Good for you! How many 70 year olds can say that?
High LDL cholesterol on carnivore?
LOL, I donāt know Robin, now all I want is a job because Iām getting bored to death being home too much. I can only do so much walking and gym workouts, I need more. Been looking for something remote, but thatās another topic
Tell your mom that you will go and get you ApoB level tested. This is now becoming the gold standard to address/predict atherosclerotic cardiovascular disease risk. While there is more to ASCVD risk than just lipoproteins, if you do not know your ApoB level, you are not fully taking advantage of the tools used to estimate you risk of cardiovascular and cerebrovascular disease. Know your risks and manage accordingly.
I will try and keep this relatively simple. There is LDL-C (commonly used to measure of cholesterol contained with in LDL) and LDL-P(the less commonly used measure of the number of LDL particles). When they are different it has been shown to be a better measure. But it gets tricky because you need to know which is the correct predictor. Apoliprotein B level - rather than LDL-C, non-HDL-C, or even LDL particle count (LDL-P)- is the best measure of potentially atherogenic lipoproteins.
Background can be found in the largest studies comparing subjects over time using āhardā outcomes, Framingham Offspring and the MESA cohorts.
Hi ffskier, Iāll look into that. Iāve been reading an interesting article, however, about a hypothesis posed regarding whether weāve misunderstood the role of cholesterol. The hypothesis was that cholesterol which is found in our cells as well as our blood, is more of a regulator then an indication of illness. And in healthy bodies, the cholesterol going up in response to what we eat, say, saturated fat, is a healthy and natural function rather than a marker of heart disease, as previously stated. Unfortunately the study was conducted in Norway, my birth place, and the article was in norwegian, so not sure how much good it would do to post the link. The hypothesis was that although saturated fat does raise LDL cholesterol it wasnāt necessarily a bad thing, and can even be seen as a healthy and natural function, the body regulating the levels, as needed. And there was an important question raised in the article whether we should reconsider how we think of cholesterol in general, how we call HDL the good cholesterol and LDL, the bad. This hypothesis was then brought forth into an american study which I will try to find, and will post a link to, if at all possible.
Iāve used a translator app in the past to read online. I canāt remember the exact app I used but I will let you know if I find one here in a minute. The article is something Iād love to read Denise
Edit: Ok, I think I used a Firefox addon so Iām sure other browsers will have those. Here are a few for PC:
ApoB is now the gold standard. If you have a family history, go get this checked asap. By taking the appropriate meds to lower your ApoB you are significantly lowering your cardiovascular risk. One of the biggest problems now in science is that there is not enough intellectual discourse. This was standard practice when a scientist would release his work, no so now. Its really bad now, because the internet allows for anybody to state what every they want and to cherry pick studies that backs up their points of view. But the study could be entirely false or very poorly designed or even have nothing to do with what the person is trying to sell you. Confirmation bias is everywhere especially when it comes to food. So I try, not always successful, to look at the larger or largest studies available as I have found them to be more accurate have no conflicts of interest or biases.
The āmanage accordinglyā part is where it gets interesting.
Iām not well-versed in ApoB to know whether studies involving drugs are reasonably expected to make a meaningful difference in outcomes. I would approach such studies very carefully and with a healthy dose of skepticism.
Of course, if there truly were a life-saving Rx for one particular deathly biomarker in isolation, well, then thank goodness for Big Pharma. But when it comes to solutions to the usual general metabolic maladies that afflict the masses, I have become convinced that proper food and exercise remain the proper medicine in 99% of the cases.
There. Thatās my personal bias⦠earned through lots of reading and personal experience with friends/family.
Well, in these appropriate meds, there is an indication though of conflict of interest. As dizzying wealth, is produced off making cholesterol meds, heart meds, etc. And so, if thatās an objective in these, non-bias studies, I wouldnāt be so inclined to think of them as wholly free of either bias or this conflict of interest. That said, my mind is open to looking into further studies, and looking at cholesterol from different view-points, as it is such an incredibly complex topic. I donāt say I hold the answers or confirmation bias is not an issue regarding a lot of these studies, but I would think twice of the lack of interest of conflict, of a study promoting both a particular medical test as well as suitable medication.
