---
title: 'The Common Pill That Raises your Risk of Diabetes (And How to Avoid it)'
source: 'https://youtube.com/watch?v=VLc1_vLZUSk'
video_id: 'VLc1_vLZUSk'
date: 2026-06-29
duration_sec: 769
---

# The Common Pill That Raises your Risk of Diabetes (And How to Avoid it)

> Source: [The Common Pill That Raises your Risk of Diabetes (And How to Avoid it)](https://youtube.com/watch?v=VLc1_vLZUSk)

## Summary

A medical doctor and PhD researcher shares his personal experience with statins, explaining why he stopped taking Crestor (rosuvastatin) after noticing a gradual rise in his hemoglobin A1C. He details the process of switching to pitavastatin and achieving better metabolic outcomes while maintaining low heart disease risk.

### Key Points

- **Personal Statin Journey Begins** [00:00] — The author stopped taking Crestor and explains the reasons. He is an MD/PhD who had been on statins for two years.
- **Real Purpose of Statins** [00:24] — Statins are prescribed not just to lower cholesterol but to reduce heart attacks, strokes, and deaths based on randomized trials.
- **Personal Risk Factor: High Lp(a)** [00:51] — The author did not have high cholesterol but had elevated Lp(a), a genetically determined risk factor for heart disease affecting about 1 in 5 people.
- **Trial of Different Statins** [01:23] — He tried atorvastatin (Lipitor) and simvastatin (Zocor). Atorvastatin raised insulin resistance, prompting further adjustments.
- **Initial Optimal Regime** [02:06] — He settled on rosuvastatin (Crestor) 5 mg plus ezetimibe (Zetia) 10 mg daily, which initially gave optimal lipid markers without raising insulin resistance.
- **HbA1c Creeps Up** [02:45] — Over 1-1.5 years, his hemoglobin A1C slowly rose from baseline ~5.1% to 5.5%, a significant change given the narrow normal range (5.7% = prediabetes).
- **Ruled Out Weight Gain** [04:16] — Despite losing weight and body fat through lifestyle, HbA1c increased, making the statin the likely cause.
- **Atypical Response** [05:12] — The rise was surprising because he had no diabetes risk factors and was on the lowest dose of Crestor, where this effect is rarely seen.
- **Switching to Pitavastatin** [07:53] — He stopped Crestor and started pitavastatin 2 mg plus ezetimibe, a statin known to be milder on glucose metabolism, especially used in Japan.
- **New Regime Results** [10:13] — After a few months, lipid markers stayed low (LDL 65, non-HDL 76 mg/dL) and HbA1c returned to 5.2%, within his normal range.
- **Key Message: Personalization** [11:21] — Optimize rather than compromise. Many options exist (different statins, ezetimibe, bempedoic acid) and patients should be empowered to discuss alternatives with their doctor.

### Conclusion

Personalization is key in preventive cardiology. By carefully monitoring biomarkers and switching medications, the author achieved optimal lipid control without compromising glucose metabolism, illustrating that most people do not need to accept trade-offs.

