of n-3 FA
- switch in n-6/3 content in brain: up to 10y, ARA content > DHA --> stabilizes in adulthood
- increase in DHA 35x from 30wk to 18 motnhs --> importance of mother's milk

Microbiome

development in offrping's microbiome coincides with brain development --> in line with brain-gut-axis-hypothesis
early life nutrition may affect microbiota and brain directly and indirectly due to the existing interactions between them

Nutrition and Brain, Baumgartner

fundamental questions & key concepts
- which concepts need to be clear in regards to timing and the relation between nutrients & brain development?
- what key concepts need to be considered: study design, timing of intervention, tools used...

Fundamental questions

Matching: does nutrient affect cognition/behavior beyond sheer brain development?
- how strong is the relationship?
  - for nutrient(s) --> additive or interactive effects with other nutrients/environment?
  - for given timeframe, e.g. first trimester
Are the consequences of a deficiency long-term or short-term?
- short-term: acute dysfunction
- long-term: cognitive development delayed/hampered

Key concepts

Matching (see above)
proper tools
- to assess deciciency per se as well as impact it has on cognitive domains
child age: early testing possible, but more reliable as child ages
study design
- rct vs interventional
- sample size

Nutrition and Brain, Baumgartner

What are the 3 types of tools used to study nutrition and brain development in children?
what are the strength and limitations?

Approaches to measuring cognition in humans

Cognition: involves many different factors, such as
- language/psychomotor/perception/attention/memory/executive functions (vgl Bild)
Global measures: IQ,
- usually paper-based, otherwise PC-based
  - motor and language based tests for infants
- limitations
  - widley applied but limited sensitivity due to global assessment of cognitive function --> score difficult to relate to nutrient deficiency
  - timing
    - must be timed properly --> difficulty of test must be appropriate to child's developmental stage
    - may overlook long-term effects when short-term effects are not present
  - high intra and interindividual variability
    - child can be distracted in room or by assessor
Domain specific testing
- test battery that assesses a given cognitive domain that is hypothesized to be affected by a nutrient deficiency at a given time point of development
- must be sensitive enough for intervention duration
- has replaced global testing because of higher specificity
- cultural differences may turn questions more difficult to certain child group --> cultural fairness
- requires validation
  - does the test depict cognitive domain of interest + does nutrient intervention affect domain of interest?
Neurophysiological tools
- MRI and fMRI measure brain anatomy and function, repsectively
- EEG: evoked potential of different stimuli can be assessed
- NIRS, non-invasive and suitable for field
- strengths & limitations
  - (-): expensive, not suitable for field, expertise required
  - (+): can be used during sleep, very sensitive thereby useful to clarify discrepant findings, potentially smaller sample sizes than with traditional assessment tools

Nutrition and Brain, Baumgartner

Iron

how distributed in brain?
what functions does it take on on brain?
- what if deciciencies occur?
what evidence available?
- hint: Nepal

Iron and brain development

Iron distribution in brain
- age specific: accumulates over time up to age 40
  - highly present in areas undergoing myelinisation during development
- area-, cell-specific: involved in neurotransmission of dopmainergic areas
Iron function in brain
- oxygen transport to brain --> high O2 needs
- energy production in cytochormes in mitochondria
- NT synthesis: dopamine synthesis is Fe-dependent
- myelinisation: Fe used as co-factor of enzymes reponsible for myelinisation as well as FAs
  - deficiency: myelin content and quality (via FA) affected --> transition speed affected in children
Iron deficiency
- crucial for myelination in 3 TM as well as up to age 3 --> deficiencies irriversible long-term damage
  - slow speed of processing and synaptic efficiency
  - spatial memory and learning affected
  - poor school achievement, attention, memory, language development, motor skills and socioemotional development --> child prone to health and psychological chalenges in later life
    - on large scale, poor development results in poverty of a nation
Evidence
- Nepal study: Fe & B9 during pregnancy until 12 months postpartum results in better cognitive outcomes and motorcontrol than placebo group
  - prolonging supplementation from 12 to 36 motnhs shows no additional benefit --> time-window pre/perinatal
- deficiency as well as anemia can lead to short and long-term consequences on congitive, motor and socioemotional domains
  - short term: O2 supply to brain insufficient?
  - long term: neurological deficits due to hampered myelination
- anemic school children benefit from supplementation --> example of short term negative consequence

