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Interventions for Preventative Heart Health

Table of Contents

ASA (Asprin)

Lowers Lp(a) as much as 46%.

Can cause constipation, and dangerous rebound effects. http://www.internationaljournalofcardiology.com/article/S0167-5273(00)00399-5/abstract

Fish Oil

Dosage is hard to judge - could it be that it is best to just eat some fish. Valid negative information.

6 G/ day of DHA + EPA (works out to 9 capsules of one brand - 3 TID ) Reduce triglycerides, VLDL, and LDL particle size; reduce risk of death from heart attack; reduce fibrinogen May reduce Lp(a) up to 48% Appears to greatly reduce inflammation.

- Possible 5-Lipoxygenase Inflammatory Pathway inhibitor?

Olive Oil

Coco (cocoa powder)

polyphenols and procyanidins My hunch is polyphenals are not really 'anti oxidants' but instead irritants that work via Hormesis.


Reduce blood pressure, contribute to correction of metabolic syndrome, reduce risk of abnormal heart rhythms 400-500 mg of Mg+ (as magnesium glycinate). May reduce oxLDL


This is weird - high dose lowers HDL raises LDL but stops angina?? Perhaps 15mg is prudent for now??

No use as a marker --

I suppose someone makes a mineral capsule - with selenium, copper, zinc in it? This might apply to folks that use RO water...

It appears that zinc might work by suppressing absorption of iron and copper?


From wikipedia:

Iodine accounts for 65% of the molecular weight of T4 and 59% of the T3. 15-20 mg of iodine is concentrated in thyroid tissue and hormones, but 70% of the body's iodine is distributed in other tissues, including mammary glands, eyes, gastric mucosa, the cervix, and salivary glands. In the cells of these tissues iodide enters direcly by sodium-iodide symporter (NIS). Its role in mammary tissue is related to fetal and neonatal development, but its role in the other tissues is unknown.[24] It has been shown to act as an antioxidant in these tissues.[24]

Iodine may have a relationship with selenium, and iodine supplementation in selenium-deficient populations may pose risks for thyroid function.

My other impression is to wonder what role the 70% of iodine that is NOT in the thyroid is doing? Antioxidant? I'm thinking 1mg

I'm thinking it may make sense to make sure we get enough selenium.

Selenium is required for the production of

deiodinase selenoenzymes. Clinical investigators in se- lenium- and iodine-deficient populations conclude the coexisting deficiencies cause increased TSH levels and contribute to goiter development.78 One French study found an inverse relationship between selenium status and thyroid volume.79 Co-existing deficiencies become problematic in areas where iodine supplementation is promoted on a population-wide basis. Selenium sup- plementation may be necessary to prevent potential thy- roid damage from iodide supplementation in selenium- deficient individuals.

Begs the question - how common is selenium deficiency?

Again from wikipedia

Dietary selenium comes from nuts, cereals, meat, fish, and eggs. Brazil nuts are the richest ordinary dietary source (though this is soil-dependent, since the Brazil nut does not require high levels of the element for its own needs). High levels are found in kidney, tuna, crab and lobster, in that order.

Sounds like sea food is important yet again..

And from

we get this little tidbit:

Some population surveys have suggested an association between lower antioxidant intake and a greater incidence of heart disease [47]. Evidence also suggests that oxidative stress from free radicals, which are natural by-products of oxygen metabolism, may promote heart disease [48-50]. For example, it is the oxidized form of low-density lipoproteins (LDL, often called "bad" cholesterol) that promotes plaque build-up in coronary arteries [49]. Selenium is one of a group of antioxidants that may help limit the oxidation of LDL cholesterol and thereby help to prevent coronary artery disease [48-50]. Currently there is insufficient evidence available to recommend selenium supplements for the prevention of coronary heart disease.

So now what is the best amount of selenium for fighting CAD?

It appears there is a role for selenium - what happens if you drink RO water? Baseline supplementation??

