3.3. Effect of Brazil Nut Consumption on Serum Lipids Profile
Three studies [17,18,24] examined alteration of serum lipid profile as a consequence of Brazil nut intervention. All pooled results were nonsignificant, including results for total cholesterol (SMD = −0.22, 95% CI: −0.57; 0.14; Table 5, Supplementary Figure S5), HDL cholesterol (SMD = −0.04, 95% CI: −0.28; 0.19; Table 5, Supplementary Figure S6) and LDL cholesterol (SMD = −0.15; 95% CI: −0.43; 0.13, Table 5, Supplementary Figure S7). Alternative imputed missing correlations did not show any significant differences (Supplementary Table S4).
Two of the three studies involved hypertensive and dyslipidaemic subjects.
When considering the results of individual studies, in one trial [17], there were no significant inter-group differences at the start of the trial in any of laboratorial variables, but at the end of follow-up, lower values of total and LDL cholesterol as well as TG for the intervention group supplemented with Brazil nuts compared to the placebo group were observed. However, in studies examining hypertensive and dyslipidaemic patients, no significant differences in serum lipids between Brazil nut and control group were detected.
Ok, just didn’t want anyone to overdo it as it would so easy to eg just start eating 5-10 or 15 nuts a day or something.
(My selenium levels were way too high a few years ago and it took a while to understand that the mixed nuts I was eating was enough to give too many Brazil nuts).
Certainly statins may not be warranted: no one, including Attia, is suggesting treating them the way some people treat multivitamins. If your apoB is 50 and all your other risk factors are under control, there’s no reason to take a lipid-lowering therapy. We’re talking, of course, about what to do if your apoB is high or you have other substantial risk factors and lifestyle alone has been insufficient. That’s exactly what makes a statin (or a blood pressure med for BP or an antidiabetic for elevated blood sugar or insulin) warranted.
All else equal, sure — but the point, again, is that people reading this want to live longer than ten years, and atherosclerosis is a progressive compounding disease. Waiting until disease is established before removing a causal risk factor (apoB or smoking) is the analogy.
CAC being present at all in a person under 70 is a calamity; having it progress is compounding neglect with failure.
Granted how little is known about either the safety or the hard-outcome efficacy of CB, taking it instead of a known lifesaving drug such as a statin would reflect a distortion in the weighing of risks and benefits.
It’s often not as simple as you suggest. We frequently see people with no risk factors other than borderline lipid levels. If it’s the lower the better, then virtually everyone will be on statins for life. .So when do we go to statins? In this case, CAC can be very helpful and can guide our decisions.
This would be easier if statins were benign, but they’re not. I’ve posted several times a mendelian randomization study showing an increased risk of cognitive decline. This matches what many of us have seen in clinical practice with people complaining of difficulty in focus and word retrieval as well as memory. Many people have muscle aches and constipation. Many of them stop the meds.
Bergamot, pantethine, amla and metamucil have multiple trials exhibiting both efficacy and safety.
I understand your preference for meds over supplements, but all medications have side effects and sometimes it takes years for them to manifest. Sulfonylureas have been around for decades and we never suspected them of leading to cognitive decline, but recent studies show them to be a significant cognitive risk. Who knew?
Yes, that terrible cognitive decline of 0.067 ms increase in reaction time per 38.7 mg/dL decrease in LDL from HMGCR inhibition.
The standard decline for each year between 18-65 is 2.8 ms.
So you’re aging about 1 month cognitively, while going back to an age of 5 when it comes to LDL.
That is also from lifelong LDL reduction and gene variation that affects the brain as far as I can tell.
Lovastatin is an older drug it is also lipophilic meaning it can cross the blood brain barrier easily.
Rosuvastatin is hydrophilic meaning it has a harder time crossing the BBB.
If you also knew about the cognitive side effects before taking it, you could’ve been primed for a nocebo effect.
It’s interesting when it comes to cognitive issues. If you just ask a patient something general you’ll get a different response than if you ask specifics like, “ how’s your focus, word retrieval, memory, and sharpness”.
Many people swear to Mendelian randomized studies on this site, unless those same studies show cognitive impairments from statins.
It’s a statin drug as it’s a HMG-CoA reductase inhibitor, it’s the first statin drug to get to the market as far as I can tell.
The size of the effect matters… like the apoB-lifespan effect or apoB-ASCVD effect, which are massive.
You will probably never find a large effect on cognition in mendelian randomization since it is highly polygenic. Meaning each gene have very small effect.
You did prove there is a mechanism, but not the size of the effect. And many of us are taking precautions by using hydrophilic statins. Simply saying statins are bad for cognition when there is hydrophilic statins seems like it is lacking nuance.
Statin use decreases the chances of dementia and Alzheimers. Statin use increasing cognitive impairment has been discredited many times. I don’t know why this is even mentioned anymore.
Here is one example of a recent meta-analysis:
There is quite a lot of debate about HMG-CoA reductase inhibition. I have not personally tried to get to a final conclusion about the arguments, but as cholesterol is a key part of cellular metabolism it would not be surprising if there were all sorts of effects from inhibiting it. On a purely personal basis I remember having specific problems recalling certain information when I was taking RYR.
I am OK with my cholesterol figures anyway. Hence I would not say I have a massively strongly held viewpoint on this.
I confess that I had not consulted this 1959 review article in a defunct state medical journal . This article contains no clinical trial at all, let alone one with hard outcomes: it lays out the author’s clinical experience that niacin lowered total cholesterol in 44 patients in his clinic.
We have several large, randomized controlled trials now showing both that niacin lowers LDL-C and raises HDL-C and yet has no effect on hard outcomes.
. This article contains no clinical trial at all, let alone one with hard outcomes: it lays out the author’s clinical experience that niacin lowered total cholesterol in 44 patients in his clinic.