ASCVD Risk Calculator

The “Framingham Heart Study (FHS”) showed that most people don’t get side effects from low to moderate doses of statins. The first statin I tried was Zocor and I did have side effects. namely muscle weakness and soreness. I switched to Lipitor and I had no side effects and took it for decades. So, if anyone is complaining about their statin, they should at least try a few others before giving up.


Just found out that my statin problems could be caused by this:

This is because it isn’t safe to eat grapefruit or drink grapefruit juice while using a statin.

Good to know. I eat a lot of grapefruit…

Rosuvastatin doesn’t interact with grapefruit, while others might so.


Statins that interact more

The following statins tend to interact more with the furanocoumarins in grapefruit juice:

  • atorvastatin (Lipitor)
  • lovastatin (Mevacor)
  • simvastatin (Zocor)

Statins that interact less

These statin medications tend to interact less with grapefruit juice:

  • fluvastatin (Lescol)
  • pitavastatin (Livalo)
  • pravastatin (Pravachol)
  • rosuvastatin (Crestor)

In 2017, I developed tinnitus. Kaiser ear doctor took some pictures, informed me that I had atherosclerosis in carotids. Bonus!

I had tinnitus for decades but did not associate it with atherosclerosis - and none of my doctors thought it was worth following up on. The audiologist focused on addressing my hearing problems, and he never brought a potential vascular issue to my attention. Somewhat similarly, no dentist has ever told me there is a link between periodontal disease and heart disease - I assume they know this is true, but all they want to do is your annual cleaning and check for cavities.

Move along, nothing to see here.

Tinnitus isn’t associated with atherosclerosis, as far as I know.

It can be.

Heart disease, hearing loss and tinnitus (

So what does your heart health have to do with your hearing? It’s all about blood flow. Studies have shown that good circulation plays a role in maintaining good hearing health. Conversely, inadequate blood flow and trauma to the blood vessels of the inner ear can contribute to hearing loss. This is also why hearing loss and diabetes are connected.

That’s because the delicate hair cells in the cochlea, which play an important role in translating the noise your ears collect into electrical impulses for the brain to interpret as recognizable sound, rely on good circulation. Poor circulation robs these hair cells of adequate oxygen, causing damage or destruction. Because these hair cells do not regenerate, it results in permanent hearing loss. When this happens, a person may also develop tinnitus, or ringing in the ears.

In a study published in the June 2010 issue of the American Journal of Audiology, authors Raymond H. Hull and Stacy R. Kerschen reviewed research conducted over the past 60 years on cardiovascular health and its influence on hearing health. Their findings confirm that impaired cardiovascular health negatively affects both the peripheral and central auditory system, especially in older adults.


The European Society for Cardiology developed an ASCVD risk calculator that incorporates Lp(a) and shows the effect of lowering LDL-C and/or blood pressure on reducing the excess risk: It also calculates risk up to age 80, unlike most calculators which only calculate 5 or 10-year risk.

The calculators are statistical tools — but of course, so is anything informative about your future risk. This is all aging and probabilities.

I’m all for coronary calcium scans, but the problem is that CAC is a lagging indicator: they can only tell you you have a problem after you already have advanced atherosclerotic lesions. Risk calculators can inform you about your risk before you’ve wrecked one of your vessels.

I assume you meant “NMR lipid tests” (i.e. 123810: NMR LipoProfile, which is a test of particle numbers not of lipids) not “MNR lipid test.” This is a good test, but it’s more expensive and no more informative than measuring apoB.

With the possible exception of corn oil, seed oils are not a problem. Canola oil greatly lowered hard CVD outcomes in a large randomized clinical trial. See also this video from Gil Carvalho on canola

Fish oil actually raises apoB. I’m not saying don’t take it — there is reasonably good evidence that it’s protective against hard CVD outcomes — but you need a different tool for lowering the driver (apoB).

Damn. I’m really sorry that happened to you. That’s terrible incompetence. ASCVD is the number one cause of death in the US and globally: any PCP ought to be prepared to be on top of this or refer you to a cardiologist.

All the 2017 emails refer to your carotids and ultrasound, whereas the 2023 email says “The Atherosclerosis of the aorta was noted by a radiologist on both a CT scan and a chest x-ray,” When did you have the (chest?) CT and X-ray?

