When I bring up Apoe4 I generally get blank stares. I am APOE4. My mother had Parkinson’s and her maternal twin had Alzheimer’s. Thank you for this forum. I drank the keto koolaid five years ago and lost 60lbs, am moderately active and still a little overweight, but feel great. I had been successfully dodging the statin push but had a TIA event last week that took me to the hospital for full stroke protocol. Morning of event…
Total Chol: 197
HDL: 71
LDL: 112
TriG: 68
Glucose: 101
A1C: 6.5
My CAC score from two years ago was 0
They promptly put me on Plavix, Lipitor and Losartan (bp med) and did a CT scan, MRI, full bloodwork, carotid artery scan and echocardiogram. The C/A scan was clean and I confess to not understanding much on the ECHO report, except there were no red flags. My question is how to talk to doctors esp. regarding the statin/apoe4 debate. I have a series of followups next week. Any suggestions for additional tests? Info?
ApoE-4 and temporary ischaemic attack
Apo E4 Heterozygous (Male) and Keto
Well, your ratio of triglycerides to HDL is less than 1.0, which together with the CAC score of 0 and the carotid artery scan and the echocardiogram all indicate that your cardiovascular risk is supposed to be minimal. But there is that TIA to contend with, and your HbA1C is quite high, even though your fasting glucose is low, so something is obviously going on.
Under normal circumstances, a CAC score of 0 means that a statin is contra-indicated. Your cholesterol numbers indicate the same thing. I’m afraid that I don’t know enough about ApoE-4 to suggest any approach to your doctor.
My only question about the TIA would be what the location of the clot was. Have they any idea? Could the symptoms possibly have some other cause?
@keeting Welcome to the forum! I wish it were on a more uplifting topic.
I had the same initial reaction as @PaulL above … My understanding is that TIA symptoms are a lot like symptoms of many other underlying conditions (or simply a fleeting confluence of sensations). Are you saying that all of the tests indicate that you are NOT exhibiting any stroke-related conditions? Or are you saying that the suspected TIA event was confirmed as such?
My symptoms were very specific and related to the speech/language center. Imagine trying to say “we need to order some…” and it coming out as “……gug…uym” for 5 minutes. From what I can gather, most small blockages resolve in 10 minutes to 24 hours and leave no trace, as was my case. The diagnosis was based solely on my description of the event, and the standard of care seems to be to look at heart/arteries first. Btw, there’s a great resource called Apoe4.Info
Scary! So glad you’re okay… So, at the end of the day, they weren’t able to identify anything that pointed at it truly being a TIA other than your description?
Thank you for clarifying. Indeed, a very scary experience.
Not being a medical professional, my grasp is likely limited, but I was under the impression that a TIA results from a temporary blockage … i.e., movement of a micro-clot. As such, I would not think a stationary calcified plaque on an artery would produce the symptoms you’ve experienced.
On the contrary, it would be micro “soft” plaque that becomes dislodged and circulates. If I understand correctly, these are the result of inflammation (somewhere) in the circulatory system. But likely systemic in nature.
Inflammation is a classic response to carbohydrate eating (especially plants, many of which contain phytotoxins). Ferreting out any/all sources of inflammation would likely be the best path forward.
A CAC score tells you about calcified plaques - which are actually stabilized (= scab ) by the calcium deposit. Sure, too much calcification will begin to narrow the passage, but (1) that’s far less likely to “throw a clot” than soft plaque which has not been calcified and (2) it’s less life threatening given today’s interventions to address a slowly closing arterial blockage due to slow-but-steady calcification.
Okay, I’ll stop practicing without a license. But that’s my “internet worthy” take on what you’ve described, given your lipid profile, etc.
Best wishes!
A few things worth considering. With an A1C of 6.5 @keeting , your diabetes risk ratio for CVD is 10.4. That is compared to one, such that as a percentage it would be a risk of 940% over baseline https://jamanetwork.com/journals/jamacardiology/article-abstract/2775559 . The risk ratio for CVD from metabolic syndrome is also high at 6.09 (for women relative risk of 509 %). Meanwhile you are all worked up over high LDL which in itself has a risk ratio of 1.3, or 30% above baseline…the MINIMUM amount of risk to even be considered a statistically relevant value. Worrying about 30% instead of the 940% risk from diabetes is, at least to me, counter-intuitive.
