krsct
GLP-1 Apprentice
Been on GLP-1 for almost 3 years. Lost 1/4 of body weight in 8 months and maintenance since then. Took a while but my doctor stopped my statins today. Never thought it would happen. It took a while but another great NSV.
It actually happened: off statins!
- Thread starter krsct
- Start date
80s.diver
GLP-1 Apprentice
That is awesome, keep us posted to see if the cholesterol numbers creep back up.
krsct
GLP-1 Apprentice
I'm at 90. My doc does not think that 55 is reasonable. Will also reassess in 6 months.
lessthanhalf
GLP-1 Specialist
Without knowing the full story it is hard to say if this is a good idea or a bad one. The purpose of statins is to reduce risk of cardiovascular disease either in the first place or after an event like heart attack or stroke has occurred. If the original assessment of absolute cardiovascular risk over 10 years was high, and statins were started for that reason, then unless that assessment is recalculated, then staying on them is the correct approach regardless of lipid levels. If they are being used for secondary protection then stopping them is always the wrong move.
If the loss of weight and improved blood pressure, lipids etc were enough to reduce risk to below 10% over the next 10 years then stopping might be correct, but it is definitely not as simple as better lipid numbers after weight loss. Looking at statin use based on absolute cardiovascular risk is the correct way to view it but it is not super simple or obvious. Anyone who has or had severe obesity is likely to have high absolute cardiovascular risk, and there is a fairly high chance of that still being the case if weight is lost especially if older. And there is a reasonable chance that damage has already occurred that will not be known about unless it is looked for.
I ended up diagnosed with early heart failure and coronary artery disease after losing a lot of weight and without symptoms, where treatment with statins and other medications reduce 10 year risk from about 25% to about 12%, but if it had not been looked into I would not have known until a heart attack years later, which might still happen , but being half as likely sounds good to me.
If the loss of weight and improved blood pressure, lipids etc were enough to reduce risk to below 10% over the next 10 years then stopping might be correct, but it is definitely not as simple as better lipid numbers after weight loss. Looking at statin use based on absolute cardiovascular risk is the correct way to view it but it is not super simple or obvious. Anyone who has or had severe obesity is likely to have high absolute cardiovascular risk, and there is a fairly high chance of that still being the case if weight is lost especially if older. And there is a reasonable chance that damage has already occurred that will not be known about unless it is looked for.
I ended up diagnosed with early heart failure and coronary artery disease after losing a lot of weight and without symptoms, where treatment with statins and other medications reduce 10 year risk from about 25% to about 12%, but if it had not been looked into I would not have known until a heart attack years later, which might still happen , but being half as likely sounds good to me.
Calm Logic
GLP-1 Specialist
It's like $100 here for a coronary CT calcium scan (CAC), if insurance doesn't pay.
It takes about three to five years for the plaque to calcify (enough to be detected on a scan). So a more expensive option is Cardiac CT Angiography (CCTA), which tells you both the past (calcified) and the present (soft plaque).
But most people who are paying out of pocket just do the calcium scan.
It takes about three to five years for the plaque to calcify (enough to be detected on a scan). So a more expensive option is Cardiac CT Angiography (CCTA), which tells you both the past (calcified) and the present (soft plaque).
But most people who are paying out of pocket just do the calcium scan.
Last edited:
skeptick
GLP-1 Enthusiast
FAREFFINOUT
lessthanhalf
GLP-1 Specialist
Agree with this, coronary calcium score is a very good way to determine if statins are needed or not, and is especially useful where calculated risk based on family history, blood pressure , lipids, blood sugar, smoking etc is intermediate, and it will still show changes if those numbers are improved by weight loss, and treatment is an extremely good idea if CCS is high even if the other numbers are much improved, as it shows very strong correlations with long term risk, possibly better than any other test including angiography. You could definitely argue than those over 40 or 50 who were or are obese and had evidence of metabolic syndrome should get this checked, even after weight loss. Not covered by medicare in Aus but costs $250 aud and gives very useful information and does not normally ever need to be repeated.
Calcium score is a lagging indicator ofr primary prevention . By the time calcium shows up on a scan, you're already well on your way to develop cvd.
sheilarae74
GLP-1 Enthusiast
👏👏👏👏👏
lessthanhalf
GLP-1 Specialist
Yes but that is the point. It is not practical or economic to treat every single person with statins. Treatment is decided by an estimate of absolute risk of MACE or major atherosclerotic cardiovascular events over the next 10 years. Biggest risk by far is age. Then the usual ones family history, smoking, diabetes, blood pressure and lipids. Calculations based on those risk factors are the standard method. Coronary calcium score is an alternate way of assessing risk and is very accurate at predicting future risk, which makes it an excellent tool for deciding if primary prevention is warranted or not.