Vitamin K2

Regulation of calcification in bones and arteries

100 mcg BID in the form of MK-7

two on reduced inflammation:

One on blocking 12-lipoxygenas

Reduced calcification


75 mg/kg/d ??? * side effects?? -- Possible down sides?

Vitamin D3

Side effects:

Stomach upset, bloating, constipation, headache, nausea, or temporary flu-like symptoms (e.g., tiredness, muscle ache) may occur. If any of these effects persist or worsen, notify your doctor or pharmacist promptly. Not likely.
The association between low 25-hydroxyvitamin D and increased aortic stiffness
Vitamin D Status Is Associated With Arterial Stiffness and Vascular Dysfunction in Healthy Humans
Vitamin D Inhibits Monocyte/Macrophage Proinflammatory Cytokine Production by Targeting MAPK Phosphatase-1

"We found that 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] suppressed foam cell formation by reducing
acetylated low density lipoprotein (AcLDL) and oxidized low density lipoprotein (oxLDL) cholesterol
uptake in diabetics only."

Possible starting dosage? 5,000 IU. Target test values? greater than 60 and less than 80ng/mL - pay attention to the units - not all labs use the same ones...

Serum 25-Hydroxyvitamin D is an Independent Predictor of High-Density Lipoprotein Cholesterol and Metabolic Syndrome in Men and Women

...after adjustment for established determinants of the HDL-C, with each 10-ng/mL increase in 25(OH)D associated with a 4.2-mg/dL increase in HDL-C concentration.

(requires blood testing to get it right - see above).

While tweaking repeat test every 2 months..

Dr. D notes: "Vitamin D has indeed been hugely helpful for raising HDL, though the effect requires at least 1 year."





Immune System

Kidney (Renal)



500mg - 2G/day Possible 5-Lipoxygenase Inflammatory Pathway inhibitor

The above study was 150m/day. Possibly increases PON-1 activity

Helps reduce niacin flush - may reduce other niacin side effects?

Improved bone density

Niacin (vit B3 )

I wouldn't take.. Failed to support all-cause mortality outcome data - and worse:

HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment

 Side effects

Found this in the Niaspan monograph:

 Acetylsalicylic acid (ASA): Concomitant administration of ASA may decrease the metabolic
 clearance of niacin (see WARNINGS AND PRECAUTIONS, General).

Interesting connection with asprin

 Metabolism: The pharmacokinetic profile of niacin is complicated due to rapid and extensive
 first-pass metabolism, which is species and dose-rate specific. In humans, one pathway is
 through a simple conjugation step with glycine to form nicotinuric acid which is then excreted in
 the urine, although there may be a small amount of reversible metabolism back to niacin. The
 other pathway results in the formation of nicotine adenine dinucleotide (NAD). It is unclear
 whether nicotinamide is formed as a precursor to, or following the synthesis of NAD.
 Nicotinamide is further metabolized to at least N-methylnicotinamide (MNA) and nicotinamide-
 N-oxide. MNA is further metabolized to two other compounds, N-methyl-2-pyridone-5-
 carboxamide (2PY) and N-methyl-4-pyridone-5-carboxamide (4PY). The formation of 2PY
 appears to predominate over 4PY in humans. At the doses used to treat hyperlipidaemia, these
 metabolic pathways are saturable, which explains the nonlinear relationship between niacin dose
 and plasma concentrations following multiple-dose NIASPAN administration (Table 3).

I don't know which of these metabolites is doing the good stuff (or is it the blockage of a metabolic path way - by the breakdown of the niacin?).

