Monday, May 4, 2026

Bike sprints, diet and disease

Yesterday did the bike sprint intervals.  Today did the 2.5 mile sprint with hills.   Both hard.  I'm thinking these types of workouts plus strength are probably better than these 25 min hill climbs where my HR is over 170 for 15-16 minutes, over 180 for 2-3 min.  I still push it to the 170s but just for short duration.   Maybe do a hill climb once a month or so.  

Bike sprint intervals  - 4 x 400m w/ 2:30 rest  

max speed: 28.4, 27.5, 28.4, 28.5

Max HR - 173




 







------------------------------------- 

Bike sprint - 2.5 miles on Laurel Branch Trl

total time - 10:18 (tied PR)

Max HR - 179 

HR over 170 - 5:18 

Avg HR - 165



 








Going for a blood draw again this week.  Kidney function tests and week after, followup with my PCP, and will press him for an angiography.  

Diet and heart disease

My brother's latest determination of celiac artery blockage was called into question by one of his Drs because it was ultrasound based, so he's pressing for a more definitive test, a CT w/ contrast.

His Dr., a DO, is one of these Keto diet guys.  I'm all for low carb low sugar diet but to be extreme about it is not particularly sensible to me.   I get the low carb thing, carb = sugar. These keto bros / carnivores are totally into this idea that you can eat unlimited fat as long as you eat zero carbs and sugar. The fact is that it does work to lose weight, but for some people, this keto diet will cause heart disease if you’re a “responder” to dietary fat.  And you don't know if you are unless you test prolifically.  Not just standard lipid panels, but more advanced tests like lipid fractionation, apolipo ratios, Lp(a), inflammation, imaging like angiography, etc... CACs are good but not enough, same with lipid panels, and it's ridiculous to draw any conclusions from the once per year lipid panel... but better than nothing. Lipid panels are cheap. Just $23 at Ulta.  

The problem with tests like LDL or Lp(a)  - these are a few of many factors that *may* contribute to heart disease / atherosclerosis. The development of CVD is a very complex and individual process, as we can see with the wide range of anecdotal experiences.   Some have established heart disease yet live long lives. Some are affected by disease from lifestyle factors like diet, yet some aren't. Medical science observes general trends among the population, but there are always a lot of outliers on each end of the bell curve.  You can definitely lose weight on carnivore / keto,  usually by replacing carbs/sugar with protein and fat. Much of the confounding and conflicting data on the subject ignores the fact that there is no general rule for all people on affect of dietary fat. Different people are affected differently by dietary cholesterol as the process for atherosclerosis is complex and dependent on many factors -including genetic disposition. Frankly, looking at it any other way is tantamount to pushing an agenda, a hasty generalization, overly simplistic, or plain disingenuous.   Not much long term data on the results of carnivore / keto diets.  

Anecdotally, I've learned I am a dietary 'responder' to animal fat intake as I learned in 2021 on my brief 'egg diet.'   My brother and I are an interesting case study, albeit ... anecdotal.

A lot of this carnivore / keto diet stuff coming from social media influencers - some professionals - seems to follow the trend of the "RFK Jr - MAGA - bro-science - pseudo-masculine - vaccine science deniers" ... long on anecdotal trends and short term results, short on science and long term studies, and certainly not looking out for individual susceptibilities, and tailoring diet to the individuals based on known vulnerabilities.  They certainly push a lot of generalizations, questionable cherry picked "science," and not much info on longevity and long lived cultures - none of which are carnivore / keto.  I also think diet can be adjusted for athletic goals and training, and can vary and be optimized according to physical needs, time of year, activity level, and body type, etc...



14 comments:

  1. Not good to live your life like a lab rat.

    ReplyDelete
    Replies
    1. Not good to live life oblivious of a treatable disease that may take years off your life. There are no guarantees, disease can be random. I live in a state, like most red states, where life expectancy is low. The avg TN male lives to 71. That's only 5 yrs away for me. It's a shorter life expectancy than Bangladesh and some other 3rd world countries. My congressman warned of migrants of 3rd world countries destroying our culture. MAGA America IS a third world country, both in health and education.

      Delete
  2. A Mediterranean and a statin covers 95 percent of individuals. The main side effect is longer life.

    ReplyDelete
    Replies
    1. Thinking about Repatha, my brother says fewer side affects

      Delete
    2. Mistake. The chance of a side effect from statin is low and it is recoverable. Follow the science and stick with statin for first line of defense. It is the only treatment that remodels and stabilizes plaques, if present.

      Delete
    3. Listen to yourself, "Statins are the only treatment that stabilizes plaque, IF PRESENT." Key words, IF PRESENT. Using that logic, if plaque is NOT present, you don't need a statin.

      Delete
  3. “Much of the confounding and conflicting data on the subject ignores the fact that there is no general rule for all people on affect of dietary fat”. This is false. There is strong evidence that saturated fat increases risk of CVD and unsaturated and mono saturated fat reduces it. It doesn’t matter if there are tails of the distribution that are outliers - if you move the entire distribution to significantly less saturated and more poly and mono unsaturated fat there will be significantly less CVD. Then add a statin. You are making it much more complicated than necessary. For 95 percent of people there is a excellent correlation between outcomes and these simple interventions (replace saturated fat with poly unsaturated and mono saturated fats and take a statin)

    ReplyDelete
    Replies
    1. "There is strong evidence that saturated fat increases risk of CVD " ... that is the conventional wisdom *for most people* ... but its probably more nuanced and complicated than that. Many more factors than dietary.

      Delete
    2. I never speak of wisdom when it comes to science matters. Wisdom is gained from individual experience. Science develops answers from thorough studies. The evidence is overwhelming.

      Delete
    3. And yes diet is not the main driver but a significant contributor. Statins address the other, more significant factors. And yes there are some outliers where statins may reduce LDL C but not lipoprotein B, and in that case there (is at least one) pharmacological therapy to add to statins to address that. This takes care of 99 percent of the population assuming intervention is soon enough. And don’t forget that for high risk individuals with abundant non calcified plaques high dose statins are a critical therapeutic component to shrink and stabilize (calcify) these unstable plaques. Everyone needs to be taught or reminded about that to counter misinformation and overcome the fear, anxiety, and unwarranted paranoia about possible transient and correctable elevations in liver enzymes, correctable by dose adjustment or statin type.

      Delete
  4. “Some have established heart disease yet live long lives. ” Actually the opposite is closer to the truth. Those who live long lives almost certainly have heart disease, it’s just that they die of something else. Nearly everyone develops some degree of it - it’s a process that unfolds over decades. The older you are the more likely you have it. Trying to be absolutely deposit free is not the goal, the goal is for it to be minimized and stabilized so it doesn’t manifest itself clinically.

    ReplyDelete
    Replies
    1. I just had another lipid panel, and I'll use it to push for an angiography. Results due in a day or 2. Also had urine analysis and C-cystatin test.

      Delete
    2. Good chance that your cystatin c will predict better eGFR than creatinine due to muscle mass. It does for me - creatinine 0.98 cystatin c 0.87. I think this is low 90’s eGFR on the combined (creatinine +cystatin c) calculator but I don’t remember exactly.

      Delete
  5. Unless someone has evidence of how they are an outlier it is logical to stick with what works/is recommended for most people.

    ReplyDelete