Nutrition and Brain, Baumgartner

Omega-3

what effects do n-3 FA have on
- brain development & structure
- brain function
how do different LCPUFAs contribute to brian health?
what are known consequences of LCPUFAs deficiencies?
what is the evidence on LCPUFAs intake during pregnancy and childhood?

Omega-3 LCPUFA

make up largest part of fats found in brain (50-60%)
mostly DHA --> EPA can affect brain via peripheral mechanisms: modulation of sysntemic inflammation and vascular health
proportions and accrual of n-3 FA
- switch in n-6/3 content in brain: up to 10y, ARA content > DHA --> stabilizes in adulthood
- increase in DHA 35x from 30wk to 18 motnhs --> importance of mother's milk
affect brain function
- via membrane fluidity --> receptor affinity in synapses increased
- some n-3 FA used as fuel source --> brain requires lots of E
- indirectly: attenuate inflammation and modulate IS via gene expression
LCPUFA deficiency
- altered FA profile
- processing speed of visual cues affected
- during perinatal period, animal model
  - myelinisation, synaptogenesis and neural membran FA composition affected
- reductions inf brain glucose uptake and metabolism
Evidence
- oberservational studies of seafood intake: beneficial effect when consumed during pregnancy as well as childhood
  - cannot establish causal relation due to nature of study
- intervention studies of omega-3 supplementation: no effects and inconclusive results

Intro lecture Baumgartner

Prevention and treatment

what factors are important to prioritize treatment and prevention?
wat are modifiable risk factors?
how is health captured, name two important factors reflecting health of a population

Prevention and treatmentent

Prioritizing of efforts necessary, but this requires knowledge about risk factors, stats and evidence
(modifiable) risk factors
- smoking
- phyical inactivity
- alcohol abuse
- unhelthy diet
statistics and evidence help to identifiy most important health problems as well as solutions to it
- Global Burden of Disease study:
  - ongoing study in entire world since 1990
  - captures data on incidence, prevalence and mortality of different conditions causing premature death or disability
    - incidence: number of new cases
    - prevalence: number of existing cases at/during a given timepoint/period
  - mortality and morbidity can be extrapolated
  - published in the LANCET: continuous epidemiological data on development of many NCDs
- population health summary measures --> not applicable to single individuals!
  - HALE: healthy life expectancy
    - compares healthspan with lifespan --> number of years to be lived in full health
    - increases if
      - risk factors are reduced
      - healtcare quality improves
    - decreases if (e.g. gap between HALE and lifespan increase)
      - with age --> usually #1 risk factor for NCDs
  - DALY: disability adjusted life years
    - sums life years lived with disability & non-fatal disease and compares to standard, normative mean of expecte life years --> basically how many years of theoretical maximum are cut short due to illness
    - time-based
    - uses factor to adjust for severity of different diseases experienced
      - not always clear where to draw line betwen healthy and unhealthy
      - death always more impactful on daly than disability/disease
    - metabolic factors make up large part of DALYs
  - DALY and HALEs allow to
    - assess burden of disease as well as efficacy of health system performance
    - target investments

Intro Baumgartner

NCDs

definition
trend worldwide
costs

Non-communicable diseases

global trend for NCDs is increasing while communicable, neonatal and maternal diseases decrease
- injuries remain indifferent
affect men and women to same degree
costs: high because ncds are chronic diseases
- usually remain for a lifetime or difficult to reverse (obesity, cancer)
- expensive medication and treatment (antibiotics or other medication against communicable diseases less expensive)

Intro lecture Baumgartner

Explain epidemiological transition

Epidemiological shift

improvement in hygene, reduction in childhood mortality and healthcare improve --> mosrtality decreases --> demographics: more aged individuals --> higher NCD risk
shift from traditional foods to Westernized diet --> obesity and chronic diseases as well as chronic burden of malnutrition increase

