I just published this, and felt it might be useful here. It covers a lot of topics, but that may be why people could find it useful. Happy to discuss here.
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The myth about exercise really explained so many variables for my situation. I have greater understanding of why sometimes I go high after exercise, then low the next time.
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I just read the posted article on MACE mentioned lower LDL and Cholesterol…LDL is important from what Ive read, and heard, and pushing LDL lowering a fix to the problem perhaps we are reducing LDL…but maybe we are treating symptom without better understanding if the problem. I do NOT want to take a statin, for this any other reasons. I still do take it… but it is VERY low dose 2.5 mg every other day. I frankly do not want to take ANYTHING…but some things may have been helpful ( doses of lisinopril and the proven kidney benefit is one example)
I know we’ve been approaching the cholesterol as a problem… I happen to disagree with this perspective, but I’m also not a fool so I take some statins.
Am I just off my rocker here and being stubborn for no reason? Perhaps… I really don’t want anyone to take this as a criticism …it just I’m trying to be honest as express an opinion.
Please set me straight if needed.
Given your comment here, it seems you’re both apprehensive to taking more, while also open to be put at ease about them. I’m not sure what you’re looking for to move you off the fence, if that’s what you’re looking for. Given the decades of medical literature on showing their benefits and minimal risk, I am not sure anyone is going to tell you anything that you’re not already aware of. I’m certainly open to hearing your concerns, so go ahead and open up.
But the good news is that PCSK9 inhibitors are extremely effective and can also lower other lipid levels that statins don’t – namely Lp(a).
Two drugs are on the market – Repatha or Praluent – both of which are injections you self-administer every other week. Given that you’re a T1D, an injection isn’t likely to deter you. 
you are quite correct my Endo wants me to take more to make sure my numbers stay under 200. I’m rather lucky as I do not have any history of heart ailments in the family, or diabetes for that matter ( I’m the family genealogist and have looked at 5 generations)
My understanding stems from 15-20 multi hour podcasts that I’ve listened to surrounding LDL, and that LDL perhaps should not be made out to be the bad guy..rather an indicator. As an engineer for 40 years I’m looking for root cause, to tackle that issue if possible
Below are some of the sources I could remember
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Dr. Nadir Ali – Oxidized LDL as an “injured firefighter”
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“Is High LDL Really a Firefighter?” from the PrevMed (Ford Brewer, MD)
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Dr. Aseem Malhotra: Short video “The Cholesterol Myth: Firefighter, Not the Culprit!”
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“The Truth About Cholesterol, With Jonny Bowden”
All four sort of follow the idea that inflammation is the driver..and that the increase in LDL is a result of the body trying to protect itself…
I am EXTREMELY skeptical about online sources but I’ve listened to roughly 70-80 hours all roughly following that idea..is is a lot of data to sift through, but mainly the idea is that the higher LDL is a symptom.
thank you for encouraging me to reply
I do not currently NEED any other other medications based on 36 years of my own medical data, at least that I am aware of.
You are also correct about that minimal risk is why I take the dosing I do!
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I’m not sure where this “firefighter” analogy is coming from among the sources you listed. But I suspect the root of the misunderstanding is what LDL does.
You said, “All four sort of follow the idea that inflammation is the driver..and that the increase in LDL is a result of the body trying to protect itself…”
I suspect the idea is that LDL is the “firefighter” in this scenario.
But that’s entirely inverted. LDL is the cause of inflammation, and “inflammation” is the body’s response to protect itself.
Let’s start with basics:
Lipoproteins are carriers. Certain types of nutrients the body needs are “hydrophobic”, which means they repel water–they can’t travel through the bloodstream to reach cells because blood is mostly water. Lipids – also called “fatty acids” – are hydrophilic, which means they like water. So, they become perfect carriers for those nutrients.
Your liver makes these lipoproteins, package the nutrients inside, and off they go: traveling through the blood and delivering their cargo. When they’re done, the lipoproteins normally get reabsorbed back into the liver. This reabsorption process requires “receptors” that will bind to the lipoproteins and carry them away.
Many people have genetic mutations where they don’t make those receptors – or enough of them – so the lipoproteins remain in the blood. Many low-density lipoproteins (LDL) will attach themselves to artery walls. And the body reacts by creating antibodies that try to get rid of them. That process is called “inflammation”.
When you cut your finger and you get a scar, that’s your body having reacted to the abrasion, sent in antibodies to kill off the molecules that don’t belong, and then rebuild the destroyed tissue. That results in a scar.
Inside your arteries, the inflammation is trying to “cure” the damage done to artery walls that the LDL caused by sticking to them. The rebuilding of the damaged tissue results in a “scar” like formation called PLAQUE. And that’s the stuff that builds up over time, and when there’s enough of it, some of the loose plaque can break off, circulate to a narrow channel, and then you have a heart attack or stroke.
Statins make the liver “hungrier” for cholesterol, and the liver responds by putting more LDL receptors on its surface, pulling more LDL out of the blood.
By clearing out these LDL particles, the body is no longer in a persistent inflammatory state, which has been shown to improve many other metabolic functions.
The only real negative effects are extremely rare. Muscle aches/cramps are commonly reported, but true statin-caused muscle injury is uncommon—about 5% of people who take it actually have genuine symptoms. Most people who feel muscle symptoms can often tolerate a different statin, a lower dose, or alternate-day dosing.
As for your levels, it’s true that it’s a genetic condition, but it’s sort of irrelevant. If your LDLs are elevated, you treat it. The cost is negligible, and the efficacy is so good, that it’s just a simple, easy way to reduce risk.
As the article points out, it’s not about your total cholesterol levels–those don’t really matter. It’s just your LDL, as those are the ones that damage your arteries.
Let me know if this helps.
I have never heard of alternate day dosing and this raises a question to ask my endo. I have been unable to tolerate any of the statins due to extreme muscle pain, even on the lowest dose available.
Keep in mind that Endos are not the primary doctor for lipid management. Cardiologists are, but their problem is not fully understanding T1D. That is, the risk profile is far higher (for reasons discussed in my article), and cardiologists don’t know that LDL levels should be targeted far lower than the non-diabetic population. So, while the endo will be great for knowing THAT you need to lower LDL levels this low, the HOW process is better managed by a cardiologist who talks to your endo.
But this all may be more work than necessary.
For those who truly cannot tolerate statins, PCSK9 inhibitors are great, if not better, actually. The problem is, they don’t come in generic form yet, so they’re expensive, and insurance won’t cover it unless the statin route has shown either ineffective or intolerable. Given your experience, you could just have your endo write the script for Repatha (insurance likes it better than Praluent) and can write the pre-authorization about your statin intolerance.
Your explanation is very detailed and highly informational. thanks VERY much for the explanation and the basics behind it I really do appreciate the information! I’ll have to add that to my understanding! thanks very very much!