So it does also detect established coronary artery disease, in my case at 645 at 58 yo this equates to 97th percentile for risk for age or about a 25% 10 year MACE risk, which is treated more like secondary prevention. I am actually quite glad my doctor talked me into getting the test when I had thought it unnecessary.
But it also often detects a CCS of 0 which translates to a low 10 year risk, which would usually mean primary prevention medications are not needed, unless calculations based on the usual risk factors were bad, but if you were going to use that to decide then doing the CCS test was pointless. So it is often used when the traditional risk factors give a borderline result as to whether primary prevention is needed or not. And it is sometimes used for more broad screening , but the science on whether this is justified is not well established.
Almost all adults on a western diet have some degree of atherosclerosis, especially after the age of 40 or so, the point is to determine those at highest risk, to decide who to treat or not , as treating everyone is not cost effective or practical and exposes a lot of people to side effects. Anti platelet agents like low dose aspirin are going out of fashion now, but they carry risks of bleeding as well, and are more typically used in secondary prevention only but this is fairly recent.
As far as I know as I have not read it in detail yet, the new US guidelines on lipid management are suggesting testing at younger ages but not recommending treatment unless absolute risk is significant, but are recommending lower LDL targets.
Prior to starting tirzepatide, my pcp put me on a low dose statin. My numbers weren’t crazy, but definitely elevated. Fast forward a year later, and now I have too low cholesterol. I think that that is adversely affecting some hormone production (mainly testosterone), and that is affecting other aspects of my life. Anyhoo, my pcp doesn’t want to take me off the statin until I talk with a cardiologist. I’m like WTF, but the more I research there are other health benefits of statins beyond lowering cholesterol, so I lowered my dose and will see cardio at some point. My pcp doesn’t think that I can split my medication, but that’s clearly not the case. So, I didn’t tell her. Lately, my numbers are more in the normal range, but I continue on the statin.
Zydeceltico
GLP-1 Enthusiast
Exactly. It was a self-chosen, self-pay CT calcium scan last August that revealed an 80% occlusion of my LCX and a stent in December that decreased that 80% to 0%. I sent the CAC results to my PCP and she put me on rosuvastatin the same day. LDL went from 141 to 54 between August and December. It was discovered that occlusion is the result of atheriosclerosis.
To your point re: secondary intentions: I am to stay on the statin due to it slowing the progression of further calcification and hardening which apparently is another function it performs.
If I had not decided on my own out of curiosity to get that CAC on my own, I would have been surprised at some point by a heart attack.
Last edited:
Statins have always been an odd decision, since they work in such a roundabout way and so strongly impact a substance (cholesterol) that your body has systems in place specifically to avoid ever getting too low and will ramp up production if it's not getting enough from your diet.
The current thinking is that the things (LDL) that transport fats, cholesterol, and other fat-soluble nutrients through your bloodstream are a key step in arterial plaque growth. The data here is rather inconclusive. We know SOME of the LDL will readily deposit in that manner and cause real problems, but we haven't nailed down exactly what it is that determines whether an individual LDL particle will do so. On average, higher LDL blood levels correlate with cardiovascular disease, but it's a fairly weak correlation (with other risk factors linking much more strongly to cardiovascular disease than LDL itself).
So instead of making an effort to explore why sometimes LDL tends to deposit in arterial walls and sometimes it does not, it's just assumed that all LDL must be bad and we should seek to reduce blood levels of this essential transporter.
So how does pharma tackle the problem? By directly going after LDL (the rationale of which is already on somewhat shaky ground)? Naw, they eventually got to doing that with PCSK9-inhibitors many years later, but instead came up with statins, which are quite the roundabout solution.
Instead of going after LDL itself, statins go after one of the essential substances that LDL shuttles around your body (cholesterol), such that your body stops making as much of it. To cope with this shortage your liver starts recalling the cholesterol transporters (LDL) more rapidly, pulling them out of your bloodstream sooner, as if it were trying to recall the cholesterol still remaining in them sooner. That succeeds in keeping the amount of LDL particles floating around in your blood lower, but also means that your body is coping with a supply shortage of cholesterol, which isn't entirely without consequence itself.