Intro lecture Baumgartner

explain Fetal Origins of Adult Disease

discovery of increase prevalence of NCDs in men stemming from areas where childhood mortality was higher
low birth weight = proxy for poor prenatal nutrition --> associated with T2D, CVD & high bp
first 1000d as key timeperiod for health
- high plasticity --> can backfire in case of maternal malnutrition due to (epigenetic) imprinting
- evidence on humans almost impossible to obtain due to duration, but evidence from animals available

Costs of chronic diet-related diseases in Siwtzerland, Wieser

explain three main dimensions of disease cost
- how do these dimensions look in CH, how have they changed and which ones are the most important ones
- how are these dimensions assessed/established?

Direct medical costs

monetary value
ressources others have to invest in order to cure/take care of diseased person
- can extend to family and non-professionals/non-medical persons
in CH: healthcare
- about 1/3 of of illness-related expenses amount to healtcare in CH
  - 9730.- Fr/y per capita
  - in CH costs are high but when adjusted for purchasing power, expenses become 20% higher (and more realistic) as opposed to 50% difference in absolute means

Production losses

of the person affected
also measured in monetary fashion --> usually based on salary of individual x time
different types of production loss
- partial loss: absenteeism (some weeks/months) or presneteeism (reduced workload/pensum)
- total loss: permanent disability or death
- potential loss: suboptimal development and cognitive weknesses, e.g. LMIC with stunting/nutrient deficiencies
how to measure production losses
- questionnaires to capture how often/long employers absent/reduced workload
- administrative data to assess partial or total disability
- epidemiological data for premature mortality
  - additionally impared physical and cognitive development in LMIC
production losses in CH
- mental and musculoskeletal disorders have greatest impact --> chronic and very low mortality cause long absence
  - more "deadly" NCDs have comparable low impact, but also because mortality higher

DALYs

disability and loss in quality of life measured in DALYs, not monetary
DALY two components: time and weight of disease
- YLD: years lived with disability --> non lethal but disabling condition
- YLL: years of life lost
severity reflect by DALY weight and must be defined --> worldwide questionnaires
- chornic diseases realtively low weight
- mental diseases and pain high weight
- good correlation between different cultures shows agreement on severity of different conditions
In CH
- neoplass responsible for large part of YLL
- musculoskeletal diseases for YLD --> larger impact than YLL, typical for country with good healthcare system
- DALY burden has declined by about 30% in last 30 years --> big progress

Costs of chronic diet-related diseases in Siwtzerland, Wieser

Give an overview of the current knowledge on costs in CH

by what categories can the data be visualized?
- what are the major causes of disease burden for these categories?
- what costs are not included
- how was GBD study used in this particular case?

Dimensions of healthcare costs in CH

by service
by type of service provider
by type of financing instance
by illness and disease
- defined using the GBD study
  - costs for pregnancy, aesthetics and similar not included
  - co-morbidities separated

Enteral and Parenteral Nutrition Meier

Malnutrition
- what is the importance of oral nutrition therapy in regards to malnutrition?
  - how's the situation in hospitals?
- prevalence
  - WW & CH
  - who's most commonly affected?
- procedures to identify malnutrition
  - what are signs

Malnutrition

Importance of oral nutritional therapy
- prevalence of malnutrition increases during hospital stay (vgl Bild: nutritiona lstatus deteriorates...)
  - 55% of served food returned --> flight attendant experiment
- affects therapy outcome and mortality
  - improving nutrition during hospital stay is economic
  - daily requirements of many nutrients not met, depending on which requirements chosen, 53-70% --> nutrition in hospital setting is highly insufficient
Reasons for malnutrition (kennste)
- Clinical: Nausea, Cancer, infections, low BMI --> can affect hunger and appetite hormones
- Non-clinical
  - mastication problems
  - monotonous food
  - food temperature & serving times
Identification of patients at risk of malnutritoin or suffering from malnutrition
- high risk patients: low BMI, disease-related weight loss
- geriatric and oncology most commonly affected
procedure of malnutritoin identification
- Risk screening
  - using screening tools: NRS 2002
- Diagnostic assessment
  - phenotypic: low FFM measured via DXA/BIA, unintentional weight-loss
  - etiologic: low food intake, disase-related difficulties eating
- Diagnosis
  - at least one phenotypical and one etiological criterion
- Severity Grading
  - moderate --> vgl Bild
  - severe --> BMI<18.5, NRS >= 3, >10% weight loss in past 6m, serum albumin < 30g/l
prevalence
- worldwide about 25%, same for CH