 Niacin functions in the body after conversion to NAD in the NAD coenzyme system. Niacin is a
 potent vasodilator, probably acting directly on vascular smooth muscle of the face and trunk. In
 gram doses, niacin reduces TC, LDL-C and TG and increases HDL-C. Reductions in VLDL-C
 and Lp(a) are also seen, and clinical data suggest a favourable effect on the small dense LDL
 particle phenotype ("pattern B") associated with increased CHD risk. The magnitude of
 individual effects varies with the underlying hyperlipidaemic condition.
 The exact mechanisms by which niacin exerts its effects are not clearly understood, but appear to
 be diverse. The rates of hepatic synthesis of LDL and VLDL are decreased, for example, as are
 serum levels of Apo B, while enhanced clearance of VLDL may also occur, possibly due to
 increased lipoprotein lipase activity. The decreased production of VLDL is thought to result
 from transient inhibition of lipolysis and from decreases in the delivery of free fatty acids to the
 liver, in TG synthesis and in VLDL-triglyceride transport. The lowered LDL levels may then
 result from decreased VLDL production and enhanced hepatic clearance of LDL precursors.

 The increase in HDL-C resulting from niacin treatment is associated with a shift in distribution
 of subfractions, with increases in the proportion of HDL2 relative to HDL3 and in Apo A-I
 respectively. Niacin is not known to affect either the rate of cholesterol synthesis, or the faecal
 excretion of fats, sterols or bile acids.

from the slo-niacin monograph:

Discontinue use and consult a physician immediately if any of the following symptoms occur: persistent flu-like symptoms (nausea, vomiting, a general “not well” feeling); loss of appetite; a decrease in urine output associated with dark-colored urine; muscle discomfort such as tender, swollen muscles or muscle weakness; irregular heartbeat; or cloudy or blurry vision.


Reduce muscle aches of statins, reduce blood pressure, strengthen heart muscle. Reduces Lp(a)?(perhaps weakly)

  • - [editors note] - I've tried taking CQ10 and lost my coffee cup 4 times in a row (OK I might lose it once regularly), but I've now heard of others having this strange effect.. On paper I want to take it.


Krill oil (containing Astaxanthin)

Not to replace fish oil - but an add on for the Astaxanthin content


Not sold that 2-glasses/day is net good - just take the polyphenols a better way?
10oz/day seems optimal -- may be that reveritrol is absorbed sublingaly?

Alcohol Can reduce Lp(a) up to 57%.


Ginkgo biloba

120 mg twice daily?


DHEA is precursive to several hormones. DHEA has also been shown to reduce the amount of atherosclerotic plaque in rabbits fed a high-cholesterol diet. Possible arrhythmia at higher levels. May help lower Lp(a) up to 18%. Does not increase Testosterone long term IMO. Possible 5-Lipoxygenase inhibitor?

reduces formation of oxLDL

lowers Cortisol?


Insist on Cinnamon verum - Cinnamon Cassia contains a potentially toxic component called coumarin, which can cause liver and kidney damage if consumed excessively. Lowers blood sugar 1-2 tsps per day.. Need to figure best dosage.. Some MDs are reporting it just doesn't work - more bad studies or the type of cinnamon

Vitamin C

Reduce blood pressure, amplify action of l-arginine 1G/day Perhaps it isn't so good for us - "Although ascorbic acid (ASA) is known as a water-soluble antioxidant, we found that it accelerated the cytotoxicity induced by oxidized low-density lipoprotein (OxLDL) in vitro."


100 - 200mg? Pssible 5-Lipoxygenase Inflammatory Pathway inhibitor


Boswellia is an Ayurvedic plant that contains anti-inflammatory triterpenoids called boswellic acids. Boswellic acid and its derivatives have anti-carcinogenic, anti-tumor, and blood lipid lowering activities. Dried extracts of the resin of the Boswellia serrata tree have been used since antiquity in India to treat inflammatory conditions.

5-Lipoxygenase Inflammatory Pathway inhibitor



Lower blood pressure, inhibit inflammation and cell adhesion, possibly reduce carotid plaque. Side effects - Arginine may increase blood sugar levels - nausea may increase stomach acid by stimulating the production of gastrin,


Reduce lipoprotein(a) 2G

These very high doses of carnitine may lead to excess energy, restlessness, perhaps insomnia and increase in blood pressure?



