My sharply rising CAC score - and why I'm staying the keto course 🖖

[SomeGuy]

Other markers of inflammation are white blood cell count (WBC), ferritin, erythrocyte sedimentation rate (ESR), and plasma viscosity (PV). All these readings should be taken into account.

Thanks for citing additional markers. I’m not familiar with all of these, but my latest CBC and CMPanels looked pretty good across the board (WBC, RBC, hemoglobin, hematocrit, all within range)

More relevant to potential inflammation: neutrophils, lymphs. monocytes, EOS, baso, all remain nicely within range: i.e., mid- to lower-end of the spectrum provided. Immature granulocytes = 0. When our internist looked at the bloodwork a few months ago she said it all looked great.

For about 18 months, I was taking regular KetoMojo readings for BHB and morning glucose. Even with dawn effect, I was typically sitting around 90 on glucose (with BHB settling in several months into keto at about +/-1.0). Never been diabetic and cutting out the carbs wasn’t particularly traumatic. Never even had the keto flu.

So either I’m incredibly healthy these days and am finally curing years of silent hidden soft plaque accumulation, or I’m missing something big here.

If it weren’t for those darn rising CAC scores, I’d be clickin’ my heels about how delightfully well everything is going.

The thing that gives me greatest comfort is that - if I had heart issues despite not having clinical symptoms - then the solution would be to cut out the carbs, eat TMAD, take K2/D3, sleep well, lower stress, etc. Yup, that’s been my lifestyle for 2 years

Keto on

[FrankoBear]

Do you have a heart arrhythmia? - harking back to the cardiologist

Do you get palpitations?

A young family member who was to be a college scholarship swimmer was diagnosed with a heart enlargement and subclinical arrhythmia and bradycardia (slow heart rate) with compensatory atrial fibrillation. The symptoms were subclinical, so he as unaware. It can lead to anatomical changes.

I disagree on Ivor. But I think he will have further nuance on stabilising the calcium score from his interviews. It may be something in the Vitamin K2 dosing - how much, what with etc.

[SomeGuy]

Do you have a heart arrhythmia? - harking back to the cardiologist

Do you get palpitations?

Good questions.

Nope, heart rhythm is steady/solid - slow resting pulse, typically 62-72 bpm. Un-medicated blood pressure: typically around 115/70.

Other than an adrenaline rush, I haven’t had a palpitation since before stepping up to give presentations to hundreds of shareholders. Happily, I haven’t been subjected to that angst in years.

K2 dosing is a very interesting issue. Cannot find reliable science on this anywhere on appropriate dosing - notwithstanding the parade of strong opinions out there.

As you likely know, D3 and K2 interact, so upping one might entail upping the other … or not. Again, opinions vary and convincing science seems to be lacking for reliable thresholds.So I’m loathe to tamper with what I’m already doing (see below)

Thanks again for the thoughtful line of questioning.

Noted above, I’m currently taking:
DAILY SUPPLEMENTS:
K2/MK4: 500 mcg
K2/MK7: 100 mcg
D3: 125 mcg (5000IU)
Fish oil: 1400 mg (330 mg Omega3)
Magnesium citrate (=500 mg of magnesium) mixed in my daily sea-salted water

[SomeGuy]

UPDATE: My wife and I both had CRP-highly sensitive (cardiac) inflammation bloodwork tests performed this week. … drum-roll…

Both of our CRP-hs serum levels are well below the <1 mg/L mark (i.e., they are well below average risk of future cardiovascular event). This would seem to suggest that - notwithstanding our recently rising CAC calcification scores - there is no evidence of active cardiac inflammation at this time.

This would seem to support the hypothesis (or bald-faced hope?) that the increasing calcification we’re both experiencing is evidence of the “healing” of previous soft plaque into stabilized hard, calcified plaque.

More wishful thinking?

[ctviggen]

That’s great news!

It’s hard to know what parameters to use. HS-CRP is one, and Ivor Cummins was all over ferritin (though, like you, I no longer know about his info).

The problem with all of these inflammatory markers, is that they are transitory. Go run 6 miles, and you’ll get a very high one. So, it’s best to take them while you haven’t done much. There are my CRP values over 7+ years:

The yellow was fasting 4.5 days, so you see what that does to you (highest value I got). The 1.2 after 1.7 is three days of eating high (saturated) fat, high calorie (Dave Feldman’s protocol).

It seems like a reasonable course just to hang out and see what happens. By all other markers, you seem to be in excellent health.

Another thing about these markers (including CAC): if you get it just once, you’ve gotten it once. You wonder what they mean. I got testosterone and c-peptide taken…once each. I had no idea what to do with those values, since there were within the “acceptable” range.