Enteral and Parenteral Nutrition Meier

Parenteral Nutrition

indications
- access to stomach blocked
  - anatomical reasons: cancer
  - gut dysfunctional: perforation, obstruction...
- tube feeding unsafe
  - excessive vomiting: pregnant women
- patients who require bowel rest
  - acute gastroenteritis, radiation etheropathy, high output fistulas
- major clinical indications
  - Acute and critically ill patients
  - Post acute patients (eg after surgery)
  - Pre operative malnutrition
  - Home parenteral nutrition (eg short bowel)
contraindications
- gastrointestinal tract fully operational
- no access to veins (vena subclavia most common)
Delivery systems
- bags/containers with different nutrients that can easily be mixed
  - All in one options also available
- Home parenteral nutrition
  - for chronic intestinal failure
  - short bowel syndrome or Crohn's
  - cancer patients with intestinal failure --> most common
must take present and future into account: assure safety and nutritional balance for existing benign condition (ex short bowel) + prevent future complications related to nutrition
will affect QoL and may become unsuited in an unpredictable time span due to laignant comorbidities
complications often occur in PN and can be reduced via monitoring
- metabolic
  - Refeeding syndrome
  - Hyperglycaemia and hypoglycaemia
  - Hypertriglyceridaemia
  - Hepato biliary complications (HPN)
  - PN induced bone disease (HPN)
- technical
  - early: pneumothorax, bleeding
  - late: vein thrombosis
- infections --> local can develop to systemic
- monitoring
  - anthropos: monitor weight, arm cicrumferences, BIA --> indicator for muscle mass
  - funtion: check hand grip strength
    - lab results of bioechical, haematological, microbiological values

Enteral and Parenteral Nutrition Meier

Enteral Nutrition

Nasogastric/enteral tube (enteral nutrition, EN)

main goal: treat malnutrition and improve outcome
performed if foods intake in coming 7 days anticipated to be insufficient or if malnutrition diagnosed
- ethical consideration: EN must improve QoL --> if it prolongs suffering of a dying patient, it is unethical
- prior to insertion of tube, expected benefit must be considered
contraindications
- gastrointestinal issues: obstruction of intestines + others (vgl Bild)
- circulatory: schock, cardiac insufficiency
- metabolic: coma, ketoacidosis (diabetes)
Different accesses types for different durations
- nasogastric & nasojejunal
  - short term less than 30d --> longer periods via parenteral or special types of enteral
- percutaneous endoscopic gastrostomy: PEG, PEG-J, D-PEG
  - access to stomach via inserted tube --> food injected into stomach with seringe (Dave having lunch)
Complications
- reflux
- infections
- malpositioning of tube in brain or lung
- refeeding syndrome: reintroduction of food results in ATP generation, yet micronutrient deficiencies limit many biochemical processed so that organism is overtaxed putting the individual in a life threatening situation

Enteral and Parenteral Nutrition Meier

ONS

Evidence: top or flop?
what types exist and when are they do be used?

