Metamucil

(Pat) #1

Last year my Dr told me my cholesterol was too high at 5.6. She asked me to see the dietitian as part of my care plan. The dietitian suggested I take one teaspoon of Metamucil every day to lower my cholesterol, she said it would take 3 months before I would see a difference. So, one year later after taking Metamucil every day, my cholesterol is exactly the same 5.6!! Is 5.6 too high? I always thought that was okay.

#2

Fiber can help cholesterol levels, but definitely not 1tsp a day.

It’s only slightly out of range (by US standards at least) and realistically fine. Your sdLDL levels are far more important since those are what can actually plaque up on you.

You can up your fiber to a couple TBSP a day and see if that helps, or if you’re doing the super fat-ified version of keto, just don’t do that. We’re told by all the fat gurus that dietary cholesterol has little effect on our blood levels, but that’s simply not the case for all of us. My total and LDLc used to be pretty high, trigs were always good as well HDL, but not excessively adding fat to everything and looking for excuses to cook things in bacon grease dropped my numbers huge.

(Bacon is a many-splendoured thing) #3

There is plenty of evidence to suggest that elevated cholesterol is not the cause of cardiovascular disease, but the idea still has a tight grip on many doctors and scientists. But even people who still believe in cholesterol have to admit that total cholesterol is not a good marker of cardiovascular risk, and that the thing to watch is the ratio between triglycerides and HDL. If that ratio is 0.9 or less (2.0 or less in U.S. measurements), then you are certainly fine, regardless of what your LDL and total cholesterol are doing.

In any case, it seems odd to claim that increasing one’s fibre consumption would lower cholesterol. We’ve known for a long time (since before the dietary guidelines were first issued, in fact) that it is carbohydrate consumption that elevates serum cholesterol levels. So it stands to reason that reducing carbohydrate consumption would have the opposite effect. But in any case, the notion that too much fat in the diet causes cardiovascular disease has not withstood very well the effect of time.

(Joey) #4

The 1970s called and they want their science back. :roll_eyes:

#5

Given they had zero clue what sdLDL was in the 70, 80, or 90s AFAIK, I’m gonna call that one a fail my man. Most docs still don’t do particle testing now. May want to read what I wrote a little closer.

(Joey) #6

Okay, I’ve re-read it multiple times. But your man is still missing the thrust of your point.

Regardless of what most docs do or don’t do… My understanding of the current research is that higher particle LDL does not necessarily contribute to clogged arteries. Context matters greatly. Meanwhile, both the association and the “plumbing model” have been debunked, no?

#7

Correct, which is why that’s not what I said, I said sdLDL.

(Joey) #8

Ah, the distinction drawn (between LDL and sdLDL) was lost on your man until now. Thanks for pointing me back to your original post. I apologize for the oversight!

Back to the larger point: Whether sdLDL “plaques up” one’s arteries remains a seemingly confused statement.

My understanding is that cholesterol particles change in size and density as they circulate and react based on the conditions encountered along the way.

As such, I don’t believe modern research characterizes sdLDL as a particle that causes plaque, but as a marker that arterial damage (inflammation) is occurring. The sdLDL are the “fireman” attempting to put out the fire… not the cause of plaque.

Best not to confuse the firemen with the fire. Better still would be to stop the cause of the inflammation - which is not sdLDL. Association is not causation.

Am I off base here?

#9

While there’s no guarantee that having sdLDL equals plaquing up on you, we know that’s the one that does it, and since particle testing became a thing that’s the one that’s now blamed. While the firemen at the fire argument I feel was valid when we couldn’t differentiate the different LDL particles, to me at least, it’s less valid now since we have a better idea of what’s doing the damage. We’re going to have plenty of it either way if our system decides it really needs to do patch work for real reasons, no reason to have tons of it free floating around either. I’d rather have less of the one that causes damage around.

Since the cholesterol gurus also seem to not be a fan of sdLDL, and given they understand way more than I do about it, for me, that’s enough for now.

We’re also told our diets don’t effect or serum levels much, but that’s definetely not the case for most it seems, myself included and one of the things that I do disagree with them on. The fact that the Feldman protocol works is a drastic dietary change within a week, which I’ve done and it works awesomely.

I don’t subscribe to cholesterol not mattering as many do, I give no credit to 200 being some magical number for being “bad”, nor do I think high LDL-C by itself is bad, but there needs to be context and unlike the original LDL = Bad thing happened, that was never really based on anything credible, but there’s way more pointing to sdLDL actually being a threat, so I want mine low, and all it took was changing how I ate slightly to achieve that and maintain it.