[SomeGuy]

Another thing about these markers (including CAC): if you get it just once, you’ve gotten it once. You wonder what they mean. I got testosterone and c-peptide taken…once each. I had no idea what to do with those values, since there were within the “acceptable” range.

Great to see how your results (over 7+ years) have remained at or below the bottom end of the risk spectrum. Most encouraging to know that what you’re doing is keeping cardiac inflammation well at bay.

As for once-and-your-done testing, as we wander down the rabbit hole in the wake of our “his & hers” rising CAC scores, we’re thinking about getting ApoE genetic testing done … although I’m not entirely sure quite why. We come from entirely different genetic stock, and are already eating the stuff that folks with ApoE-4 ought to be eating, so I’m beginning to wonder: why bother getting it (yeah, even once )

[ctviggen]

I can’t advise you there, as I would like to get the same test done…even though I don’t know what I’d do with that info. (For instance, I have ridiculously high Lp(a), but getting a test to confirm I have genetics that causes me to have high Lp(a)…how does that help?)

A lot of these markers, I didn’t know existed 7+ years ago. I didn’t even know to get HbA1c and fasting insulin done. Often, I paid for my own blood tests, and I bought “packages” for a while. These included things like Lp(a) and HS-CRP, and for a while, I didn’t know what they were. When I finally started entering everything into a spread sheet, and figured out what was (potentially) important, I had to go back and get this info.

For ApoE4, I’m not familiar enough with it, other than some people have high LDL and will adjust what they eat to try to lower their LDL. I’m not sure that does any good, though. (If you eat a higher PUFA diet to lower your LDL, is that a good thing? I don’t think so, but I could be wrong.)

[SomeGuy]

For ApoE4, I’m not familiar enough with it, other than some people have high LDL and will adjust what they eat to try to lower their LDL. I’m not sure that does any good, though. (If you eat a higher PUFA diet to lower your LDL, is that a good thing? I don’t think so, but I could be wrong.)

Not so sure about trying to change LDL, rather than focusing on HDL/Trigs and letting the rest of your body’s lipid system adjust itself accordingly … aren’t much of our brains made of the stuff?

From my limited research: while ApoE-4 is clearly linked with higher risks of Alzheimer’s, an ApoE-4/4 gene profile is also associated with the risk of systemic inflammation (viz. many now refer to Alzheimer’s/dementia as “diabetes of the brain” due to its inflammatory connections).

Bottom line: While ApoE4 is NOT a guaranty of getting Alzheimer’s (more don’t get it than do), still, whatever one can do to reduce systemic inflammation would be highly advisable for an ApoE4 type - i.e., even more so than for those who are ApoE-3 or -2, (in some combination; two alleles).

How? Through lifestyle changes … like restricting carbs, OMAD/TMAD, exercise, sunshine, healthy sleep, etc.

So yeah, if you’re doing these things already, then it’s hard to grasp any practical usefulness either way. I’m thinking that ApoE testing for keto’ers is more about curiosity than as providing helpful guidance for what to do next. Kind of like your Lp(a) concerns.

[PaulL]

My understanding is that the ApoE4 gene is the human default, and the others are later mutations. For what it’s worth, and from what I recall of what I’ve read, ApoE4 doesn’t so much lead inevitably to Alzheimer’s disease, as it makes people more vulnerable to the effects of a high-carb diet.

The designation of Alzheimer’s disease as “Type III diabetes” is because it is linked to insulin-resistance of brain cells. Apparently the glucose metabolism of brain cells is insulin-dependent, so excessive insulin puts that pathway at risk if the cells have to down-regulate their insulin receptors. The advanged-glycation end products of glucose metabolism can also cause damage.

Fatty acids are too large to cross the blood-brain barrier, apparently, but ketone bodies are small enough to do so, and they are metabolised in the mitochdondria of brain cells, so they can usually be metabolised even when the glycolytic mechanism is damaged. And ketone/fatty-acid metabolism has the added advantage of not producing AGE’s.

[fitbod]

I wonder what reducing saturated fat might do? Based on my reading it seems likely that saturated fat does contribute to higher LDL. High LDL is a good indicator for coronary risk in the general population. But when we go keto even though LDL goes up, HDL also goes up and trigs fall which are indicators of lower risk in the general population. It is often asserted that in a low carb person we should focus less on LDL and more on Trig/HDL but it doesn’t seem like we have the studies to be sure.

I haven’t had my bloodwork done since going keto in March 2020. My LDL when last checked in 2019 was only 63. It will be interesting to see what it is after 15 months of keto.

[PaulL]

It is often asserted that in a low carb person we should focus less on LDL and more on Trig/HDL but it doesn’t seem like we have the studies to be sure.

The triglyceride/HDL ratio is supposed to indicate low cardiovascular risk in everyone, not just people on a low-carb diet. I don’t know how good the studies are that showed this, but everyone who believes that cholesterol has something to do with heart disease accepts them.