Oral Nutritional Supplements

first line adjuvant nutritional therapy
different types
- polymeric: entire foods, commercially available --> usually better tolerated and used most often
- oligomeric: broken down macros --> peptides & micro's
- disease specific: diabetes, CKD...
- isolated macros
Forticifaction of foods first step of malnutrition treatment, further step taken with sip feeds if fotification insufficient
concinving evidence for the effectiveness of ONS in the clinical setting (multiple meta-analyses)

Enteral and Parenteral Nutrition Meier

Oral Nutrition Hospital

special types of criteria to adapt nutrition to patient
- protein requirements can differ between patient groups
  - restricted: e.g. renal insufficiency
  - elevated: e.g. dialysis patients
- Energy
  - elevated: malnutrition
  - restricted: obesity
- medical indications
  - gastroenterogical: gluten free, lactose free...
  - speicial conditions: frc free, germ reduced, phenyl-alanine free
Protected Mealtime Policy
- assistance for people who need help (paralysis, e.g.)
- give patients enough time to consume meal -->no doctors or nurses present
- in between snacks to increase kcal intake
Monitoring of food intake via supervisisoin of tray collection

Infant and young child feeding, Baumgartner

Breastfeeing practices

what is the rationale for breastfeeding
what are short and long-term effects on breastfeeding
- on child --> name 3 main domains, then exemplify
- on mother
possible mechanisms mediating the above effects

Breastfeeding practices

Timing
- within one hour of birth
- until up to age 2 or even beyond, on-demand
exclusive breastfeeding for first 6 months
- HIC: introduction of complemetary foods as of fifth month recommended
rationale
- no adverse outcomes on growth & natural (mother’s milk much more complex and rich in diverse nutrients/bioactives than formulas)
- short-term (infancy)
  - decreased newborn mortality --> protects against diarrheal and pneumonic infections
    - sudden-infant-death syndrome (SIDS)--> two months reduce risk by 50%, longer breastfeeding further reduces risk of SIDS
    - compared to non/partially breastfed children: not breastfeeding increases infection-realted mortality 2x
  - beneficial effect on gut health --> necrotisation of enterocolitis prevented in pre-term infants
- long-term (later life)
  - protective against neurodevelopmental delays
    - potential enhancement of motor development
  - protective against metabolic diseases (hypertension, diabetes, obesity)
  - protective against immune-related diseases (allergies, coeliac, IBS)
    - WHO meta-analysis: non or sporadically breastfed children prone to develop obesity whereas breastfeeding for at least 6 months protects children
  - Protective effect possibly mediated but gut microbiome modulation during first 1000d
    - Microbiota of breastfed infants differs from formula fed à more commensal, less pathogenic strains
  - Protective effects also for mother à diabetes, obesity, breast/ovarian cancer

Infant and young child feeding, Baumgartner

Complementary feeding practices

what importance of complementary feeding, what is the goal?
- what if complementary feeding fails?
what foods shoould be consumed
- amounts
- rythm
- type
- foods to avoid
how many children get appropriate complementary feeding worldwide?
important aspects of compl. feeding during illness
explain:
- responsive feeding
- early protein hypothesis

Complementary feeding practices

necessary to cover increased needs as of 6 motnhs that cannot be covered by mother's milk anymore
- sub-oprtimal complementary feeding à stunting
complementary foods (= first foods)
- semi-solid and soft
- complement mother's milk --> closes the gap between requirements covered by milk and requirements milk cannot cover but that the growing infant has
- from month 6 to 23 --> some children ready earlier, around 4 months
- 70% children WW are introduced to first foods, but only 20% with minimum diversity and frequency à breastfeeding from 12-23 months persists in 65% of cases WW
weaning: stopping breastfeeding and switching over to semi-solid foods
complemenary feeding practices & recommendations
- quality of foods important:
  - ensure food variety by feeding at least 5/8 food groups
    - animal foods incl. mother’s milk
    - fruits & veggies
  - avoid empty calories --> high nutrient density foods important
  - Portion sizes: start with small portions, soft and little variety and 2-3 meals per day
  - Variety increase variety, volume and frequency of feeding
- other important aspects & special situations
  - hygiene & proper food handling
  - use fortified foods if necessary
  - in case of illness --> increase drinking volume and offer favorite foods to ensure proper food intake
- responsive feeding: watch out for and respect child’s reaction to feeding à foundation of (good) eating habits
- early protein hypothesis: protein intake > protein requirements primes metabolism to become obese

