Quick review. I started Keto in January of 2017. My Coronary Arterial Calcium, CAC , score in 2018 was 76 and rose to 375 by 2019. At this same time, I was diagnosed with a bifascicular block. Another check 8 months later and I slowed it down to almost a halt with 386 and finally dropped it to 355 after another 8 months which defies the estimated 12>% increase in calcification most cardiologists expect. Instead, I generated an 8.2% decrease in hard plaque and furthermore increased my ejection fraction from 45% to 60%. In the following, I recount what I did to diagnose my condition’s primary driver, on top of the healthcare community diagnosis.
Reviewing the Data
The Plan to repair my damage was formulated in May of 2020 after a great deal of research and applying this however poorly understood into my own situation. This occurred just as I was making predictions about Covid (early February was when I told my employer we were going to have troubles). As the world shut down and when I wasn’t focused on the pandemic, I was reading up on heart disease. As stated previously I devoured many of the leading low carb lipid and heart experts. I then reviewed the AHA literature which basically said it was hopeless to even attempt to alter the Agatston Score. Yet I saw people on the forums and Facebook groups who claimed to have done so. I had faith that if they could do it, so could I. The idea was to review the health markers I knew from the data I had and then apply what I was learning to see if I could find patterns. If I saw a correlation and the intervention could not create a larger problem there was no harm in attempting it. Basically Pascal’s Wager for Heart Disease. I would still see my primary care physician and my local cardiologist as well as monitor my health markers. This plan suggests I might not win but at least I will not fail.
I started with the obvious, blood pressure. Hypertension over time is linked to increased arterial stiffness. Arterial Stiffness considered the main driver of why hypertension leads to blockages in the heart. The continued high pressure responds to growth in the arterial wall thickness which then loses its elasticity. Think of it this way: a garden how to small for the amount of pressure that is left out in the sun all season loses its ability to be flexible and coil back around the lawn reel. I knew of no easy test for arterial stiffness but using the proxy of blood pressure has up to now, usually been good enough. Fortunately I have kept daily blood pressure readings averaged monthly and charted over the last three years.
Looking over my blood pressure, although there was high and lows, and I could overlay other statistics such as resistance training, calories, sleep and other data nothing other than heart rate variability jumped out at me. I could see that my training as measured by Heart Rate Variability (HRV) and the time of year had some pronounced effects. Indeed, my level of activity was a greater influence on BP than even my pulmonary embolism which I suffered as the result of the second Moderna shot and my particular genetics.
I have measured my body fat according to a Dexascan and have kept my body fat between 16 and 22%. This would place me in the top 7% of body composition according to the CDC for someone my age. While blood pressure must be playing some role, I am going to make a working hypothesis that the negative effects are seen more in body fat accumulation and not muscle mass. My body fat percentages do not always correlate well with a gain in weight, the second highlighted area shows a gain of body fat but an overall decrease of body weight and a very low blood pressure reading. in The third highlighted area of December 2020 to March 2021 also has an increase in body fat and a decrease in blood pressure and weight. At best I can only say that the mixed results are not enough for me to say “aha!! Gotcha”
I had GREAT muscle mass and as such have determined that while I see a correlation and maintaining a healthy weight is important in maintaining a healthy blood pressure, I am going to continue to work more on body fat AND not overall weight as a primary driver to good health. I will avoid beta blockers and calcium channel blockers for now- side note I was prescribed diltazem in May 2021 as a result of the PE. As such I think it has had little bearing on these results coming into the game for two months. I would continue to monitor BP without excessive intervention.
How’s Those Lipids?
Most of know the Cholesterol Theory of Heart Disease. Much of the medical community is beginning to accept that this theory has been misapplied. I am not going to dissect that here. I am going to say that as a member of the ketogenic community I do not believe blood lipids are the sole driver, if at all, of heart disease. I will however review my data with the reader.
According to 23&me I am a person who thrives on a high fat diet and my APOE Alles are 2/3. I am stating this only in that I do think what genes one has do play a role on the lipids effect in the body.
The regular annual draw. I have done many tests on lipids during an extended fast and have charted some outrageous cholesterol numbers. What I can say with all sincerity is that WHEN you do a lipid sample matters as much as to what the numbers say. I can tell you much more about your recent history with food far better than some. In my case, I will filter out some of this noise from all my extended fasting labs ( 96 hours plus) and show my lipids only near the standard 14 hours fasted. My LDL is has traditionally been high. Conversely my HDL skews low unless I supplement Carlson’s Super Elite DHA or add Cod Livers & Sardines to my weekly nutrition. At the time of diagnosis my lipids were high but the previous years accumulation was well within any medical providers acceptable levels. As there is no smoking gun showing direct mechanistic causation of lipids being the cause of a blockage my assumption remained that my lipid levels were not the reason for my block. It is fun to note that as my lipids rise my heart health improves as can be seen all the way in the right of the first graph. Something to be mindful of later.
