LDL may or may not correlate to cardiovascular outcomes

Unsaturated fats are the siren call of lower cholesterol to fight coronary heart disease (CHD). IMHO, it was the whole point of developing products, like canola, of which Soylent has plenty. So said the American College of Cardiology (ACC), and many others. For decades.
Now the president of the ACC is telling us that LDL may or may not correlate to cardiovascular outcomes. :open_mouth: (read the link)
In the same link, I see this from the BMJ (British Medical Journal?);

Consumption of saturated fats is not associated with all-cause mortality, cardiovascular disease, coronary heart disease (CHD), ischemic stroke, or diabetes2.’

There is probably lots of resistance to this idea, but the trend here is against unsaturated fats. Soylent has enough battles to fight, without taking on more. But my concern is that inclusion of unsaturated fats within Soylent will be a new battle very shortly. Please don’t respond with research stating otherwise, this post alone is enough evidence to suspect researchers of opportunistic collusion with a now failed premise. Instead, I am reaching out for evidence/research that unsaturated fats are the new enemy, in the hope of putting Soylent at the head of the class,

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So, you only want evidence that supports your already-held view.

How very un-scientific of you.


It seems unsporting not to quote my whole sentence. That being said, you may find some overlap discussed here;

If you have something relating to cholesterol and saturated fats, and you have read the link, ok, I concede, please post it.
[edit] But beware, my only response may be to say, the behemoth medical associations no longer agree with that view. The fact that they changed their view, IMHO, is a thumbs down on prior research in support of lower LDL to fight CHD, and avoiding saturated fats to fight obesity.

Okay, I have some questions:

  1. Why am I looking at a blog post that cites other blog posts as sources?
  2. Since when does “LDL may or may not correlate to cardiovascular outcomes,” mean “that unsaturated fats are the new enemy”
  3. How is a blog post that uses a single comment as the basis for the majority of its claims a dependable source?
  4. How can these studies be taken as conclusive when they only search for correlations rather than investigating causative mechanisms?

And some comments:
We need both LDL and HDL. They play very different roles in the body, both being essential to our survival. And in theory, a healthy person should be able to regulate their LDL and HDL levels automatically as needed since the production mechanisms of both are tied to negative feedback systems. So rather than fighting over who’s good vs evil fats research is more conclusive, wouldn’t it be more productive to look at why some people can’t seem to control their LDL production and what mechanisms are failing when lipids delivered by LDL end up accumulating in the arteries?


Yes, I wonder that myself. Who cares whether or not LDL is bad. What relevance does that have to anything?

Blog post?

I’m outta here.


@Prairiepanda, Ok, perhaps I should put in the Reuters and Medscape links that are list at the bottom of the blog. For the benefit of board members that are not MDs, you may find the blog helpful.

You may wish to re-read my post. No such conclusion was drawn, but a request for information on such a hypothesis.

Did you read it? How many in your extended family have had cholesterol tests over the decades in the fight against heart disease?

Precisely. We have been on the cholesterol march for decades for exactly this problem.

My hunch is unsaturated fats, or carbs. That is the point of this thread, and Soylent has both. Can you shed any light on this?

Monounsaturated fats can lower LDL. http://www.ncbi.nlm.nih.gov/pubmed/10584045.

The high-MUFA diets lowered total cholesterol by 10% and LDL cholesterol by 14%.

Polyunsaturated fats (omega-3) can lower LDL. http://www.ncbi.nlm.nih.gov/pubmed/6712540.

We conclude that dietary omega-3 fatty acids lower plasma LDL levels in normal human subjects by reducing the rate of synthesis of apoprotein B.

@Syke, controlling LDL is a mission without a goal, or even a point.

Some prominent cardiologists have questioned the 2013 guidelines, but the ACC and AHA have shown little appetite to return to LDL targets. “LDL may or may not correlate to cardiovascular outcomes,” Dr. Kim Allan Williams, president of the ACC, told Reuters last week.

Okay, the post I wanted to respond to seems to have disappeared, so I’ll just paste my quotes from the email copy:

The problem is that those articles do not cite their sources either, so it would take considerable digging to identify the papers they referenced, if it is at all possible with the little information they gave. The original blog post does improperly cite a couple of papers at the end, but these are not what the bulk of the post is about.

I read your post. Since you started by talking about the blog post, I assumed that your later hypothesis was prompted by that. But if not, it would be helpful to know what the basis of your hypothesis is.

Yes, I read it. I also read the other articles that it referenced. At least 4 of my extended family have had cholesterol tests done, but I do not see how that relates to my complaint that most of the blog post is based on a single comment(“LDL may or may not correlate to cardiovascular outcomes”)

The arterial buildup that we’re concerned with in this case is comprised of largely of lipids, not carbs, so carbs are out unless you’re aware of some reason that certain carbs(or excess carbs) would mess with the regulatory processes that are supposed to prevent arterial lipid buildup. Cholesterol is a part of it, and may contribute to the stability of such buildups, but most of the plaque consists of other lipids. The exact lipids involved vary a great deal, presumably dependent on what is most abundant in your system at the time, for whatever reason(not necessarily due to diet, but that might be a factor). Most(not all, obviously) naturally occurring lipids are unsaturated, so many of our fat-metabolizing enzymes are built to take advantage of this. Saturated fats are more difficult to break down due to crowding, but we’re certainly equipped to handle those as well, with a different set of enzymes. So I’m skeptical of any source that claims one or the other is “good” or “bad”, or even “better” or “worse” compared to the other, unless someone can point at some suspicious metabolic byproduct or other cause for concern that is unique to that fat type. The only dietary fat that I’m a bit weary of is trans fats because their steric configuration is pretty incompatible with our metabolic pathways.


Thank you, @Prairiepanda, I have read your response with great interest. My original reply is being held purportedly for spam inspection, it is my second such hold. I’d be happy to drill into those references, but I hesitate to expend the effort under the circumstances. Thanks, again.