Best home lipid monitor - Recommendations?

Hey Everyone!

I would love to be able to monitor my own lipids at home. I live in the UK and testing can get £££ - especially when you want to make plenty of changes and monitor the results (testing every month or even every few weeks).

I am weighing up the options to see what is best based on reliability/accuracy/cost-efficiency/etc.

Here is one device I am considering, which gives a standard lipid panel:

Other alternative would be to get a device that measures total cholesterol (cheaper) and then just get ApoB tested every 6 months. My diet is stable to I don’t expect HDL to budge too much - so I suspect I can still monitor changes month to month through TC.

Anyone using one of these devices, have any advice or any alternatives? Thanks

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Would love to hear from anyone with experience of these too.

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Why would you want to do that? I think test every 6 months should be ok (maybe 3 if you are looking into whether changes you implemented are having any effect).

TC are mostly dependent on volume of carbohydrates in your diet both LDL and TC are also related to stress as stress mobilizes your body reserves and liver produces more of both… from what I know the most you can do with diet is to reduce carbohydrates and add fiber (eg. more vegetables, legumes etc.), decrease some dietary fat intake and increase protein in your diet. Of course you need to practice some sort of caloric restriction as these factors wont matter if you eat more than you need. Reducing stress and adding some sort of activity is what would help having lipids in your blood under control. Of course it would be different if you are genetically predisposed and you need to monitor lipids to see if the medication is working…

I would not want to monitor my lipids all the time. Especially TC as a random high carbohydrate intake (e.g. party, holidays…) could make them higher for few days… and if your diet is stable otherwise they should be stable as well.

ps. I read some reviews on the machine you mentioned and similar and they seem quite difficult to operate properly and readings are not really very accurate plus you must add the cost of testing strips… IDK how much would you pay for a lipid profile test out of pocket in UK, but I pay 8,5 EUR at the clinic if my doctor would not be willing to get one on insurance (I think I can do if previous test is within range only one additional in next 12 month period)


Last time I looked, Thriva was the cheapest option for lipids including APOB. I use them.
I have managed to get a free nhs lipid panel out of my gp on one occasion though there is no chance you will get APOB with that.

Hi - yes I am already working with NHS GP on lipid testing. I have got them ‘on my wavelength’ so to speak - but still fairly long breaks between tests.

I want to optimise my rapa intake based on lipid profile. Also want to calculate my ‘minimum effective dose’ of lifestyle/phara interventions - without it taking 5 years (like if I just had annual or once every 6 months).

The above monitor works out at £4 roughly per test - pretty great value. Of course, there is the upfront cost, but still a better investment in the long term if you test regularly.

On a side note, NHS do get non-HDL which is almost as good as ApoB - and definitely much better than LDL or TC - so this is one advantage of the NHS.

As much as I know lipid profile is just one of the measurements you want to monitor regarding cardiovascular health, IMPO inflammation (hs-CRP) gives you more of an idea what is happening in your body. Rapamycin generally reduces inflammation in body so raised lipids wouldn’t matter that much I guess (inflammation is crucial as the root of arteriosclerosis, not the lipids alone). I remember reading an animal study on that subject, can’t find it ATM but sounded pretty convincingly logical.

ps. found the study I mentioned above

No, lipoproteins and lipids is an independent risk factor, CRP is just a marker it seems like as there is no statistical significant effect on CAD in mendelian randomization. It’s like smoke from a fire. IL-6 causally increases risk for CAD though, but remember the importance of independent causal risk factors. Increasing or decreasing risk from one independent risk factor does not mitigate risk from the other, it’s still there. Only overall risk decreases, and I think apoB/LDL covers most of the causal risk space (explaining most of the risk).

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" . It is an acute-phase protein of hepatic origin that increases following interleukin-6 secretion by macrophages and T cells."

The correlation between CRP and IL-6 seems to be around 0.3-0.4.

“the acute phase protein C-reactive protein (CRP), whose production
in the liver is stimulated by IL-6.”