Hi Denise, Iām only on my phone at the moment, and donāt know how to post the link, but as soon as I have access to a computer again, I will. I think youād find the article interesting if you were able to translate it.
I so agree with you, weāve been led to believe for every disfunction and irregularity we experience within our bodies we should run to Big Pharma. When a healthy lifestyle, a healthy WOE combined with exercise could achieve a better, healthier outcome than any prescribed meds, and of course, better quality of life. Iām not saying thatās so in every case, but there is far too much emphasis on prescribing preventative meds currently than doctors encouraging people to achieve the same through a change of WOE/lifestyle. It doesnāt even seem to be factored into the various diagnoses and subsequent treatment plans reccommended.
They are available in various sources on PubMed. The reason the ratio is different between mmol/L and mg/dL, is that the conversion factors from masses to moles are different. For instance 1 mmol/L of total cholesterol, LDL, or HDL = 38.6698 mg/dl, whereas 1 mmol/L of triglycerides = 88.5740 mg/dL. Doing the arithmetic shows that a ratio of 0.9 in mmol/L is equivalent to 2.0 in mg/dL.
(Remember that a mole is a specific number of molecules, but the mass of a mole depends on the molecular mass of said molecule. This means that a mole of hydrogen will weigh less than a mole of oxygen, and a kilo of hydrogen will contain more molecules than a kilo of oxygen.)
Hi Denise, here is the link to the norwegian article about a new hypothesis regarding the role of cholesterol. If you can manage to translate it, I think youāll find it interesting. https://forskning.no/hjertet-mat-og-helse/ny-norsk-modell-kan-forklare-kolesterol-mysterium/1806166
Iām not saying this hypothesis is right or wrong, but I certainly found it food for thought. There needs to be more research into this. It was my mom who shared this link with me, even after voicing all her concerns regarding the carnivore WOE, as I had sent her studies to make her rethink the danger she thought it posed, in raising cholesterol. Which led her to do a bit of her own research, and sheās now reading up on it a bit more.
More power in a study is always a good thing, but we also need to look at both the hazard ratio and the clinical significance of the study, as well. Bradford-Hill thought that unless the hazard ratio was at least 2.0, there was no point in worrying about it. It is also possible for a result to be statistically significant but clinically unimpressive.
For example, one study showed a clearly significant life-extension benefit of taking a particular statin, but the benefit was around four or five days. Most people would not consider that worthwhile, especially given the risk of undesirable side effects. Likewise, if the number needed to treat is very large in order to produce a benefit, that also says the treatment may not be worthwhile.
Ok, thanks so much! I am always looking for more info on the high cholesterol just to get peace of mind over it. I do have good ratios on my Trigs/hdl. I mean theyāve improved since starting keto 2 years ago.
And here is the same article Denise, written in english https://sciencenorway.no/cholesterol-fat-heart-attacks/new-model-could-explain-old-cholesterol-mystery/1810159
The woman behind this new hypothesis is Marit Kolby Zinƶcker. If you want to research her, and find out more regarding her hypothesis about the role of cholesterol, you can probably google her name and find additional info.
Hi Denise, I accidentally replied to myself instead of you so I am posting the link I found again to the same article written in english https://sciencenorway.no/cholesterol-fat-heart-attacks/new-model-could-explain-old-cholesterol-mystery/1810159 The womanās name is Marit Kolby Zinƶcker, I googled her name just now and several more articles came up, but this is the same article I read in norwegian. And now Iām off to bed, hopefully soon to the land of sleep.
If I understand the hazard ratio correctly, Iāll try to illustrateā¦
If thereās a 1% chance of something happening, and the odds increase to 2%, then the āhazardā has doubled. 2:1.
Looked at differently, the risk of that thing NOT happening declined from 99% (100% minus 1%) down to 98% (100% - 2%). From this perspective, the odds of having avoided the risk remain virtually unchanged.
Is that significant enough? Well, āenoughā depends on the stakes and consequences. The lower the stakes and the less onerous the consequences, the less Iād be worried about a remote risk (1% or 2% is still pretty remote).
And 98% to 99% are pretty good odds of dodging the proverbial bullet. Not likely worth a major change in policy, medication, lifestyle, ā¦
Sorry, I wrote āhazard ratio,ā when I meant effect size. Apologies. Relative risk was not what I was talking about.