Now if someone had a prior cardiac history or was at significant risk, such a bargain might be very reasonable. Instead, it's just routine for your doctor to push statins on you as soon as your LDL hits a slightly elevated number on a couple of lab tests, as if it were as benign of a decision as taking a vitamin supplement. 🤷♂️
The current thinking is that the things (LDL) that transport fats, cholesterol, and other fat-soluble nutrients through your bloodstream are a key step in arterial plaque growth. The data here is rather inconclusive. We know SOME of the LDL will readily deposit in that manner and cause real problems, but we haven't nailed down exactly what it is that determines whether an individual LDL particle will do so. On average, higher LDL blood levels correlate with cardiovascular disease, but it's a fairly weak correlation (with other risk factors linking much more strongly to cardiovascular disease than LDL itself).
So instead of making an effort to explore why sometimes LDL tends to deposit in arterial walls and sometimes it does not, it's just assumed that all LDL must be bad and we should seek to reduce blood levels of this essential transporter.
So how does pharma tackle the problem? By directly going after LDL (the rationale of which is already on somewhat shaky ground)? Naw, they eventually got to doing that with PCSK9-inhibitors many years later, but instead came up with statins, which are quite the roundabout solution.
Instead of going after LDL itself, statins go after one of the essential substances that LDL shuttles around your body (cholesterol), such that your body stops making as much of it. To cope with this shortage your liver starts recalling the cholesterol transporters (LDL) more rapidly, pulling them out of your bloodstream sooner, as if it were trying to recall the cholesterol still remaining in them sooner. That succeeds in keeping the amount of LDL particles floating around in your blood lower, but also means that your body is coping with a supply shortage of cholesterol, which isn't entirely without consequence itself.
Now if someone had a prior cardiac history or was at significant risk, such a bargain might be very reasonable. Instead, it's just routine for your doctor to push statins on you as soon as your LDL hits a slightly elevated number on a couple of lab tests, as if it were as benign of a decision as taking a vitamin supplement. 🤷♂️
tendency
GLP-1 Enthusiast
TL;dR re: LDL. The latest research shows, to my understanding, that if you have significant CVD risk factors then you should be paying attention to your LDL numbers. If you don't have CVD risk factors then LDL numbers are probably not that important.
Last edited:
latviantower
GLP-1 Enthusiast
Excellent point. I recently had my calcium CT and guess what? Despite being on a statin for 20 years and keeping my my cholesterol well below even borderline, my calcium score is off the charts. So now I have a cardiologist! Good news? The calcium is in my arterial walls, stabilizing the whole thing. No narrowing. Aced stress test. Hit the gym every day. Only have to see the cardiologist once a year. My LDL is 40 (yes still on a statin, different one at higher strength), total cholesterol <100.
A high calcium score is not a death sentence - it can be a wake up call. The key is to have to scan earlier in life - for example, my trainer (37) had a scan showing very mild calcification (horrible family CVD history), but they are being aggressive NOW to slow the process before it gets critical.
I think what’s missing here is that LDL alone doesn’t define cardiovascular risk.
The more complete question is: what is this person’s actual risk right now?
That usually involves ApoB, Lp(a), inflammation (hs-CRP), and sometimes CAC.... not just LDL.
So LDL of 90 and stopping statins could be reasonable… or premature.
It depends on factors we’re not seeing discussed: ApoB, LDL-P, Lp(a), inflammation, family history, insulin resistance, CAC, etc.
Without that, it feels like an incomplete picture
The more complete question is: what is this person’s actual risk right now?
That usually involves ApoB, Lp(a), inflammation (hs-CRP), and sometimes CAC.... not just LDL.
So LDL of 90 and stopping statins could be reasonable… or premature.
It depends on factors we’re not seeing discussed: ApoB, LDL-P, Lp(a), inflammation, family history, insulin resistance, CAC, etc.
Without that, it feels like an incomplete picture
Completely agree with this, but there is a greater implication here too. It's very likely OP was put on a statin without evaluating these factors to begin with and purely based on one or two LDL-C (estimated) values from a basic lipid panel alone, as is commonly done in the US and a rather disappointing state of affairs.
Zydeceltico
GLP-1 Enthusiast
@tubby
I am seriously interested in your take on my numbers.
I had my CAC on 10/8 and my PCP started me on rosuvastatin on 10/9.
My stent was placed on 12/9.
Again -seriously curious about your take. thx
I should add that I started tirzepatide on June 6, 2025.
SW: 242 lbs, GW 187 lbs reached 11/1/25 and have maintained since.