@Destrider: as others have indicated, you really ought to consider trying another statin — particularly rosuvastatin if you’re a grapefruit-gobbler. These things are quirky, and rosu is minimally affected by CYP3A4.

@RapamycinCurious The statin that caused problems for me was Rosuvastatin. It was the worst muscle soreness I have ever experienced. I am still recovering from it. I have developed new chronic pains, mainly in my right hip, that I did not have before I started Rosuvastatin :frowning:

I have thought about trying ezetimibe, but I read that it is toxic to take both GFJ and ezetimibe. Any idea how much time spacing you should take between the two to avoid side effects?

Also, ezetimibe may cause muscle myopathy as well…

I’m sure you can find a study that shows that, but I can produce just as many that show fish oil reduces apoB. Fish oil is one of the 2 or 3 supplements I’d say almost everyone should take.

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I’m sure you can find some small trials that report lower apoB due to being underpowered, but there are quite a few large trials on fish oil, and they consistently find either no effect on or an increase in apoB or LDL-C. For instance, the STRENGTH trial:

A total of 13 078 patients were randomized at 675 academic and community hospitals … to receive 4 g/d of omega-3 CA (n = 6539) or corn oil, which was intended to serve as an inert comparator (n = 6539), in addition to usual background therapies, including statins. …

Results When 1384 patients had experienced a primary end point event (of a planned 1600 events), the trial was prematurely halted based on an interim analysis that indicated a low probability of clinical benefit of omega-3 CA vs the corn oil comparator…

LDL cholesterol levels increased in the omega-3 CA group but not in the corn oil group (1.2% vs −1.1%; GMR, 1.03 [95% CI, 1.01-1.04]; P < .001), while greater increases in HDL cholesterol were observed in the omega-3 CA group (5.0% vs 3.2%; GMR, 1.01 [95% CI, 1.00-1.02]; P = .002). Apolipoprotein CIII levels decreased in the omega-3 CA group but not in the corn oil group (−7.0% vs 5.9%; GMR, 0.88 [95% CI, 0.87-0.89]; P < .001). In contrast, no significant difference was observed with regard to percentage change in apolipoprotein B levels (−2.0% vs −1.0%; GMR, 0.99 [95% CI, 0.98-1.01]; P = .34) between the omega-3 and corn oil treatment groups, respectively.
Omega-3 Fatty Acids vs Corn Oil and Major Adverse Cardiovascular Events in Patients at High Risk

And just over a week ago:

84 patients (mean age: 68.2 years, male: 85%) who achieved low-density lipoprotein cholesterol levels of <100 mg/dL were enrolled. … Serum LDL concentrations in the no-treatment, 2-g EPA/ DHA, and 4-g EPA/DHA groups were lower than 80 mg/dL and showed no significant difference. No significant difference was observed in Δ (changes from baseline to follow-up) LDL among the groups. [All were around 70 mg/dl before and after treatment — Table 2l]. The [plaque-to-myocardium signal intensity ratio (PMR) of coronary high-intensity plaques] was reduced in each group over 12 months. There were no significant differences in PMR changes among the three groups in the primary analysis or analysis including total lesions. The changes in CTA parameters, including indexes for detecting high-risk features, also did not differ.

As I said in my original post, I’m not saying don’t take it — there is reasonably good evidence that it’s protective against hard CVD outcomes — but you need a different tool for lowering the driver (apoB).

“Fish oil (FO) contains omega-3 long chain fatty acids, eicosapentaenoic (EPA) and docosahexaenoic acid (DHA), and FO has been shown to effectively target fasting TG, nonfasting plasma TG and total apoB-lipoproteins in the MetS [40-43]. Meta-analyses have shown that FO lowers fasting plasma TG and ApoB-lipoproteins by 15% to 45%, and FO specifically targets the nonfasting or postprandial excursion in plasma TG following a high-fat meal “

I give you the last word as I have no interest in arguing. But don’t want forum readers to think fish oil is raising their apo b.

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I don’t have time to reply in detail but I completely disagree. When I was looking at the subject in 2021, I found plenty of sources that convinced me that seed oils increase CVD risk, decrease metabolic health, and increase obesity.