Could tryptophan be a link in the depression/inflammation axis of CAD?

Seeing or hearing things that are not really there (hallucinations)
Fast heartbeat (tachycardia)
rebound Anxiety attacks
Feeling faint
Muscle spasms
Difficulty walking

 ALA (Alpha Lipoic Acid)

Not so interested in this one:

CONCLUSIONS: Studies examining the relation between ALA and prostate cancer have produced inconsistent findings. High ALA intakes or high blood and adipose tissue concentrations of ALA may be associated with a small increased risk of prostate cancer. However, these conclusions are qualified because of the heterogeneity across studies and the likelihood of publication bias.

One should probably recheck thyroid if taking ALA (Alpha Lipoic Acid)

Vitamin E as γ-Tocopherol

γ-Tocopherol has been mentioned by Bruce Ames Vitamin E in most pills is alpha

Gamma Tocopherol is available..


At least 100 mcg, up to 1000 mcg sublingual preparation is an excellent alternative to lower homocysteine.

Folic acid Vitamin B9

Do not take!!

"Recent study shows 2x increase of prostate cancer with folate doses of 1 mg (1000 mcg) and higher."

TMG (Trimethylglycine) (Betaine)

Side Effects of Trimethylglycine

Trimethylglycine if taken in high dosages, such as more than 750 mg, can cause nausea, increased body temperature, restlessness and insomnia and perhaps muscle tension headache.


Found in green Tea - I'm trying 600mg - reduces oxLDL


Looks like 5 to 15g/day in various papers.

From D. Burke et al published in the Canadian Journal of Applied Physiology (23 (5):471, 1998) After three weeks of either creatine or placebo supplementation, 40 male varsity athletes were interviewed and filled out a questionnaire detailing all side effects during the double blind study. Two side effects showed the greatest difference between the creatine and placebo group: sleep irregularity (creatine 47%, placebo 7%) and muscle soreness (creatine 53%, placebo 14%).


Anthocyanins (red polypheols )

Elderberry seems to be the best source. (iHerb.com ?)

Source Naturals Wellness - Elderberry (still out of stock)
NOW - Elderberry Extract (substitute for the above)
Eclectic Institute - Aronia (Chokeberry) was out-of-stock, but is now available
LEF Pomegranate Extract (expensive, but the best - looking for an effective substitute)

The CETP inhibition in the above study means that small-LDL may be reduced by this regimen of 160 mg twice per day.

LDL -13.6%
HDL +13.7%


It seems chokeberry juice also "decreased the activities of enzymatic markers of cytochrome P450, CYP1A1 and 1A2. NDEA treatment also decreased the activity of CYP2E1 but enhanced the activity of CYP2B." Medscape article here. As pointed on a recent thread on curcumin, this could negatively affect those taking pharmaceuticals, so caveat emptor.

ORAC = Oxygen Radical Absorbance Capacity (this is based on food storage not in vivo -and probably works via hormesis NOT as an antiox - dosage could be key - to high may do damage?)

Acai Berry raw 100gm: with ** mono-fats, saturated fat palmitic , omega-6, phytosterol**
ORAC 18,500
Anthocyanins 320

Chokeberry raw 100gm
ORAC 15,820
Anthocyanins 1480

Blueberry raw 100gm
ORAC 6520
Anthocyanins 558

Pecans 100gm
ORAC 17,524

Blackberry raw 100gm
ORAC 5245
Anthocyanins 317

Walnuts 100gm
ORAC 13,057

Almonds 100gm
ORAC 4282

Red Wine 100gm
ORAC 3873
Anthocyanins 24 - 35


May increase PON-1


Could be that only in the form of wine sublingal absorption of dissolved - most of the studies promoting resveratrol were not oral dosages.

