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Diet, Lipid and CVD - Coggle Diagram

- - - - SFA and LDL-C relationship determined by many factors: type of fat replaced (PUFA, MUFA, Carbohydrtae), not all SFA’s have same effect on cholesterol and depends on food eaten
    - - WHY? Association between SFA and death from CVD, not causation. Mediated through third factor such as LDL cholesterol. SFA also impacts on other aspects affecting CVD.
      - What is the relationship between SFA and cholesterol influenced by?
        
        substitution- better effect with PUFA, than MUFA than Carbs
        
        replace SFA with PUFA beneficial at reducing CHD risk. When replacing SFA with Carbs. can see adverse effect, especially if free sugars. can see NO net effect if replace with PUFA and carbs at same time which is why some studies show no effect
        
        Differential effects of different fatty acids on LDL and HDL (not all SFA have same effect at raising LDL-c)
        
        Lauric acid raises LDL > myristic acid > palmitic acid and stearin acid doesn’t effect LDL. same observed with HDL
        Varying effects on total c : HDL c
        Composition of fatty acids in food important
        
        Coconut oil: 91% SFA (15% lauric acid which behaves as a medium chain fatty acid and no effect on swerum LDL cholesterol, directly to liver and not incorporated into CM. 80% long chain fatty acids which raise LDL and HDL as incorporated into CM).
        
        Nutrients versus complex foods- interpretation of CVD risk and reccomendations
        
        We don’t consume fatty acids in isolation. We eat in foods with varying compositions. SFA from processed meats associated with increased risk CVD and reduction in CVD risk seen when dairy and plant SFA replaces meat SFA
        
        when milk fat wrapped in milk fat globule membrane (whipping cream MFGM) in modulating plasma lipoproteins, reduced LDL-c (reduced bioavailability of fat). Native SFA without milk fat globule membrane (butter) has increased effect on LDL-c.
        
        Effects of cheese in lowering blood cholesterol: cheese lowers LDL-c whereas butter raises LDL-c when compared to habitual diet. WHY? Cheese has calcium which may be precipitating SFA which reduces bioavailability
        
        Mechanism: why SFA in cheese and dairy has less effect on serum LDL-c than butter
        
        Ca2+ precipitates SFA in cheese and decreases cholesterol solubilisation in gut so absorb less effectively compared to butter so doesn’t raise LDL-c to same effect
        
        Seen in dutch cohort study - when looked at effect of SFA on ischaemic heart disease, no effect seen as driven by intake of short and medium chain fatty acids and SFA from dairy sources (dutch eat high amount of cheese and dairy so counteracted risk of other SFA)
        
        Compliance to diet
        
        Biological variation in serum LDL-c in response to. changes in intake of SFA
        
        When group changed from baseline diet to NCEP diet (lower fat and SFA diet), highly varied LDL-c reduction (varies on how absorb fat, LDL receptors etc) . Huge variation in LDL response to changes in SFA in diet in other studies
  - - - Diet high in SFA (palmitate) raises LDL-c and LDL receptor gene and reduced with oleate (MUFA) / LDL receptor gene shut down
        
        One mechanism to explain: 1. Intracellular pool of free cholesterol important in transcribing LDL receptor (when high, low LDL receptor transcription).
        
        When cells sense SFA, ACAT enzyme does not form cholesterol esters (does not like SFA) so cell level of free cholesterol remains high and LDL-receptor transcription remains low = HIGH blood cholesterol
        
        Conversely, ACAT favours MUFA AND PUFA as substrates for forming cholesterol esters so reverse occurs= LOWER blood cholesterol
- - - - PREDIMED- Med diet either supplemented with nuts or extra virgin olive oil. Compared to control diet, incidence of end point CVD reduced significantly
    - - Designed to reduce hypertension. Has significant effect on systolic and diastolic lowering
- - - - Fructose and sucrose (fructose and glucose )
      - Direct: Sugars in high quantities (20% + total energy) increases metabolic risk
      - Indirect: ~12-13% free sugar intake leading to CVD risk over time
      - In USA, above 20/25% sugar total energy , 2 fold increase in risk of CVD death
      - Fructose vs glucose sweetened beverages effect as 25% total energy : fructose more lipogenic sugar . Post-prandial TAG higher with fructose .
      - fructose in cola increased VAT, liver fat and muscle fat in comparison to drinks not containing free sugars (milk, diet cola, water) over 6 months
      - Dietary intakes of non-milk extrinsic sugars in UK adults and adolescents - on average 12% total energy from free sugars. Upper 2.5th percentile,get up to 30% total energy from free sugars= overall little risk in terms of DIRECT sugar s metabolic effects but INDIRECTLY through body weight
      - Post-prandial TAG response in children with NAFLD given sugar-sweetened beverage: higher baseline and higher response, worsening cardio metabolic risk at early age
      - Sugar and body weight: Free sugars and sugar-sweetened beverages are determinant of body weight in free-living individuals (not one particularly sugar like fructose)
        effect mediated through energy intake from sugar and not type
        