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Yes, I understand that. But here we are talking about rapamycin and raised lipids profile. Rapamycin decreases adiposity which might be associated with a rise in serum cholesterol (like when loosing bodyfat HDL migh decrease, and total cholesterol and HLD particle numbers might increase giving a temporary showing increased risk of cardiovascular disease). But at the same time rapamycin is reducing inflammation so it is possible that at the same time reduces also the inflammatory reaction in which inflammatory cells can infiltrate the arterial wall and interact with oxidized LDL cholesterol particles, leading to the formation of foam cells, which are beginning of atherosclerotic plaques. I am just guessing here as there are not many studies done on people taking rapamycin and CAD risks.

Thanks, I don’t know why I found that correlation, many other sources suggest they’re very correlated.
Right now I might say CRP is useful because it indirectly measures IL-6, like how LDL measures apoB. IL-6 blood tests seems practically impossible, while CRP is very easy to measure.

This is the study for my claim about IL-6, lower CRP via IL-6:

Since they are independent, whatever you do with other risk factors couldn’t influence the other.
Increasing apoB is bad regardless how much you decrease inflammation, since it is independent, that’s my point. I don’t think it’s possible to sum up a decrease in inflammation with an increase in apoB and figure out what the total risk is.

Although I understand and appreciate your perspective, I keep getting reminded how often we’re wrong when using mechanisms to guide our decisions, rather than outcomes. There’s a lot of things in vivo and ex vivo that does not pan out to help at all.

But lower IL-6 measured by CRP does decrease causal cardiovascular risk, diabetes, and other diseases.
While it might increase pneumonia risk.

So keep apoB low, keep CRP low (due to IL-6), seems good to me.
I’ll have to look into downside of low IL-6 / CRP on pneumonia more and if overall risk for pneumonia could be decreased in other ways (determined with outcomes).

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The problem is that if IL-6 causes the creation of CRP you would expect a time delay which is not going to necessarily cause an immediate correlatation.

This is a proposed mechanism that is not substantiated by enough data to drive decision making - based on my own personal risk/reward analysis.

  • based on my read of the available evidence - ApoB (as measured by using LDL as a proxy by the lipid panel monitor discussed in this post) is causal in ASCVD regardless of inflammatory status. Maybe inflammation is a catalyst, but still atherosclerosis can develop independently.

I prefer to ‘play it safe’ and keep lipids under control. I am not happy to walk around with dyslipidemia on a ‘wing and a prayer’ that rapa is attenuating all risk. I might be totally wrong and actually raised ApoB on rapa is no problem - but again, my risk analysis tells me to keep lipids well managed.

I personally would rather not take rapa and have normal lipids, than take rapa and have dyslipidemia.

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I use Thriva too as in the UK most primary care physicians (GPs we call them) inthe NHS know little about anything beyond LDL-C, HDL, TGs or tot-C.
Thriva do ApoA and B. All fine, even on Rapa.

Although it isnt Rapa-related I also had to beg my GP to do my Lp(a). Mine is 190 ie moderate risk. My dad had an MI at 59 so I see tge risk as way higher. In north America Im sure Id get a PCSK9i but the lipidologists here say I either have to be in the high risk group (200+) or have an is ischaemic event to qualify. To by PCSK9i’s would be about £400 a month.
So Im using niacin, red yeast rice, L-carnitine etc to try to modify it. Those studies suggesting statins increase Lp(a) are concerning but there is insufficient evidence as to the clinical significance.

I am all for playing safe. There seems some evidence on protective properties of rapamycin in ASCVD. I agree on ApoB but the way I understand and read literature (and I am in no way saying I am right and correct on this) is that ApoBs are capable of causing inflammation, so it is enough to have high enough levels of ApoB to start the process of plaque development (which is most evident in people who are genetically predisposed to abnormal high ApoB levels).
My serum lipids before rapamycin were perfect (my diet not so much) so of course any dyslipidemia will be a concern of mine too.

castro2004.pdf (261.4 KB)

One thing I like about the UK NHS GP is that they’re now using non-HDL as a marker. This measures the total of all atherogenic particles - basically a poor man’s ApoB. I am content with this metric.

I have found the nurse practitioner at my GP surgery to be great. Easier than ‘convincing’ the doctor and willing to work with me on mutually agreed approach to lipids re pharmacology. I also have clients who have the same experience.

I checked out Thriva - prices are not extreme actually. Still a big outlay compared to £40 for 10 lipid profile tests with the above monitor I have suggested.