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Thread: Dietary saturated fat intake and risk of stroke: Systematic review and dose–response

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    Default Dietary saturated fat intake and risk of stroke: Systematic review and dose–response

    Dietary saturated fat intake and risk of stroke: Systematic review and dose–response meta-analysis of prospective cohort studies
    • Higher dietary saturated fat intake is associated with a decreased overall risk of stroke.

    • There is a linear dose–response relation between dietary saturated fat intake and the risk of stroke.

    • It is necessary to re-evaluate the restrictions on saturated fat intake for future dietary guidelines.
    Do bear in mind these studes are based either on Food Frequency Questionaires or 24 hr dietary recall interviews.Neither of which are particularly reliable.
    It will be better when researchers actually collect data by asking trial participants to photo everything they eat though the day I'm sure something like these apps could be adapted to record actual food/beverage consumption without leading/encouraging trialists to limit calories/macros The 9 Best Food Tracker Apps of 2020

    It is sad there appears the British Heart Foundation is still sticking to it's anti-saturated fat stance.

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    It can be so depressing Ted that they think they “know” and are not open to the possibility of having been wrong for all these years.
    Gilli - DLTBGYD but more importantly KCHO

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    Default High-Risk Atherosclerosis and Metabolic Phenotype

    This new paper is worth reading even if you just look at the images and read the sections headed LIFESTYLE LINK
    It's helpful when the rather dense scientific text is interspersed with more basic sections explaining what you may in practice, be able to do about what they have just been explaining.

    High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation

    Lifestyle link
    Notably, levels of small LDL-P are primarily responsive to dietary carbohydrate intake (increase with higher carbohydrate consumption), while large LDL-P are more responsive to dietary saturated fat (increase with higher saturated fat consumption).
    Both weight loss and carbohydrate restriction decrease the expression of the small LDL-P pathway.71
    These considerations provide some biological plausibility for the observation that in large populations, higher dietary saturated fat consumption is associated with higher LDL-C, but not with higher all-cause or CVD mortality.72
    LDL-C might thus provide misleading information as to the effect of diet on ASCVD risk and may therefore be an inappropriate marker for informing dietary advice.73,74
    A further level of complexity regarding recommendations for dietary fat intake is the fact that dietary fats comprise heterogeneous molecules with diverse structures even within conventional fat classes (i.e., saturated, monounsaturated, and polyunsaturated fatty acids).74
    For example, odd-chain SFAs (C15:0 and C17:0) are relatively unique to dairy fat, are not synthesized by humans, and are therefore regarded as reasonable biomarkers of dairy fat consumption. Cohort studies measuring these biomarkers of dairy fat intake show associations with protection against diabetes, and meta-analytic evidence from prospective studies suggest that C17:0, but not C15:0, intake is inversely associated with the risk of CVD.74 Collectively, this does not speak to restricting all food sources of dietary saturated fat for cardiometabolic health and supports food-based, instead of nutrient-based dietary recommendations.

    Lifestyle link
    Adequate intake of EPA+DHA and/or EPA only at doses of >3 and 4 g/day, respectively, is an effective and safe option for lowering triglycerides87 and hepatic fat content in NAFLD
    For those who may think 3-4g omega 3 is a lot it may be worth understanding better how much omega 3 (EPA +DHA) is actually present in omega 3 softgels. How much EPA and DHA is in your omega-3 supplement?
    May I also remind you that the omega 3 index is the balance between omega 3 and omega 6 and while people continue to consume fast foods fried in omega 6 seed oils it will remain the case that pro-inflammatory omega 6 overwhelms the anti-inflammatory potential of omega 3. Most of the omega 3 trials fail to reduce omega 6 intake so show disappointing results from omega 3 supplementation
    If they measured omega 3 index at start of omega 3 research trials and at the end so we could see how near to an Omega-3 Index of over 8% they actually achieved and how long the trialists had to heal, before the study ended.
    Same happens with vitamin d research, they know naturally early and indigenous humans attained maintained 25(OH)D around 40-60ng/ml (100-150nmol/l) from daily UVB exposure but you never see a vitamin d3 study where they use sufficient cholecalciferol daily to maintain natural levels even though there is good research showing the anti-inflammatory actions of D3 require the presence of cholecalciferol in serum and we can only measure free available cholecalciferol in serum in significant amounts at natural optimal 25(OH)D levels around 125nmol/l 50ng/ml. Why does anyone expect cholecalciferol to work as a signalling molecule when it isn't present in that form in serum. No one is stupid enough to expect a mobile to work when there is no signal present.


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