Reduction in saturated fat intake for cardiovascular disease

(Mike) #1

In May, Cochrane updated/released this meta-study, which showed that a reduction is saturated fat led to a reduction in risk of combined cardiovascular events by 21%, but no significant reduction in
all-cause mortality or cardiovascular mortality. I generally consider Cochrane to be a fairly good source. These results, which seem neutral at best (all-cause mortality findings), and contradicory to other low carb studies at worst (cardiovascular events findings) are a bit surprising.

Hoping that someone here who is more skilled in parsing study results has some insights.

https://pubmed.ncbi.nlm.nih.gov/32428300/

Thanks, Mike

(bulkbiker) #2

Their main results

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Would seem to completely negate their conclusionā€¦

Full paper is here ā€¦ look like a longggg read

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011737.pub2/epdf/full

#3

A reduction in overeating is always favourable.

(bulkbiker) #4

Depends what you are ā€œovereatingā€ I guessā€¦

(Bob M) #5

This has been handled quite well by DiscoStew on Twitter, and others. Basically, they still did not use certain studies, in addition to making other errors.

And whenever I see relative risks of 21%, I ignore it.

(Bacon is a many-splendoured thing) #6

Cochrane is apparently getting less objective, with some founding members claiming that the board has sold out. Iā€™m surprised by the 21% reduction in events, however. First of all, it seems high, and second, how clinically relevant is this reduction? (It is quite possible for statistically significant results to be irrelevant from the clinical point of view.) I wonder what the selection criteria were for this metanalysis. Have you seen any critique by ZoĆ« Harcombe or any of the other usual suspects?

#7

Iā€™m sure itā€™s possible to develop a foie gras liver by overeating or force feeding oneself on fat.

(bulkbiker) #8

Although oddly it would seem that the geese and ducks need grains to achieve itā€¦
I donā€™t see the ā€œgavageā€ involving much ingested fat so maybeā€¦ just maybeā€¦ your sweeping statement was incorrect?

(Bunny) #9

Increasing Vitamin C intake is also the best ā€˜strategyā€™ to increase and maintain the glycocalyx shield on the endothelium and not eat more of any fat than necessary meaning watch your portion size, and being your Vitamin K intake is adequate, your veins and arteries will be clean as a whistle?

No kind of fat is going to protect you from CVD or CHD risk, period!

Another one to add to the list of ā€˜strategiesā€™ is to try to keep endogenous and dietary sugars as low as you can coupled by adequate Vitamin C intake?

Authorsā€™ conclusions: The findings of this updated review suggest that reducing saturated fat intake for at least two years causes a potentially important reduction in combined cardiovascular events. Replacing the energy from saturated fat with polyunsaturated fat or carbohydrate appear to be useful strategies, while effects of replacement with monounsaturated fat are unclear. The reduction in combined cardiovascular events resulting from reducing saturated fat did not alter by study duration, sex or baseline level of cardiovascular risk, but greater reduction in saturated fat caused greater reductions in cardiovascular events. ā€¦More

(Edith) #10

I donā€™t see how they could have said all those things about not finding any evidence that supported lowered saturated fat intake improved health outcomes and then come to the conclusion that they did.

(Gregory - You can teach an old dog new tricks.) #11

The number needed to treat for an additional beneficial outcome (NNTB) was 56 in primary prevention trials, so 56 people need to reduce their saturated fat intake for ~four years for one person to avoid experiencing a CVD event.

Give me a breakā€¦

#12

We considered studies that performed experiments with C57BL/6 mice (non-knockout) with NAFLD induction by hypercaloric diet, and whose treatment was based on lipids. (oils)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949901/

Overfeeding on isolated fatā€¦

Elevated PAI-1 is a risk factor for thrombosis and atherosclerosis[5]
https://en.wikipedia.org/wiki/Plasminogen_activator_inhibitor-1

Keogh at al53 recently demonstrated that 8 weeks of a
very-low-carbohydrate, high-saturated-fat weight-loss diet reduced plasma PAI-1 levels in severely obese individuals with
a body mass index of 33.64.1. However, the beneficial
effect of this diet seems rather to be a result of weight loss,
because plasma PAI-1 levels are also reduced by an isocaloric
high-carbohydrate, low-saturated-fat diet in the obese subjects. On the other hand, the effects of kDa on blood
fibrinolysis have not been examined in nonobese individuals
as far as we know. Our present findings suggest that the
nature of kDa with respect to the prevention of thrombosis is
a double-edged sword. The morning increase in PAI-1 plays
an established role in the mechanisms underlying transient
morning resistance to thrombolysis using tissue-type PA, as
the activity of PAI-1 is 2- to 4-fold higher in the morning than
in the evening.5 Therefore, the kDa-induced circadian augmentation of PAI-1 expression in a phase advanced manner
not only contributes to an increased risk of myocardial
infarction but also alters the efficiency of thrombolytic
therapy when applied in the morning.
https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.109.190140

(bulkbiker) #13

Oils not fat thoughā€¦ see it gets complicated this stuffā€¦

I could feed you rancid seed oils and make you ill with ingested fats unlikely to make you fat though.

(Bacon is a many-splendoured thing) #14

The fat we eat gets metabolised, if itā€™s not used structurally. (This is from studies involving radio-labelled foods.) The structural problems caused by eating too much polyunsaturated fat, especially trans-fats, are well-known.

Liver fat, on the other hand, is produced by a process called de novo lipogenesis, which occurs when the liver is overwhelmed with ethanol, fructose, branched-chain amino acids, or a fourth thing that Iā€™m not recalling at the moment. Dr. Robert Lustig, the well-known neuroendocrinologist and food activist, explains the metabolic pathway involved during the course of this presentation (should you wish to do further reading, he supplies references to the studies he refers to on each slide):

#15

I did say ā€œovereatā€ and provided evidence.
Figure 1 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949901/)

Robert Lustig is right to an extent. Eat real food. However he doesnā€™t explain why modern humans are consuming all this junk food in the first place. Why this junk food was created in the first place.

(Bacon is a many-splendoured thing) #16

Ah, I see. From what the article says of the studies they reviewed, all of the studies gave their mice high-sugar diets, which seems to be the standard practice in all these studies of ā€œhigh-fatā€ diets in mice.

I fail to see how to disentangle the effect of the sugar from the effect of the high-PUFA oils the mice were given. Though we do know, come to think of it, that overloading the liver with trans-fats causes fatty liver, in the same way as does overloading the liver with ethanol, fructose, or branched-chain amino acids.

(Gregory - You can teach an old dog new tricks.) #17

Because itā€™s cheap to manufacture, has a long shelf life and targets kids who get addicted to sugar and carry their addiction into adulthood.

(Bob M) #18

Not sure what to say hereā€¦other than their conclusions seem misplaced:

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The only location where they say sat fat might have an effect is for ā€œcombined cardiovascular eventsā€. Otherwise, the data isnā€™t great.

#19

Junk food was created before the manufacturing of junk food. :wink:

Try again. :slightly_smiling_face:

(Gregory - You can teach an old dog new tricks.) #20

Not sure what I should tryā€¦

What is your idea of pre-industrial junk food consumed by modern humans?

The obesity, CVD and T2D epidemics did not take off until the mid 20th century, coincident with the ramping up of the mega processed food conglomerates.