Infant and young child feeding, Baumgartner

DOHaD

explain framework --> draw!
hints
- environment
- early nutrition
- adult health & disease

DOHaD Framework

environmental stressors prime organism à organism becomes prone to diseases if environment changes / is not-well prepared to environment
- genetic
- epigenetics
  - DNA
  - Histone
  - Chromatin structure
  - miRNA
trajectories in early life more modulable/plastic, relatively low effort and pronounced impact on later life
- little known on how breastfeeding and complementary feeding affect epigenetics and microbiota
  - obesity incidence more strongly correlated with microbiome at 3 months than at 12 months
- partial breastfeeding with additional formula à microbiota more similar to formula-fed infants
- breastfeeding/mother’s milk has epigenetic effects
epigenome and microbiome interact with phenotype and early nutrition à 1000d for microbiota modulation

Eating disorders, Milos

Definitions

General characteristics of eating diorders
three types of eating disorders
- prevalence
common co-morbidities
- mortality

Risks and complications of eating disorders

Types
- Anorexia nervosa (AN)
  - typical symptoms: worry about body shape, self-esteem linked to weight/appearance, fear of gaining weight
  - 1.2% women
  - weight 15% below expectation
  - BMI < 17.5 kg/m2
  - weight loss caused by active or non-active measures
    - active: vomiting, laxatives
    - non-active. eating-restriction
  - always a behavioral and psychologic features
- Bulimia nervosa (BN)
  - typical symptoms (same as AN): worry about body shape, self-esteem linked to weight/appearance, fear of gaining weight
  - normal weight, but preoccupation with weight --> self-esteem related to weight
  - high food intake due to food attacks --> 1/week
  - vomiting to compensate for food attacks
- Binge eating
  - food intake >>> during at least 3 months
  - characteristic behavior: fast and abnormally bulky food intake despite absence of hunger followed by disgust and guilt
Characteristics
- often slowly and gradually developing bnormal eating behavior with tendency of becoming chronic
- eating disorder is hidden from family/friends and third parties
- profound impact on life: physical, psychological, professional, and social
Co-morbidities
- mostly psychatric nature
  - high rates of suicidal tendencies amongst eating disorders
  - difficulties to assess own and other's emotions
  - difficulties to see big picture, obsessive with details
- mortality in anorexic people ~6%
- hormonal foundation: leptin-like effect observed in AN
  - increased activation of HPA and HPG (gonads) axes --> reduced BMD, increased physical activity but also reduced reproductive activity
- organ specific --> vgl Bild
  - gastric emptying
  - osteoporosis --> 40% of patients have low BMD
  - amenorrhea --> fertility affected
  - cortical brain atrophy

Eating disorders, Milos

Etiology & Therapy

name three main areas of etiology and exemplify each
give an overview of therapy
- who is involved?
- who is targeted?
- what are the main goals of therapy?

Multifactorial etiology

Biological and genetic factors
- genome-wide association found 8 loci involved in AN
- pre- and perinatal factors:
  - infections during pregnancy
  - SGA
  - birth complications
  - feeding disorders in infant
  - childhood: obsessive, perfectionistic behavior
- Neuro
  - alteratino in the dopaminergic system leads to self-starvation becoming a trigger of motivation --> viscous cicle
Personality and individual experiences
- Character traits
  - low self-esteem
  - obsessiveness
  - anxiety
  - emotional inhibition
- trauma
  - sexual abuse or other trauma
  - strict diets in family
  - critical experiences towards appearance/weight/eating
Socio-cultural factors
- beauty standards
  - fashion standard
- overabundance of food
- unhealthy role models

Therapy

interdisciplinary --> communication is key!
- medical entities (family physician, specialists, gynecologists, dentists, internal medicine)
- employer
- social services
- psychiatry
target patients as well as patient's surrounding
- get insight and enhance trust, and motivate change
- family, relationship
- work
major goals
- reach at least BMI = 18.5 or stabilize weight if normal BMI
- normalize eating habits --> 3 meals/d with 2-3 snacks
- treat comorbidities (somatic/psychiatric)

Musculoskeletal diseases and nutrition, Andersson

Bone basics

bone homeostasis
- renewal duration
- BMD pattern throughout life --> draw
  - same for all?