## Transcript

I recently stopped taking Crestor, which is a type of statin known as Rousseauva statin. So in this video, I'm gonna explain what happened, why I stopped taking it, and what I started doing instead.
I'm an MD, PhD, research scientist, and I've been taking a statin every day for about two years. Now, most people misunderstand this about statins, even a lot of doctors.
You might think the point of taking a statin is to lower your cholesterol, but that's not really the point. You look at cholesterol levels as a readout, as an indicator of how well the statin is working, how powerful it is in that individual, but the real reason that statins are prescribed
is that they reduce heart attacks, strokes, and deaths in randomized trials. There are a number of other drugs that lower cholesterol, and yet they're not prescribed because they don't meet that standard.
In fact, in my case, I didn't have high cholesterol in the first place. And I had high is something called LP Little A. About one in five people have that elevated and it's mainly determined genetically, it runs in families, and it raises risk of heart
disease. So I started taking the statin, not to lower cholesterol per se, but to lower the overall risk of heart disease, of a heart attack or a stroke in the long run. Now, I've been on three or four different types of statins over time.
I've been on a tour of a statin, which has sold as lipitor. I've been on cymbastatin, which has sold as zoocorp, and for different reasons, I switched around. Cymbastatin isn't that powerful, so the effect was kind of mild.
A tour of a statin is stronger, but in my case, it raised my insulin resistance. So I kept tweaking things. I wanted to find a regime that gave me the best of all worlds. I wanted those lipid indicators in the optimal range that we know is linked to a very low
risk of heart disease, of heart attacks and strokes, and at the same time, I wanted none of the undesirable effects, like increased insulin resistance or blood sugar.
So after playing with this for a while, I landed on a regime of Rousseauvastatin, the Crest War five milligrams a day, plus a zeta-mime, which has sold as zedia at 10 milligrams a day.
And the reason we combined those two is that those drugs potentiate each other. So when you take them combined, the effect is stronger. And that regime seemed to be working perfectly for me, at least initially, the lipid indicators,
the cholesterol, but more accurately, something called APLB was in the optimal range, and insulin resistance did not go up, fastened blood sugar did not go up. So everything looked hunky-dory.
But then something changed. I kept doing blood work periodically every few months over the next year to year and a half, and I noticed that my hemoglobin A1C was slowly creeping up.
Hemoglobin A1C, also known as glycated, hemoglobin is an average of your butchered levels over three months. And my usual value is around 5.1 percent, give or take, between 5.0 and 5.2 in that ballpark.
And what I noticed was that over a period of about six months, first it went to 5.3, then it went to 5.5 percent, which I had never seen before in my life. Now if you're not used to hemoglobin A1C values, this might seem strange because the difference
is tiny. But the thing with A1C is it varies within a very narrow numerical range. So just to give you an example, an A1C of 5.1 is perfectly healthy, good A1C, whereas 5.7
is prediabetes. And then 6.5 percent is full bone diabetes. So a difference in numbers that might seem small makes a huge difference physiologically. So going from my usual 5.1, give or take, 0.1 to 5.5 was meaningful.
It definitely caught my attention. Now here's another thing we need to clarify, because you might be wondering, well, was it the statin? Was it something else? Great question. When fasting blood sugar or hemoglobin A1C go up, the number one thing we think about,
especially in a Western population, is weight gain, people putting on fat. That's the most common cause of blood sugar or hemoglobin A1C going up. But I've actually lost weight, I've actually lost body fat since I started the statin a
couple of years ago, not because of the statin, but because of lifestyle diet and exercise. So that didn't explain the increase. So I had no other plausible explanation. The statin was the most likely.
So I decided to pause the crest or the russava statin also as a test. If I pause it and the hemoglobin A1C comes back down, it was indeed the statin. If it doesn't, it's something else. Now, before we go into what I started doing instead of the crest or there's something fundamental
that I need to clarify to you. This change was very atypical and surprising for two reasons. We do see blood sugar and hemoglobin A1C go up in certain individuals on statins that's known that's been described.
However, that usually happens with higher doses. I was on five milligrams of crest or which is the lowest dose. On that dose, we don't usually see that. But more importantly, we usually see this in people who have some predisposition, who have
some risk factors already for diabetes. So people who are pre-diabetic or have metabolic syndrome or have a lot of overweight or obesity. In my case, I have none of those risk factors and so we was quite surprising.
In fact, people that are very knowledgeable in this field were very surprised to see that raise in hemoglobin A1C. But precisely because it's atypical, it makes for an interesting case study to share and discuss with you because in science, we look at data sets of large populations, randomized
trials, cohort studies, and that's super important. You don't want to neglect that, but we also want to personalize. We want to apply what is known scientifically to your individual case, to my individual case,
to the person that's in front of us. Science shows us what happens in average to most people. Your individual results show what's happening to you and both of those matter. So my situation was atypical, but the fact is hemoglobin A1C was going up.
Maybe there's some individual susceptibility there. Now this next clarification is possibly the most important thing in this entire video because this is often misunderstood.