I am seriously interested in your take on my numbers.
I had my CAC on 10/8 and my PCP started me on rosuvastatin on 10/9.
My stent was placed on 12/9.
Again -seriously curious about your take. thx
I should add that I started tirzepatide on June 6, 2025.
SW: 242 lbs, GW 187 lbs reached 11/1/25 and have maintained since.
Last edited:
Let me preface this by saying that I'm not a doctor and you shouldn't listen to anything resembling medical advice that I might say. It's not medical advice and I'm not qualified to provide that.
I'd start by ignoring the LDL-C numbers entirely. On a basic lipid panel they don't actually measure LDL, they estimate it using something called the Friedewald Equation (Google that if interested in learning more). In addition, even if LDL-P (a proper measure of LDL that is actually a direct measure of it rather than a crude guess) was done, since you're going through a period of weight loss, that can bias your LDL result significantly, making it less reliable than it would be if you were at a stable weight prior to having the lab done.
However, looking at the numbers on your lipid panel that actually are strongly correlated with cardiovascular risk as well as directly measured rather than estimated (triglycerides and HDL), I do see some cause for concern there. At present, the best estimator of cardiovascular risk is the triglyceride to HDL ratio, which is much more strongly correlated with it than LDL-C. And honestly, that's not looking great. 140/34 = 4.1 is bad, but then that was before you started taking a GLP-1 and you don't need me to tell me that you were in bad shape before the GLP-1.
Jumping ahead to 9/17/25, your trig/HDL ratio is now 96/30 = 3.2. That's still bad, but a significant improvement over where you were before the GLP-1 and honestly a pretty positive change over a 3 month period. And honestly with such a rapid weight change in such a short period of time, I'd probably want to see things "settle" for a bit before making any sort of judgement call there.
Now jumping to your January numbers, 44/35 is looking a lot better at 1.3. Of course, getting to that ratio via a statin is very different than getting to that ratio via lifestyle changes. Just as holding a bunch of helium balloons as you step on the scale isn't going to lead to any of the health improvements that actually losing weight would come with, I don't know that examining statin-mediated numbers is really going to tell us anything useful there. Also, you probably have many years at which your cardiovascular system was under strain and built up plaque, which has to be factored in too.
The traditional school of thought with that is that by taking a statin you'll increase the amount of calcified plaque in your arteries. Normally that's a bad thing, since more calcified plaque means more cardiovascular risk. Of course, cardiologists being the dogmatic people that they are, upon discovering that rationalized it as actually being a good thing since it meant plaque was more stable and less likely to break off from a deposit (which could potentially be fatal). I can't say I disagree with them on that point to be honest, but just throw the dogmatic dig in there because, while likely true, it's also the kind of rationalization one would invent in trying to justify their own past actions and practices, and such things are probably worth considering when evaluating recommendations. They also have a long history of giving bad advice based on very limited evidence, but I digress...
Another school of thought (that hasn't been studied extensively) is to seek out other ways of reducing plaque deposits (natto kinase shows some promise there) rather than calcifying them, but I don't think that's well enough understood for a responsible recommendation to be made there, since one could argue that's just as easy to lead to catastrophe for you as improvement, based on things I don't know the answer to. But you kind of have to pick a lane there: Either stabilize/calcify the plaque via the traditional/statin route or attempt to actively reduce it somehow.
I guess my main takeaways going forward if I were you would be that your low HDL is hurting your trig/HDL ratio (if not for that, your triglycerides are at a really nice level right now). At the same time, you can't really trust your lipid panel numbers to tell you anything useful in the future, as they're biased by the statin that you're taking, making them suspect at best when applied to risk models that may conflate statin and statin-free numbers. I might consider seeking out an "LDL skeptical" doctor and pay for a consult with them. In the end there's a good chance they will also recommend staying on the statin that you're on, but they're going to have less blind spots than I will and be in a position to actually give you a proper recommendation.
Calm Logic
GLP-1 Specialist
Regarding calcium CT scoring for intermediate risk:
Risk calculators:
Related guidelines:
Risk calculators:
The PREVENT equations estimate absolute 10–year risk for total CVD (PREVENT-CVD), ASCVD (PREVENT-ASCVD) and HF (PREVENT-HF) for adults aged 30–79 years and 30-year risk for total CVD among adults aged 30–59 years. In addition to absolute risk estimates, the calculator provides complementary risk information, including PREVENT–Age and age- and sex-specific 30-year risk percentiles, to help contextualize predicted risk and support clinician–patient discussions.