My other ratios look good as well. Sometimes they do skew towards a level of insulin resistance. I also know that I have had episodes of more insulin resistance than others, even while being in keto. With all this in mind, I reviewed my lipids and they are within the window I expected. Much like my blood pressure they ebbed and rose according to activity and meal frequency. Moving forward I worked under the acceptance as confirmed by NMR Lipoprofile that my Pattern A LDL was large and akin to fluffy tumbleweeds instead of the dangerous smaller dense particles. It was my belief that LDL was part of the immune system, and it was their accumulation at the site of the damage in my heart that was caused by something else other than LDL. LDL has been thought to be the cause rather than the response. Think of it this way, LDL was a metaphorical ambulance trying to mitigate the crash site. However the observer (medical researchers) who arrive only after the ambulances do then in assessing the situation say “look at all these ambulances (LDL) they caused an accident!!” I believe it was either Carl Franklin or Siobahn Huggins who coined this metaphor. I could be wrong on this. Check out this podcast for more insight: 2 Keto Dudes #83 – Lipid Dysregulation with Siobhan Huggins . For the 60 years of the Heart Cholesterol Theory no one has provided a mechanistic “smoking gun” showing definitely HOW LDL was the issue let alone why the “excess” was bad. I like many others began to believe the filter of LDL as villain was flawed and we need to look elsewhere.
An injury had still occurred in my heart, and my heart arteries were getting blockages in the form of calcification, hard plaques. If it was not the blood pressure or the blood lipids, could it be the same problem that made me obese, osteoporotic with spinal injuries as well as some other metabolic issues? Could it possibly be insulin resistance? I have previously stated that I did know my insulin had been an issue and in keto crept up. During a 120 hour fast I could be as low as 1.0 uIU/ml but tended towards 6.0 uIU/ml for a 14 hour fast. However in early 2019 I was eating a great deal of over the counter keto labeled items, in particular Keto Ice Creams, and this I was doing daily. Whether it was the sweeteners used in there or the fibers something during that time spiked my insulin.
My working hypothesis then was I had some level of insulin resistance that was not yet under control through a ketogenic diet OR that my particular keto diet was at times was rather sloppy or “dirty keto”. Keto store-bought items infiltrated my WOE and this possibly created havoc. I could see it reflected in other measures. I had a HBa1C of 5.9 after daily consumption of store bought keto ice cream for at least 6 months even though my morning BG was not outrageous it was elevated from the previous 2 years. My Beta-hydroxybutyrate or BHB was slowly decreasing showing either a fat adaptation OR less need for ketones as I was getting energy from sugars. KETO Cookies and small cakes also made their way to my table shouting BUT WE’RE KETO. See? I needed the god dammed KETO Police!! It was this incident that made me create The Keto PD.
Insulin Resistance and Endothelial Cells
Elevated Insulin as a driver of heart disease? Isn’t insulin a diabetic issue. Yes but diabetics usually die of heart disease and not their “diabetes”. There is a link. And as insulin when working properly stores excessive energy in the body for later but when its excessively high the cells become resistant to its signaling and this creates all kinds of havoc. Excessive insulin can damage the endothelial cells, those that line the arterial wall and as such if they are damaged perhaps the immune system just might send LDL there to shore up the weakened arterial walls. A plug in the dike so to speak. What if the excessive glucose from the Standard American Diet (SAD) had created the problem? Although I wasn’t inflicting as much damage as I had in SAD, what if my particular dirty keto diet continued to exacerbate the issue? If all this was true, then it was this I needed to fix much more readily than I already had? Could this be me primal driver, i.e. root cause?
Could it be that insulin and glucose could create the damage? It turns out that yes, it very much could. Glucose and Insulin lead to arterial wall thickening and stiffness. I had already looked at arterial stiffness from the point of view of hypertension. I hadn’t considered that insulin could create it and that it could still be a main driver of my issue. At this point I have to remember that my issue was undiagnosed until 2019. I have no idea if I had it prior to my Ketogenic Way Of Eating, WOE, or if it manifested as a result of this WOE. That my diagnosis could be the result of the removal of the source of injury and as a result the healing manifested itself as the disease. Again I had to remind myself that I had lost body fat, gained muscle and healed osteoporosis and lowered my pre-diabetic HbA1C. I found it ridiculous that this WOE was harmful until proven otherwise. SO I began to operate under the assumption that my issue was lingering from the SAD way of life and possibly that I was creating flare ups with my current type of dirty keto.
The key then was to focus on lowering my fasting insulin. To lose visceral fat which I understand to be a proxy for excessive insulin and metabolic dysfunction. To balance my Trig/HDL ratio and furthermore once I had removed the primary driver of the damage what could I do to reduce the calcifiaction or more bluntly how could I reverse the damage I had done?
Part Three of this Three part look at my heart disease reversal will complete how I lowered my CAC by 8.2% and improved my overall heart & general health. All this while suffering a bi-saddle pulmonary embolism! It’ll take me about a week to type it up. It will include my exercise, keto nutrition, fasting schedule and supplements as well as my reasoning for each. I have no definitive proof that anything I did will work for others. I am only sharing my story to expand or community of N=1 anecdotes.