I don’t know if saturated fat raises LDL, but Dr. Phinney says in some of his lectures that it definitely raises HDL, and he compares it to an HDL-raising drug he worked on that never made it to market because of its side effects.

Not that it really matters in any case; after several years of watching lectures by Dr. Phinney, Dr. Ludwig, Prof. Diamond, Dr. Kendrick, Prof. Bikman, Dr. Berry, Dr. Ede, Dr. Eades, and Dr. Mason, I’ve stopped believing that cholesterol and dietary fat have anything at all to do with cardiovascular disease, they are just convenient scapegoats, it would seem. When you learn about the roles cholesterol plays in building cells; in making Vitamin D, progesterone, and testosterone; in building and fueling the brain; and in fighting infections, you wonder why we ever feared it in the first place.

[SomeGuy]

My understanding is that the ApoE4 gene is the human default, and the others are later mutations. For what it’s worth, and from what I recall of what I’ve read, ApoE4 doesn’t so much lead inevitably to Alzheimer’s disease, as it makes people more vulnerable to the effects of a high-carb diet

That’s consistent with the more credible sources I’ve seen on the topic. The way you’ve phrased it is quite succinct.

When you learn about the roles cholesterol plays in building cells; in making Vitamin D, progesterone, and testosterone; in building and fueling the brain; and in fighting infections, you wonder why we ever feared it in the first place.

I’ve read that the brain consists of a significant amount of cholesterol. It would seem odd for the body to produce a “toxin” - and then develop one of its most essential organs of this same material.

Yeah, hard to understand how scary we’ve made it all sound. Then again, if you’re marketing a drug, it becomes more understandable.

[FrankoBear]

More wishful thinking?

The growing body of information is looking good. I like that you are so aware of wishful thinking and confirmation bias.

I was wondering if the shape of the calcium scan deposits indicate an anatomical reason for increased blood turbulence?

[SomeGuy]

I like that you are so aware of wishful thinking and confirmation bias.

Thanks - wishful thinking coupled with confirmation bias are my strong suits.

I was wondering if the shape of the calcium scan deposits indicate an anatomical reason for increased blood turbulence?

Considering a turbulence effect from calcium deposits is an intriguing thought.

My guess: evolutionary culling (viz. heart failures) has likely produced a balance between (a) closing up an artery through excessive calcification and (b) letting unchecked gooey soft plaques head downstream to clot somewhere unexpected.

The herd survivors (at least within the window of reproduction) are likely blessed with the better balance between (a) and (b).

Then again, other than rare genetic disorders, few humans suffer from coronary artery disease before we’re done making more humans - so evolutionary forces associated with calcification - or lack thereof - have likely run their course by that point, either way …

[Razzic]

I’d second this. It is well known that the Ca will circulate the body and nor be absorbed without all 3 of those (Mg, K2 l & D3).

I read a study a few years back saying too much calcium was bad (linked to overall death mortality) and the better approach was less calcium, and more of the above related vitamins / minerals.

How much D3 are you having a day? How much K2? And how much calcium and Mg?

[JonAddison]

First thing that jumped out when looking at the regimen for SomeGuy is the fish oil.

Yes, if one Googles one will come back with a trillion hits with favorable fish oil articles.

However, polyunsaturated oils may lead to calcification thru more than one pathway.

[SomeGuy]

First thing that jumped out when looking at the regimen for SomeGuy is the fish oil.

Yes, if one Googles one will come back with a trillion hits with favorable fish oil articles.

However, polyunsaturated oils may lead to calcification thru more than one pathway.

@JonAddison Thank you for this. I’m not sure then how to proceed…

If taking a daily fish oil supplement pill is doing harm - not good - this would represent a major “fail” in my approach

[flap_jack]

No science, just ‘gut feel’, but I worry about HIIT, and inflammation / turbulance thus caused. Those of us in the UK got a fright by Andrew Marr’s story. I have a CRC of 333, and now ride for long distances below MAFF threshold in the hope that I won’t provoke anything.

[SomeGuy]

No science, just ‘gut feel’, but I worry about HIIT, and inflammation / turbulance thus caused. Those of us in the UK got a fright by Andrew Marr’s story. I have a CRC of 333, and now ride for long distances below MAFF threshold in the hope that I won’t provoke anything.

I know what HIIT stands for … can you kindly translate CRC (is 333 good or bad?) and MAFF? Sorry, just not following these terms.

[flap_jack]

sorry typo. CAC 333.
MAFF is the training popularised by Phil Maffetone, which is really zone 2 (he advocates HR180- your age for a max during these sessions). Lots of others now recommending it, as I’m sure you know. I’m like you on the CAC, not sure what else to do but continue on this road, so following this thread with interest.