Bone homeostasis

Bone basics
- trabecular: 15.25% calcified
- cortical bone: 80-90% calcified,
- cells
  - osteoblasts & osteoclasts: build/resorb bone
  - osteocytes: derive form osteoblasts and represent mature cell, 80-90% of bone
renewal every 10 years
peak bone mass between age 30 and 40
- gender differences:
  - women have lower BMD to begin with --> 60-80% genetically inherited, rest modulated by environment
  - menopause-caused fall in estrogen results in greater bone resorbtion and therefore lower BMD in females

Musculoskeletal diseases and nutrition, Andersson

Osteoporosis
- prevalence --> how many falls
- burden of fractures
- risk of fracture depending on first/seonc fracture and gender
- how measured/proxy
- reatment and preventive strategies

Osteoporosis

loss of bone mass (quantity) and deterioration of bone archtecture (quality)
consequences
- greater fracture risk
  - most commonly spine, hip or wrist fractured
  - 5-6% of falls actually result in fracture
- collapsed vertebra --> tooped posture
prevalence
- gender differences --> 20% females, but also 5% males affected
- worldwide variance in prevalence assumed to have genetic reason, not nutritional
- 75% of osteoporotic fractures in >70 year-olds
- risk for first fracture differs between gender (50% or more for females vs 20% males), but not for second fracture: 20% both gender
  - risk for second fracture highest in the year following the first fracture
cost & disease burden
- 13'000€/hospitalization --> greater than cancer, heart, and stroke combined due to greater prevalence of osteoporosis fractures than other
link to sarkopenia
- fear of falling reduces mobility and thereby muscle mass --> ultimately increases fall risks
- muscle strength correlates with BMD

Musculoskeletal diseases and nutrition, Andersson

Sarkopenia

prevalence
consequences
etiology
risk factors

Sarcopenia

prevalence: 20-75%, depending on population and source of information
consequences
- poor hospital outcomes, risk of falls, loss of independence
definition and diagnosis not always clear --> muscle mass measurements, handgrip strength
muscle strength via handgrip
- peak in early adulthood
- bi-phasic decline --> gradual as of age 40, substantial as of age 50
etiology
- systemic inflammation
- ageing-associated processes
  - reduced autophagy
  - loss of mitochondria with additional decline in mitochondrial function
  - impared stem cell regeneration
- los protein intake and negative protein turnover --> decrease in MyoPS and MitoPS
Risk factors
- sarcopenic obesity
- extreme weight loss
- drugs & pharmacological therapy --> ACE inhibitors
- smoking & alcohol
- sedentariness
- genetic/intrsinsic factors: gender, sex hormone deficiency, comorbidities
Prevention
- sarcopenia considered to be a nutritional disorder
- lifestyle interventions effective
  - exercise: less conclusive evidence
  - nutrition: evidence more equivocal and in favor of greater protein intakes
- pharmacological treatments use hormone replacement --> testo / SARMs

Musculoskeletal diseases and nutrition, Andersson

Osteoporosis

Risk factors
- what clinical RF exist?
Screening
- typical tool used
- cut-off values
- how do informatics play a role in risk assessment? Exemplify!
What typical areas of body fractured?

Risk assessment

Risk factors
- clinical --> vgl Bild
- BMT-D score --> assessed using DXA
  - < -1 SD: osteopenia
  - <= -2.5 SD: osteoporosis
  - <= -3 SD: severe osteoporosis
- BMD is integrated into the FRAX algorithm (fracture risk assessment tool) with clinical risk factors to predict 10-y risk for certain fractures
- sometimes no BMD assessemtn available (e.g. men or subsequent to typical fracture) --> recommended treatment if:
  - FRAX risk > treshold (country specific)
  - fracture of hip, vertebrae, proximal humerus, pelvis, distal arm
who to screen
- essentially, screening is recommended to postmenopausal women, especially >65y
- men >70 recommended to screen depending on Consensus/Foundation