If I looked at those values of hemoglobin A1C going up and I went, oh, so I'll just stop, the regime, I'll just stop the statin and do nothing instead. That would be a step backwards.
That would be a net negative because we know from randomized trials that the net result of the statin is a reduction in what we call the hard outcomes, the actual things we care about, the heart attacks and the strokes and the deaths at the end of the day.
And we see that even in people at higher risk of developing diabetes and even in populations that have type 2 diabetes already. So if I had no other option, I would take that trade off of the higher hemoglobin A1C, not
on some theoretical speculation or some gut feeling, but on the actual data from randomized trials. In fact, my cardiologists that I talked to were not that impressed, were not that alarmed
with that increase. They said, well, it's not that big a deal, we'll just watch it and not change the regime for now. And that's a reasonable position, it's not crazy, but I decided to change because I'm still
young in my 40s and because I had the luxury of options. So I can afford to experiment, to make a change, and I don't have to take that trade off.
I'm not forced to do that. I decided to change. So I stopped the crestor and I started something called Patava statin, which is a member of the big statin family, but it's something that was developed and it's mainly used in
Japan. It is not prescribed that often in the West, nowhere near the crestors and the lipitors. But the randomized trial data shows something very interesting, not only does Patava statin reduce those hard outcomes we talked about, like the actual heart attacks at the end of
the day, but it actually seems a little milder on the glucose metabolism, the insulin resistance and the blood sugar. So it made total sense in the situation. And when I brought it up, I actually suggested it to my cardiologist.
She said, yeah, that's a good idea, we can try that. So I started two milligrams of Patava statin, plus that a zetamide, that zedia, we talked about, same dose, ten milligrams, same as before it didn't change that.
I just took out the crestor, the rousseauvastatin, and I started this Patava statin instead. So I did that for a few months and I just got blood work. Before we get into that, I want to address a very likely question.
You might be wondering about things like burberry or nato kinase, which you might have heard about on social media. Many of those supplements have been shown to reduce cholesterol levels.
Some of them might even reduce the thickness, the size of the plaque in the arteries according to some studies. I don't take any of those supplements, even though I could get them essentially for free. For the same reason that we covered earlier in the video, if you remember, the whole point
here is not the lower cholesterol per se, it's the lower the actual risk of a heart outcome of an event, as we call it in cardiovascular medicine, a heart attack or a stroke. And the fact is, those supplements, although some of them have very interesting, promising
data, they haven't met that standard. So it would be much more of a coin toss for me to go take one of those supplements that hasn't cleared that bar, although I think the data is really interesting and I'd be open
to taking one of those if the data in the future at that level is convincing. But right now, it's a no brainer. I'm going with what has the strongest outcome data. Okay. So let's go over my results, my blood work on the new regime, Patavastatin and azadamide.
Basically, the lipid indicators stayed in a low optimal range. So my LDL cholesterol is 65 and my non HDL cholesterol is 76, all of this in milligrams per deciliter.
So these are ranges that tell me that the risk of heart disease is extremely low in the future. There's another test that I always like to get, which is called APLB, which measure the actual number of particles in the blood that cause heart disease.
Ironically, the lab made a mistake and did not measure that, although we requested it. But that's okay. I'll get it next time. The non HDL cholesterol, which is total cholesterol minus HDL being 76 already tells me that the
APLB is going to be pretty decent. So that looks pretty good. And then my hemoglobin A1c came back down to 5.2, which is roughly in my normal range.
So basically, the desired outcome overall. So my cardiologist was pretty happy with that. I think overall is a success. I'll continue to monitor, I'll make changes if necessary. I'm not married to any strategy or any med or any bill.
It's whatever gets me the results and whatever has the strongest scientific evidence. The bottom line of the real message I want you to get from this whole video is personalization. Because we have so many options nowadays that most people do not need to compromise.
Optimize, don't compromise. Just a lot of that. It works. Take it to the bank. Many people don't need medication. They can get all of their blood work looking really solid. Just with lifestyle, if you don't have any genetic kinks, some people need the extra nudge.
For those people, we have all these options. We have seven classes of statins now all validated in actual randomized trials looking at hard outcomes. We have azetamide, azetia.
If those are not enough, people can add rapata. Some people do. And for people who can't tolerate any statin, some people are really statin-intolerant. There's been pedoic acid, which does a similar thing.
Or you can use azetamide by itself. That's another option. There's so much wiggle room and your doctor might not have time to go over all of this with you in a short appointment. So being aware of this information empowers you to have that conversation at a different
level. If you want to know more about this topic, the little particles in your blood and what causes heart disease and how to avoid it, we have a whole breakdown in detail explaining all of this and the tests that you want to ask your doctor for, so I'll link that right here, check it
out, and I'll see you next time.