        Fat contributes to increase in percentage body fat (not sugar and starch) = high fat foods top of list in terms of foods contributing to obesity . Combination of sugar and fat in foods that give greatest propensity for increase in body weight
  - - - SACN 2015- Intake of free sugars <5% total energy because of contribution to energy and body weight and dental issues
      - SACN 2015 findings: no association between total carb intake and incidence of T2DM and CVD, vascular function, inflammatory markers, risk factors for T2DM= total carb is neither detrimental nro beneficial to cardio-metabolic health (likely due to varying types of carbs)
      - SACN 2015: Intake dietary sugar not related to cardio-metabolic risk or coronary events or T2DM, blood glucose or insulin (sugars contribute to energy intake which in turn contributes to insulin resistance)
      - SACN 2015: Greater consumption of sugar detrimental to health
      - Intake of sugar sweetened beverages are source of free sugars that were associated with T2DM
      - Should low fat high carb diet be reccomended? TAG increases and HDL reduces (due mutual lipid exchanged reactions) and LDL shrinks becoming atherogenic= if replacing fat with carbs, make sure complex variety containing large proportion of fibre
- - - - more studies showed egg intake not associated with risk of CVD and cardiac death in general population but may be associated with increased incidence of T2D and CVD population
      - OTHER FACTORS CONFOUND RELATIONSHIP OF EGG INTAKE AND CHOLESTEROL IN T2DM: Jackson Heart Study: cohort with T2DM stratified by egg intake . High egg consumers much stronger history of smoking, ETOH intake and less education and ate more red meat and SFA and trans fats (same BMI)
      - ALTERNATIVE EVIDENCE: DIABEGG study: high egg diet fed to people with T2DM and effect on CVD risk factors assessed. Cholesterol, LDL, HDL, TAG and glucose and Hba1c all reduced .
      - SUMMARY: Systematic review of egg consumption, CVD and T2DM: eggs not associated with increased CVD risk in T2DM. Risk seen could be due to dietary pattern and other risk factors associated with those having high egg diet. CONCLUSION: dietary pattern, PA. and genetics gave have greater impact on CVD and T2DM than a single food like egg. Up to 7 eggs per week can be safely consumed with emphasis on healthy lifestyle in those with CVD and T2DM.
  - - - Weight loss: reduced cholesterol biosynthesis in general
      - SFA replacement: reduces intracellular free cholesterol
      - Soluble/ insoluble fibre: bile salt sequesterants / energy displacement
      - Plant sterols/stanols: compete with dietary and biliary cholesterol
      - Soy protein: stimulates LDL receptor expression directly as phytosteriols have estrogenic-like activity
- - - - 36g fish/day (2.2 servings / week) delivered 0.9g EPA/DHA (as fresh salmon)
    - - TAG lowering : fish oil supplementation accelerate clearance of TAG-rich lipoproteins in postprandial phase . Up-regulates lipoprotein lipase activity (fish oil upregulates gene expression of LPL)
      - Hear rate lowering
      - BP lowering
      - (At higher doses) Antithrombosis
      - (At lower doses) Antiarrythmia
      - Very little effect of LC n-3 PUFA on total cholesterol. LDL-c tends to increase/ gets larger with LC n-3 PUFA intake
      - LC omega-3 reduces liver fat . In people with NAFLD, hepatocytes lack LC omega-3 . DHA particuarly effective
      - Deficiency of LC n-3 PUFA leads to depletion of them in membranes of key metabolic tissues (liver, adipose tissue) = metabolic dysfunction and ‘cardio metabolic risk’ which increases development and endpoints of CVD
        
        N-3 INDEX (percentage of EPA and DHA in membranes)= if 10%, you get the most cardiac protection from sudden cardiac death compared to addressing other risk factors
        
        As LC N-3 PUFAs increase in diet, ventricular tachycardia and fibrillation reduces (antiarrhythmia and preventing sudden cardiac death)
  - - - if have heart disease, should have 2 portions a week to have 0.5g/day
    - - target populations for LC n-3 PUFA studies: all mechanisms of action of LC n-3 PUFA’s are found in metabolic syndrome so population needs to be with this group (dilution effect with general population so no effect seen)