Karin, great write up on blood testing. Do you have a preferred lab? I've normally used Life Extension every two years, but I have to check if they do all of these tests....Doug Williams
Doug, my insurance doesn't cover many of the advanced tests because I don't have a "diagnosis". Like Karin, I also use Anylabtestnow but also compare prices with ultalabtests and walkinlab as well as labcorp and Quest. I go with whoever has the best sale.
Great summary! The omega3 index is not in the same framework and we used it to screen for an omega3 dietary pattern marker and not a supplement guide. Our cut off is 6.
I agree that mainstream science does not focus enough on APOE4, and instead focuses too much on amyloid and tau. Amyloid and tau are clearly downstream products that seem to be the result of the disease rather than the cause. However, I also think focusing exclusively on APOE would also be a mistake, because Dr Bedesen has compelling evidence "Alzheimer's" is not even truly a disease. Instead, it is better described as a syndrome with several subtypes that are actually completely different diseases. There are three main subtypes though in his theory, as well as several less common ones, and the most common "subtypes" of his are an inflammatory subtype caused by bacterial or viral infection, a cold or atrophic subtype caused by nutritional deficiency, and a toxic subtype caused by toxin exposure, which can include heavy metals and fungal mycotoxins. If you are not familiar with Bedesen, you should look into him. I predict that as long as scientists think of Alzheimer's as a disease instead of a syndrome, they will never find out what causes it.
You might resonate with researcher Juan Fortea's view that ApoE4 confers it's own set of risk factors for pathology that makes the argument that in AD, ApoE4 genotype should be recognized as a specific form...new nomenclature needed...and that even having ApoE4 could be better recognized medically as a prodromal condition.
Great post! I recently convinced my cardiologist to order me an ApoB test. Can't wait to get it done. Your post will surely be helpful for fellow E4 carriers seeking to go beyond a basic lipid panel...
Hi Karin , very impressive and I will up my lab work. From an earlier article of yours and elsewhere, I understand you have experience with 2HP B Cyclodextrin. The idea if I ‘m remembering correctly is that it appears in eg Niemann Pick where currently used generally to reduce the useless and harmful buildup of non lipid particles in astrocytes that gum up the axonal transport and create inflamation and create hyponutrition . I’m wondering re your thoughts on any way to infer this action is happening from lipid or other tests but also did you notice any changes with use? I’m considering this and also wondering as cavadex has so little info on their site and how to compare that with atherocare product? Are many people using this here? The underlying science looks solid and toxicity low, eg see cyclotherapeutics although they unnecessarily it appears seem to prefer an iv preparation . Any thoughts, how would this fit into an overall set of measures? Best wishes and thanks again for your writing.
Karin, this is a carefully reasoned framework and the APOE4-as-lipid-trafficking-vulnerability framing is, I think, the most mechanistically honest way to orient prevention strategy.
One question worth putting to the panel: is the Omega-3 Index correctly positioned as the seventh marker, or does the evidence support treating it as upstream of several of the markers you've listed above it?
The basis for the question is this. The markers you weight most heavily (VLDL, remnant lipoproteins, triglycerides) are measures of how much stress the lipid system is currently under. The Omega-3 Index is at least partly a measure of how well the system can handle that stress. Membrane DHA status influences receptor fluidity and recycling efficiency, including LDL receptor activity. A membrane depleted of DHA is less able to cycle receptors competently, which feeds directly back into the clearance burden you identify as the core APOE4 vulnerability. If that mechanism holds, two people with identical lipoprotein profiles may not be in the same position if their membrane substrate differs materially.
Which leads to the second question, and the one I'm most curious about. You don't mention the AA:EPA ratio. For someone tracking the Index seriously and aiming for 9%+, the ratio feels like the natural complement. It speaks not just to how much EPA and DHA is incorporated into the membrane, but to what the membrane is actually doing with it. A membrane can be omega-3 replete and still be primed toward inflammatory signalling if AA accumulation is high, driven by exactly the insulin and glycaemic dynamics you list elsewhere in your targets.
I ask partly because the ratio is absent from a lot of otherwise sophisticated lipid frameworks, and partly because someone managing this as carefully as you are almost certainly has a view on it. I'd be genuinely interested in how you're thinking about it.
I placed the Omega-3 index a bit lower simply because I still see the main drivers (triglycerides, remnants, ApoB) needing to be addressed first. But your point is well taken two people with similar lipid numbers may not be in the same place if their membrane composition is very different. On the AA:EPA ratio, I do track it, but I haven’t included it in my core list, probably because I think of it more as context than a primary signal. But I agree, it adds an important layer, especially when trying to understand inflammatory tone alongside lipid patterns. I really appreciate the depth of your comment to help further clarify an important topic.
I'm well impressed with your protocol. Well done indeed. I can't see much room for improvement on that.