When my sdLDL came back terrible I had a followup to pass and my doc would have sawed my head off if I couldn’t, and she’s cool and isn’t brainwashed, she only does NMRs so I cheated the process with Cardarine, and in all honesty if was probably bad because of some other supps I regually use, but I’ve been able to maintain awesome numbers since then without any help just from the diet change.

(Joey) #10

Although we agree that higher sdLDL is a sign of trouble, for me the issue remains as to whether sdLDL cholesterol is the cause of a problem versus part of the solution.

My understanding is that LDL (especially sdLDL) helps keep damaged arteries from tossing life-threatening clots into circulation (where they cause heart failure, stroke, brain aneurysm). That’s a good thing.

Sure, I’d rather not have a fire. And too many firemen trying to put out a fire can leave a lot of broken windows - but that’s still better than letting it burn.

Whether cheating on one’s bloodwork is a useful exercise might make for a separate interesting topic :thinking:

(Bacon is a many-splendoured thing) #11

My view is that manipulating markers is an ineffective way of dealing with a problem, because it leaves the real cause unaddressed. So it is crucial to know whether we are dealing with a marker for a problem or the (or a) cause of the problem.

I am not convinced that small, dense LDL is a cause of cardiovascular disease. I’m no expert, of course, but what I’ve read leads me to the marker-not-cause hypothesis. I am old enough to have seen the focus shift from saturated fat to cholesterol to LDL to type of LDL to specific aspect of LDL, and the shifts feel more like grasping at straws to prop up a failing hypothesis than true advances in our knowledge.

The problem is that for decades research has not been funded unless it is intended to reinforce the prevailing view that fat/cholesterol/LDL just has to be harmful. Yet several large studies intended to support that prevailing view not only failed to support it, but also produced data that showed cholesterol can’t be the cause of cardiovascular disease.

Keys’s own Minnesota Coronary Study is a case in point. Yet despite this, Keys and Franz never changed their hypothesis. Instead, Keys removed his name from the study, and Franz withheld publication for 17 years. This behaviour is a pretty good indication that they knew their hypothesis was wrong but lacked the courage to admit it.

(Joey) #12

@PaulL +1 to everything you’ve laid out above.

Serum cholesterol becoming smaller and denser (thus, sdLDL) is likely a response to arterial inflammation - not a cause.

Although I would not be pleased to see high concentrations in my NMR lipid profile, I’d regard elevated sdLDL the same way I feel about scabs on skin wounds … better to scab over than to bleed out. Better yet to get to the cause of the wounding.

[As for bloodwork hacking: Instead of trying to rig my test results to mislead my doc about biomarkers (in fear of getting crap about concerns that are not scientifically correct), I’d spend my energy looking for a better physician. Just me?]

(Bacon is a many-splendoured thing) #13

I would say, rather, that it is not a response to arterial inflammation, but rather is caused by the same cause. A slight nuance, perhaps, but possibly significant. (This is an idea along the same lines as Peter Attia’s TED talk, which introduced me to the idea that diabetes was not a response to obesity, but an independent problem caused by the same mechanism that caused obesity.)

In any case, my favourite analogy is to say that manipulating a marker is like cheating on a school exam. The exam is intended to to measure one’s mastery of the subject matter in a course, and cheating may get a better grade, but it won’t increase one’s knowledge. Would people rather see a doctor who paid someone to take her tests for her in medical school, or a doctor who actually knew her stuff?

Circumstances alter cases. Not everyone lives near a keto-friendly doctor.

If you need life insurance, hacking your lipid numbers, while not entirely ethical, avoids bringing up an issue that might cause trouble later on. Also, if you are one of Dave’s lean-mass hyper-responders and can manipulate your lipid results like that, then what it actually shows is that when you eat according to the dietary guidelines, you officially have no cardiovascular risk. Which is what they are looking for. How you actually eat to minimise your cardiovascular risk is not truly relevant, in that sense, anyway.

One the other hand, fooling one’s doctor is not really a good idea, generally speaking. Far more honest either to refuse the prescription for a statin, or take it and simply never get it filled. And you can insist on a CIMT or CAC scan, and get a more realistic estimate of your condition, which might actually help to revise the doctor’s understanding. (Remember Dr. Berry’s line about how many patients it takes to convince a doctor!) It’s worth noting that Dave Feldman has a challenge to anyone who can produced a patient to show that elevated cholesterol is harmful in otherwise healthy people (he phrases it more precisely, but that’s the gist).