Musculoskeletal diseases and nutrition, Andersson

Calcium

requirements increase slightly after 50y from 800 to 1000 mg/d
recommendations
- 800-1200 mg/d
- foods preferred source
- addition of vitamin D in institutionalized individuals
calcium rich foods: mostly dairy and animal-based, although present in many fruits and vegetables too
- average intake in Western 700-900 mg/d
- dairy product effective in preventing the decline of BMD, but not in its restauration
  - under debate: evidence for persisting bone loss in postmenopausal women despite intakes of Ca of 300 - 2000 mg/d
supplements
- supplements sometimes necessary to meet recommendations --> 30-50% of older women in western countries prescribed supplements
- uptake kinetics between dairy and supplemental Ca differs
  - supplements peak vs dairy plateaus --> potential mechanism for vascular complications, but not yet clearly identified
Evidence
- may increase risk of vascular diseases
- inconsistent results on fracture reduction (meta-analysis)
  - reduction total fractures and vertebral fractures but not forearm or hip
  - often supplementes combined with vitamin D --> no additional effect
  - overall: no convincing evidence and, if any beneficial effects of Ca on BMD, then only minor
- increased BMD by 1% after 1y --> not cost-effective

Musculoskeletal diseases and nutrition, Andersson

Vitamin D & risk of fractures and falls

what is the recommended dosing
deficiency
- what is special about cut-off values?
- compare different regions: Northern EU vs rest of EU vs middle east
evidence
- inconsitsent findings: why?
- what is still recommended
- who is liekly to benefit?

Vitamin D

deficiency
- serum 25(OH)-D best marker for Vit D status
- disagreement regarding cut-off values but unanimity that <25 nmol/l severe deficiency
- values <50 nmol/l increase from Northern Europe to Western/Southern/Eastern Eruope and up to 80% of individuals deficient in Middle East --> more sun not necessarily more Vit D
Evidence
- link to muscle function
  - mechanistic
    - muscle has vit-D-receptor (VDR) and converts it to 25OH-D --> supplementation increases VDR expression
    - deficiency affects mostly type 2 fibers
  - lower strength & functional decline in vit D deficient individuals observed in observational studies
  - supplementation shows reduced fall incidence
- Lancet meta-analysis suggests no benefit of vit D supplementation to decrease fall incidence
  - negligable effect on vit D vs control as well as high vs low dose
  - small effect on selected populations (es = 0.83)
  - critiqued by mani experts in the field
    - biased study selection: no studies of vit D an calcium --> 40% of high quality data not included in meta-analysis
    - deffectiveness of daily dose of 800-1000 IU well established
- Dosing
  - 2000 IU no effect on fall and fracture incidence
    - DO-HEALTH
    - doses of 20'000 IU/d for prolonged period may increase risk of falls
  - 800 IU usual recommendation to at-risk population (elderly and little exposure to sunlight)
  - >4000 IU not recommended, unless malabsorbtion
Supplementation & approach
- in case of deficiency, supplementation is required and likely to reduce risk of falls
- replete individuals are unlikely to benefit from supplementation

Musculoskeletal diseases and nutrition, Andersson

Protein

intake recommendations
evidence on protein intakes and bone health (not muscle!)
- how do types differ?
- what are the advantages and disadvantages of greater protein intakes?

Protein

1.2-1.5 g/kg/d to overcome anabolic resistance --> often unfeasible due to lack of appetite, too much food, mastication problems...
- 25-30g protein per meal required
Evidence for protein & bone health
- moderate evidence: protein with Ca and vit D might improve BMD and
- amount: higher protein intakes are generally better than low in terms of bone health --> no effects on bone biomarkers
  - meta-analysis across life-course shows different result depending on data used
    - non-adjusted: greater protein intake associated with better bone health
    - covariate adjusted: no association between amount or type of protein and fractures
- higher protein intakes have at least no deleterious effects
- type: soy and animal-based protein seem indifferent in terms of how they affect bone health

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