Karin, great write up on blood testing. Do you have a preferred lab? I've normally used Life Extension every two years, but I have to check if they do all of these tests....Doug Williams
Doug, my insurance doesn't cover many of the advanced tests because I don't have a "diagnosis". Like Karin, I also use Anylabtestnow but also compare prices with ultalabtests and walkinlab as well as labcorp and Quest. I go with whoever has the best sale.
I either get everything from my PCP or get the Spectracell lipid test through my local "AnyLabTestNow". Costs about $300.
Great summary! The omega3 index is not in the same framework and we used it to screen for an omega3 dietary pattern marker and not a supplement guide. Our cut off is 6.
I agree that mainstream science does not focus enough on APOE4, and instead focuses too much on amyloid and tau. Amyloid and tau are clearly downstream products that seem to be the result of the disease rather than the cause. However, I also think focusing exclusively on APOE would also be a mistake, because Dr Bedesen has compelling evidence "Alzheimer's" is not even truly a disease. Instead, it is better described as a syndrome with several subtypes that are actually completely different diseases. There are three main subtypes though in his theory, as well as several less common ones, and the most common "subtypes" of his are an inflammatory subtype caused by bacterial or viral infection, a cold or atrophic subtype caused by nutritional deficiency, and a toxic subtype caused by toxin exposure, which can include heavy metals and fungal mycotoxins. If you are not familiar with Bedesen, you should look into him. I predict that as long as scientists think of Alzheimer's as a disease instead of a syndrome, they will never find out what causes it.
You might resonate with researcher Juan Fortea's view that ApoE4 confers it's own set of risk factors for pathology that makes the argument that in AD, ApoE4 genotype should be recognized as a specific form...new nomenclature needed...and that even having ApoE4 could be better recognized medically as a prodromal condition.
Great post! I recently convinced my cardiologist to order me an ApoB test. Can't wait to get it done. Your post will surely be helpful for fellow E4 carriers seeking to go beyond a basic lipid panel...
Non should be ‘ non useful’- note typo
Hi Karin , very impressive and I will up my lab work. From an earlier article of yours and elsewhere, I understand you have experience with 2HP B Cyclodextrin. The idea if I ‘m remembering correctly is that it appears in eg Niemann Pick where currently used generally to reduce the useless and harmful buildup of non lipid particles in astrocytes that gum up the axonal transport and create inflamation and create hyponutrition . I’m wondering re your thoughts on any way to infer this action is happening from lipid or other tests but also did you notice any changes with use? I’m considering this and also wondering as cavadex has so little info on their site and how to compare that with atherocare product? Are many people using this here? The underlying science looks solid and toxicity low, eg see cyclotherapeutics although they unnecessarily it appears seem to prefer an iv preparation . Any thoughts, how would this fit into an overall set of measures? Best wishes and thanks again for your writing.
Karin, this is a carefully reasoned framework and the APOE4-as-lipid-trafficking-vulnerability framing is, I think, the most mechanistically honest way to orient prevention strategy.
One question worth putting to the panel: is the Omega-3 Index correctly positioned as the seventh marker, or does the evidence support treating it as upstream of several of the markers you've listed above it?
The basis for the question is this. The markers you weight most heavily (VLDL, remnant lipoproteins, triglycerides) are measures of how much stress the lipid system is currently under. The Omega-3 Index is at least partly a measure of how well the system can handle that stress. Membrane DHA status influences receptor fluidity and recycling efficiency, including LDL receptor activity. A membrane depleted of DHA is less able to cycle receptors competently, which feeds directly back into the clearance burden you identify as the core APOE4 vulnerability. If that mechanism holds, two people with identical lipoprotein profiles may not be in the same position if their membrane substrate differs materially.
Which leads to the second question, and the one I'm most curious about. You don't mention the AA:EPA ratio. For someone tracking the Index seriously and aiming for 9%+, the ratio feels like the natural complement. It speaks not just to how much EPA and DHA is incorporated into the membrane, but to what the membrane is actually doing with it. A membrane can be omega-3 replete and still be primed toward inflammatory signalling if AA accumulation is high, driven by exactly the insulin and glycaemic dynamics you list elsewhere in your targets.
I ask partly because the ratio is absent from a lot of otherwise sophisticated lipid frameworks, and partly because someone managing this as carefully as you are almost certainly has a view on it. I'd be genuinely interested in how you're thinking about it.
I placed the Omega-3 index a bit lower simply because I still see the main drivers (triglycerides, remnants, ApoB) needing to be addressed first. But your point is well taken two people with similar lipid numbers may not be in the same place if their membrane composition is very different. On the AA:EPA ratio, I do track it, but I haven’t included it in my core list, probably because I think of it more as context than a primary signal. But I agree, it adds an important layer, especially when trying to understand inflammatory tone alongside lipid patterns. I really appreciate the depth of your comment to help further clarify an important topic.
Thank you Karin!