While I am more on the side of LDL-C is meaningless and maybe apoB as well, I appreciate @ffskier providing the standard viewpoint which is not supported by most in these forums. I am making a list of all valuable publications on CVD currently, so in this regard @ffskier, which is your BEST publication that supports the standard viewpoint that you espouse? Just want to make sure I do not miss anything worthwhile.
I would caution not to be too overly alarmist … sure, diabetes is extremely unhealthy. But an A1c of 6.5% is at the lower end of where a diabetes diagnosis typically begins. And those identified as T2 diabetics often present with markedly higher glucose levels. And that’s where the study is a bit opaque…
I couldn’t find anywhere in the study where the average or range of HbA1c results of those “diabetic” subjects were provided. That subgroup could have had significantly higher HbA1c levels (than 6.5%) for many years … leading to a range of metabolic issues, perhaps including CHD of some type as tracked as an outcome endpoint in the study.
But even more importantly, this same study explicitly states: "Compared with the LPIR score, the hemoglobin A1c level was weakly associated with incident CHD."
Between these two considerations (plus favorable HDL/Trig ratio), I’d try to be less alarming about the risks of this individual currently faces - although I fully agree that the glucose levels are more concerning than LDL.
To be clear, I’m not suggesting an HbA1c of 6.5% isn’t cause for corrective lifestyle changes. But to lump the CHD risks faced by this person with those of all of the diabetics - when the study itself discounts an A1c & CHD association - might be raising more anxiety than is warranted given the facts as presented.
These posts were moved from the other ApoE-4 thread at the suggestion of a member.
A fair response, but I was just quoting the numbers to point out, that regardless of the level of diabetes risk at A1C 6.5, it will by necessity (if you also consider that it must be part of metabolic syndrome), much higher than the risk from LDL. Or at least that is the claim in the paper, and I am confident that it is a much more reasonable perspective than ldl as a main focal point. Having said that, it is odd that the A1C risk ratio is so low if lp-ir and diabetes are so high. I wonder how that works.
Someone can correct me if I’m wrong, but if I recall from listening to a “2 Keto Dudes” podcast, @richard chose to stay on metformin because even though he had been eating low carb/keto for many years, he still couldn’t keep his A1C in the normal range without the help of medication.
So, even though you have been keto for 5 years and your cholesterol and triglycerides look great, there may still be something going on with your blood sugar and insulin resistance? Maybe getting that A1C all the way into the normal range (with some help from medication) is the final piece to your puzzle? (Also, not a doctor 
)
I think we’re in full agreement. Perhaps it was more about tone.
I was trying to lower the angst that may have been created. It’s clearly worth resolving an elevated A1c. But the looming high risk of CVD seemed overdrawn given his eating pattern, favorable lipids, and statement about weak association between A1c and CVD within the cited study itself.
Regardless, we’re also on the same page re: LDL … worrying about that given his context is getting distracted by the wrong ball.
Don’t forget about the limitations of HbA1C, either. As Bikman points out, a healthy person’s erythrocytes (red blood corpuscles) can live longer than the assumed 90 days, which means that the reading is going to be artificially elevated, because they will be picking up extra glycation during their longer life spans. And conversely, a sick person’s erythrocytes might not be living for the full 90 days, thus giving an artificially low reading. Also, I understand that variations in how well-hydrated a patient is at the time of the blood draw can also affect the reading.
Excellent points.
Our family internist is a believer in the “longer-lived” red blood cell idea - which, as you note, pick up more glycation as a result of being around longer in the bloodstream - hence elevating reported HbA1c by the lab. So we have an easier time with such wellness visits.
Still worth keeping close track of carbs/sugars in the diet. But a fasting serum glucose of “just over 100” for a fat-burner isn’t unusual at all. It’s often the mark of a stable glucose level with minimal excursions.
I’d suggest he get a home blood glucose meter for a few bucks at the drug store or grocery and measure every 30 minutes for about 2-3 hours after a typical meal and see how much it changes. I believe that’s what separates the “healthy” gluconeogenesis-derived serum glucose from the S.A.D. insulin-resistance-producing glucose spikes.
Found this video and thought I would share. Nadir is a cardiologist who tackles apoE4 in this video https://m.youtube.com/watch?v=A78RxVZnXgI