Don’t you think it’s how seed oils are used? Unless added to a recipe, and not too many recipes ask this, the amount of canola oil that I use is a fraction of a gram daily. Most modern non-Teflon, nonstick pans require only the slightest amount of oil to coat the surface. Most health-conscious people are not doing deep fat frying. So, I think the discussion of whether or not seed oils are good or bad is not applicable to people who are already following healthy diets.

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For me, seed oil avoidance primarily applies to eating out, and I do very little of that these days. Happily there are apps now to help you find seed oil free restaurants. At home, I can always find a substitute if a recipe calls for seed oil.

As my CRP and NMR lipoprofile numbers look good in a diet that is seed oil free as much as possible, I’m going to stick to the plan.

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You’re quoting from the discussion in this paper. This passage cites five references. Despite what the passage says, none of them is a meta-analysis.

[40] is a small RCT (33 people) from Korea, and did find that fish oil lowered apoB-100 by 24%. This is an exception rather than the rule on the claims of the authors of the cited passage.

[41] Was another small RCT, this one in men with hypertriglyceridemia (average TG 225.66 mg/dL): “Thirty-four men (17 in each group) completed the study, but for the analyses reported here, we had samples from only 14 subjects in each group.” The cited paper does not actually contain the effects on lipids, but refers back to their previous paper, which found that DHA “elevated concentrations of LDL cholesterol (12.6%), small VLDL particles (133%), and large LDL particles (120%) and the mean diameter of LDL particles (0.6 nm) in fasting plasma.” So the exact opposite of what the paper from which you’re quoting says.

[42] is a review on the mechanisms whereby omega-3s affect lipid metabolism: its only section on levels says “Comparing EPA treatment with DHA treatment, or DHA treatment with OM3FA treatment, generally shows similar and small or no effects on LDL-C levels [18, 19, 23,24,25,26]. However, it is reported that treatment with DHA, but not EPA, increases LDL-C levels and LDL particle size [22, 54]. In contrast, one study showed no effect of DHA, but EPA treatment decreased TG levels and increased LDL-C levels in normolipidemic individuals [20].” So certainly no support for it lowering LDL-C/apob.

[43] was an RCT that “randomly assigned [metabolic syndrome] patients to 1 of 4 diets: high-SFA [HSFA; 38% energy (E) from fat, 16% E as SFA], high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA], and 2 low-fat, high-complex carbohydrate [LFHCC; 28% E from fat] diets supplemented with 1.24 g/d of long-chain (LC) (n-3) PUFA (ratio 1.4 eicosapentaenoic acid:1 docosahexaenoic acid) or placebo (1.24 g/d of high-oleic sunflower-seed oil) for 12 wk each.” At the end of the trial, the LFHCC with fish oil led to a nonsignificant −5.3% reduction in postprandial LDL-C and a nonsignificant 5.9% increase in postprandial apoB48; no data are given on total apoB, apoB-100, or fasting lipid values.

[44] is a review about omega-3 fatty acids in CVD; the only thing it says about lipoproteins is that “In patients with this degree of TG elevation [135 to 499 mg/dl], a 20 to 30% reduction in fasting [TG] values is typical and often accompanied by small reductions in nonhigh-density lipoprotein cholesterol and apolipoprotein B.”

So the quoted passage misrepresents or exaggerates its cited studies.

As I noted, none of the cited studies is a meta-analysis. This study actually was a meta-analysis. It forund that omega-3 fatty acids had no effect on LDL-C (WMD 0.03 [—0.08 to 0.15]).

Reviewing this I’ll retract my statement that FO elevates apoB/LDL-C: it appears that it has no effect. But it certainly doesn’t meaningfully lower it.

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Hi your canola oil reference links to a Mediterranean diet study, not canola. Do you have the correct link please?

That is the correct link. If you read the study, the only direct intervention was that the experimental group was given free canola-based margarine. They were also advised to use canola oil or olive oil for salads and in various aspects of a Mediterranean diet — but if you look at the dietary data in the paper, there were no major differences between the two groups other than the lower consumption of deli meat (low in controls, lower in the Meds) and the substantial change in fat intake from using the canola margarine and canola oil.