The American Heart Association PREVENT™ Online Calculator
Welcome to the American Heart Association Predicting Risk of cardiovascular disease EVENTs.professional.heart.org
CVD Risk Estimator Plus - American College of Cardiology
Combining traditional ASCVD risk modeling with modern cardiovascular kidney metabolic (CKM)–inclusive risk equations, CVD Risk Estimator Plus provides clinicians with a comprehensive, personalized cardiovascular disease (CVD) risk assessment.www.acc.org
CVD Risk Estimator Plus computes risk estimates using:
2013 ASCVD Pooled Cohort Equations (PCE), which calculate 10‑year and lifetime risk of atherosclerotic cardiovascular disease using age, sex, race, blood pressure, cholesterol profile, diabetes status, and smoking status.
2023 PREVENT™ Equations, which estimate 10‑ and 30‑year risk for total CVD, ASCVD, and heart failure (HF), incorporating kidney and metabolic health measures such as BMI and estimated glomerular filtration rate (eGFR), and supporting optional predictors including urine albumin‑creatinine ratio (UACR), hemoglobin A1c (HbA1c), and social deprivation index (SDI).
MDCalc uses the 'Hard' coronary Framingham outcomes model, which is intended for use in non-diabetic patients age 30-79 years with no prior history of coronary heart disease or intermittent claudication. This version was selected because it is the most widely applicable to patients without previous cardiac events.
Framingham Risk Score for Hard Coronary Heart Disease Calculator
The Framingham Coronary Heart Disease Risk Score estimates risk of heart attack in 10 years.www.mdcalc.com
See the official Framingham website for additional Framingham risk models.
Related guidelines:
(2026)
In adults at intermediate risk and select adults at borderline risk with no prior ASCVD, if the decision regarding LLT [lipid-lowering therapy] remains uncertain, a CAC score should be used for further risk stratification and to guide the decision to withhold, postpone, or initiate therapy.
Major Global Coronary Artery Calcium Guidelines (2022)
The figure elucidates an algorithm for suggested CAC scoring and assessing ASCVD risk. CAC = 0 suggests withholding statin therapy, while CAC = 1 to 100 favors lifestyle improvement. CAC = 101 to 400 indicates treatment for individuals >75th percentile, and CAC >400 requires initiation of statin therapy.
Last edited:
And for those curious about what diet can achieve, these are my pre to post-diabetes lipid and A1c results (achieved through diet). I don't have any labs with GLP results yet so not sure how those will impact me. Ignore the weird trend-line from the left on my A1c plot as there was about a 5 year gap between results so it's just connecting those dots.
Also note that I engaged in no significant exercise during that period other than walking around the neighborhood a bit. All diet.
Also note that I engaged in no significant exercise during that period other than walking around the neighborhood a bit. All diet.
Attachments
Can't speak to those specific links, but I'd take anything the AHA says with a huge grain of salt. They have a history of making claims that seem to benefit industry (pharma and big food) and are scientifically dubious at best and then digging into their positions even after it's clear that claims they've made are flawed (e.g. their long-standing positions on saturated fat and low-carb diets). At a minimum I would check to see if there's a Cochran review article on the same topic and if Cochran supports the AHA position and guidelines or comes to a different conclusion.
Otherwise, I'd just assume that most positions promulgated by the AHA are primarily a means of influencing doctors (who themselves wouldn't knowingly behave unethically towards their patients) into giving bad advice that benefits industry. There isn't really a smoking gun that proves that's happening, but they've just been wrong so much historically that it would be naive to take them at face value.
Last edited:
Zydeceltico
GLP-1 Enthusiast
Firstly, thank you for the thorough review. I know you're not a doctor nor would I be tempted to consider an anonymous post from a complete stranger as medical advice. That said (mostly as a caveat for others who may read this), I do appreciate your thoughts.
To the recognition of the short amount of time: yes - I am happy to report that I am apparently a super-responder. It should also be noted that due to the almost immediate balancing of blood sugar levels that I experienced, decades of what I used to believe was constant hypoglycemia has finally and completely subsided. Gone. With that, I was able to negate a vast quantity of daily food stuffs that I would intake simply to keep my energy, mental acuity, and emotions in precarious balance. For years I had desired to simply "eat clean" and had success a couple of times for several months at a time but not without the internal struggle of food noise. So it was relatively simple to instantly begin eating clean (no simple carbs, no sugar, no junk). I also immediately began strength and cardio training 5x/week and getting +2 more hours of sleep per night as my insomnia was also mitigated. So yes - lifestyle changes are a huge factor. I've been at GW since late October and eat without issue. Very happy and content with the -necessary for me - lifestyle changes.
