Food and Nutrition for Disease Prevention
752-6102-00L
752-6102-00L
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Karten | 68 |
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Sprache | English |
Kategorie | Biologie |
Stufe | Universität |
Erstellt / Aktualisiert | 07.03.2021 / 11.06.2021 |
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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)
- nasogastric & nasojejunal
- 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
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
- protein requirements can differ between patient groups
- 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
- decreased newborn mortality --> protects against diarrheal and pneumonic infections
- 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
- protective against neurodevelopmental delays
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
- ensure food variety by feeding at least 5/8 food groups
- 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
- quality of foods important:
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
- little known on how breastfeeding and complementary feeding affect epigenetics and microbiota
- 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
- Anorexia nervosa (AN)
- 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
- mostly psychatric nature
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
- Character traits
- Socio-cultural factors
- beauty standards
- fashion standard
- overabundance of food
- unhealthy role models
- beauty standards
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
- gender differences:
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
- greater fracture risk
- 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
- mechanistic
- 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
- 2000 IU no effect on fall and fracture incidence
- link to muscle function
- 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
- meta-analysis across life-course shows different result depending on data used
- 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?
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?
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)
- cancer patterns--> cancer type and total prevalences differ between countries
- 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?
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?
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
- insulin resistance as key driver of cancer
- 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
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
- Red and processed meats: 1.2% increase
- 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
- Overall chance of contact between carcinogens & enterocytes is reduced
- Fruit
- Decrease in cancer risk limited
Cancer and Nutrition, Andersson
- What strategies exist to prevent cancer?
- How do they work?
- On what levels?
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?
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?
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
- CVD: increasing rates ever since population infectious diseases could be prevented/reduced --> opulations ages and becomes prone to CVD
- 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?
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
- most nutritional sciences studies do not fulfil criteria sufficiently, so causality remains weak
- 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
- do not necessarily correlate with actual CVD mortality, although increase risk factors --> use of hard facts as more reliable information
- 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
- intermediate risk factors & soft vs hard outcomes
- 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
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
- negative impact on risk factors but associations show decrease in mortality
- 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
- high agreement:
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
- many studies suggesting beneficial effects of moderate alcohol consumption may be biased due to overestimation + residual confounding of moderate drinkers vs abstainers
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
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