(Joey) #14

Interesting twist. Then from this perspective (i.e., two effects stemming from the same cause): what would be the cause of inflammation that also causes serum cholesterol to become smaller and denser (having begun circulation as larger and less dense)?

(Bacon is a many-splendoured thing) #15

Elevated serum insulin is one factor. Excessive carbohydrate intake would be another. Dave Feldman says that the primary job of LDL is to carry energy from adipocytes to the cells to supply their energy needs. What happens if elevated serum insulin is preventing fatty acids from leaving adipocytes?

In any case, I seem to remember that it is the age of the lipoproteins that is more relevant than their size (size being a factor of age, as they yield up their cargo of fatty acids), and the longer it takes for a lipoprotein to be scavenged, the more likely it is to become oxidised and cause damage. I believe that Dave Feldman explains all this on his Web site. The reason the triglyceride number goes up on a high-carb diet is that the triglycerides that excess glucose gets converted to are then packaged into chylomicrons, to be transported to adipocytes for storage.

If I got any of this wrong, please alert me, and I will edit this post.

(Joey) #16

Having deeply consumed Dave Feldman’s content at one point (and supporting his efforts financially), I no longer recall the more detailed mechanisms as you do. So I certainly won’t suggest you’ve got it wrong.

My simplified takeaway: sdLDL becomes smaller and denser (starting out its journey in a larger, less dense form) by picking up compounds in circulation that need to be removed in order to maintain (restore) healthier tissues. They are the solution, not the problem.

Perhaps it’s merely semantics but it seems odd to consider sdLDL as being “caused” by either elevated insulin and/or dietary carbs. Applying the “firemen to the rescue” analogy I don’t regard firemen as being caused by fires.

Then again, perhaps it’s just that classic distinction between causation and association - and in my struggle to comprehend, my metaphors and analogies only get me so far. :man_shrugging:

(Bacon is a many-splendoured thing) #17

Now, see, I’m glad I asked for correction, because I thought it was the HDL that picked up stuff, especially cholesterol, to take to the liver.

I did know that LDL begins life as VLDL (very low-density) and gets smaller and denser as it goes on, but I thought it was because it was giving up its cargo of fatty acids to cells to use for energy. Dave has a cute lecture in which he pictures LDL as boats and cholesterol as the life preservers. I forgot who the passengers were supposed to be.

(Joey) #18

Or perhaps I did! Now I need to go back to basics to make sure I’m not totally confused on which particles are which … on the metabolic Titanic. Will get back to you…

(Joey) #19

@PaulL I’d promised to return to the literature on this…

So, there are several studies noting the association between sdLDL and atherosclerosis & coronary heart disease. Whether it’s association or actual causation seems to be unclear (and “causation” is loosely addressed without further support).

However, there is strong evidence for the idea that circulating sdLDL picks up triglycerides … which is said to be the reason they become more dense and compact around this trig “cargo.”

With this in mind, it would seem to follow that elevated trigs - known to cause atherosclerosis and eventually lead to CHD - would be associated with higher serum levels of sdLDL inasmuch as picking up trigs is what makes for sdLDL to become more prominent in the lipid profile.

BTW, higher concentrations of sdLDL are associated with a “Pattern B” profile, so it all hangs together in that sense.

So how ought we regard sdLDL? Causation, associated symptom, body’s cure?

Well, that’s about as far as I got in rereading old studies based on a simple search. :thinking:

(Bacon is a many-splendoured thing) #20

A positive association is not proof of anything. After all, there is a positive association between reading comprehension and shoe size, and also a positive correlation between the divorce rate in the State of Maine and margarine consumption. Does that mean that learning to read makes our feet bigger? Or that getting divorced (if we live in Maine) causes us to eat margarine? (I suppose it might, if the judge awarded a high alimony payment . . . .)

On the other hand, a negative correlation, such as has been found between cholesterol and cardiovascular risk in several large, government-funded studies is definite proof of a lack of causality.

Now that is a study I’d like to read, since fatty acids are not particularly dense, and I’d expect the expansion of the LDL from taking on triglycerides to make it larger and less dense, instead of smaller and denser, as might be expected if the LDL started out carrying triglycerides and yielded them up to feed the body’s cells.

I don’t believe that this has actually been established. I can perfectly well believe that someone has observed an epidemiological correlation, but see a couple of paragraphs earlier.

This is indeed true, and it is why a high ratio of triglycerides to HDL is considered a marker of high cardiovascular risk. If we lower triglycerides by eating less carbohydrate and raise HDL by eating more saturated fat (as Dr. Phinney advises), it has the effect of changing our LDL profile to the healthy Pattern A.

I lean towards associated symptom, myself.