Also pertinent: I had approx. 38% body fat last June. Now at 18% per DEXA in February. The great majority of my weight loss was VAT fwiw. According to a DEXA in Oct. and the second one in Feb., I have apparetly increased lean muscle mass by 6+ lbs in that amount of time, so it kinda feels like the plan is working as hoped.
Not certain where I stand on the statin question. I am not really concerned about it as I also have zero sides from the statin either and I feel better at 62 y.o. than I have in a decade.
Last edited:
Your situation is too complicated for me to have useful advice on, obviously.
One thing I will add is that there are a large number of studies out there that study the relationship between total cholesterol and all-cause mortality in very large populations (thanks to readily available public health data). A nice trait about all-cause mortality is that it's harder to fake/manipulate than an intermediate marker.
When a statin brings down cholesterol, it's impossible to know how that compares to bringing cholesterol down through other means or how much of a benefit it will actually lead to without studying it. Fortunately, this has been studied in large populations. Unfortunately, those who conducted the (expensive) research are mostly unwilling to share the raw data with groups that might be critical of their work so we're kind of stuck trusting that the pharma-friendly researchers have conducted a fair analysis of the data and haven't applied dubious correction factors or other tricks to skew the data towards a particular conclusion.
What we do know from population-level cholesterol data is that having too low of cholesterol and too high of cholesterol are both associated with significant increases in all-cause mortality. The curve varies by both age and sex. Here is an example of the first curve I could easily find on Google, but there are many studies and they all have somewhat similar results. Choose your favorite if you wish to read more.
Some of the low-end risk can be explained by cancer (in late-stage cancer your cholesterol does tend to drop), but that doesn't seem to explain all of it.
And that's why I suggest finding a physician who is skeptical of statin therapy (instead of listening to me) who can better flush out the other side of the equation, enabling you to make a proper objective comparison, since at that point you'll have heard both sides of the story.
Last edited:
Turbo-Farmer
GLP-1 Enthusiast
I highly recommend the book “Statin Nation” by Dr Malcolm Kendrick He has been a GP for over 25 years and has worked with the European Society of Cardiology.
Key Arguments:
Minimal Lifespan Increase: Kendrick cites data suggesting that even for high-risk individuals, taking statins for five years may only increase life expectancy by an average of four days.
Pleiotropic Effects: He argues that if statins do work, it is not because they lower cholesterol—which he views as an "unimportant bystander"—but because they increase nitric oxide synthesis. This helps dilate blood vessels and prevent clotting.
Hidden Side Effects: The book claims that side effects (such as muscle pain and cognitive issues) are often dismissed by researchers who have financial ties to the pharmaceutical industry.
The "Black Swan" Logic: Using Karl Popper's scientific method, Kendrick points out "black swans"—cases where people with high cholesterol live long lives—to argue that the "all-high-cholesterol-is-bad" theory is fundamentally flawed.
The also argues that the relative risk of death from heart disease is lower. The absolute risk of death is greater when taking statins. The book also examines the drug approval process and how the results are obtained by taking the best case scenario for the drug approval. Without taking into consideration the overall benefit.
My personal opinion on statins is that it increases insulin resistance and the side effects made running more difficult for me as I was combating my diabetes.
I gave this book to my Dr to enjoy while she’s on maternity leave. So she can understand my viewpoint on statins. ( this isn’t the first time I’ve given her a book assignment as her patient)
I suspect there's at least some truth to the points you raised (or perhaps they're completely correct). There's enough of what I might call suspicious tells in regards to the history of statins to give me pause at the very least.
I will say that if someone is going to consider a statin, they'd likely be foolish to do so without assistance from a GLP due to the blood sugar issue/insulin resistance issue that you brought up. The GLP won't eliminate all of the risk associated with statins, but at least it should partially mitigate that particular one.
I still maintain that there are good reasons to believe that GLPs are going to prove to be more cardioprotective than statins as the data emerges where even if someone buys into the AHA guidelines for LDL many "borderline" people will drop below that simply from taking a GLP.
Trending Topics
Latest Posts
-
-
-
-
My compound was solidified on arrival, is this normal?- Latest: flipperdosan
-
-
-
-
-
Have you found any method or supplement that has improved your sleep?
- Latest: notfatanymore123