Possible 5-Lipoxygenase Inflammatory Pathway inhibitor

May be increase PON-1 activity.

Oscar Puig, Tian-Quan Cai, Rebecca Kaplan, John Menke, Pek Lum, Gerry Waters, John Thompson, Andy Taggart.
Merck Research Laboratories, Rahway, NJ and Rosetta Inpharmatics, Seattle, WA oscar_puig@merck.com
Oral doses of 1-3 grams of nicotinic acid (NA) per day lower serum triglycerides, raise high density lipoprotein cholesterol, and reduce mortality from coronary heart disease. The molecular mechanism(s) leading to these favorable effects are currently unknown. The leading hypothesis is that NA inhibits lipolysis in adipocytes by acting through the NA receptor GPR109A, thereby reducing serum non-esterified fatty acid levels which leads to an improved lipid profile. However, other mechanisms may account for some of the beneficial effects of NA. In this study we present evidence suggesting that NA has the capacity to activate sirtuins, a class of enzymes that have been shown to extend life span and protect against different forms of cellular stress. Molecular profiling in animals treated with NA revealed gene signatures that statistically overlap with signatures from other nuclear receptors like PPARg, aryl hydrocarbon receptor, mineralocorticoid receptor or steroid receptors. A common link among all these transcription factors is that they are regulated by the acetylation/ deacetylation status through SirT1/NCoR. We therefore investigated whether resveratrol, a known SirT1 activator, and NA would have similar gene signatures. Indeed, our preliminary results suggest that resveratrol and niacin could act in a common pathway by activating sirtuins. NA activation of sirtuins would lead to general cell stress resistance and could explain, at least in part, its beneficial effects in atherosclerosis protection.




From wikipedia:

After ingestion, lycopene is incorporated into lipid micelles in the small intestine. These micelles are formed from dietary fats and bile acids, and help to solubilize the hydrophobic lycopene and allow it to permeate the intestinal mucosal cells by a passive transport mechanism. Little is known about the liver metabolism of lycopene, but like other carotenoids, lycopene is incorporated into chylomicrons and released into the lymphatic system. In blood plasma, lycopene is eventually distributed into the very low and low density lipoprotein fractions.[15] Lycopene is mainly distributed to fatty tissues and organs such as the adrenal glands, liver, and testes.

pyridoxal-5'-phosphate P5P (B6)

May help peripheral neuropathy

A starting dose of 50 mg usually works, to lower homocysteine



??? You can find kaempferol in many berries, including strawberry and cranberry, along with tea (Mayo Clinic is doing research on cranberry and CAD) Dosage?


500-1000 mcg from kelp tablets?

Might act directly in arteries and other tissues. Antioxidant?

As inhibitors of lipid peroxidation, via 50 -monodeion dinase activity, T4 and reverse T3 were found to be more effective in this antioxidant activity than vitamin E, glutathione and ascorbic acid (17).

Lots of thyroid receptors in the heart..

Everything you want to know about iodine is here

Pyridoxamine and pyridoxal-5’-phosphate

It appears to be an anti glycation agent - prevents AGE(Advanced Glycation Endproducts)??


PhosChol PPC (Polyenylphosphatidylcholine ) may also lower lipids? and raise HDL Protects Liver - helps lipids a bit and reduces oxidized lipids. 2700 mg per day

But from :

However, a review of 24 such studies in 1989 suggested that, when controlled for the effect of linolenic acid (lecithin is especially rich in this fatty acid), the cholesterol-reducing effect was eliminated (Knuiman JT et al 1989).

What else? -- lots of paper showing it helps with alcohol liver problems.

Reduces oxidation of LDL???

Oxidation of LDL in baboons is increased by alcohol and attenuated by polyenylphosphatidylcholine

If I understand this right - we want to reduce oxidized LDL - , this seems to be liver protective and might be a good idea for anyone taking niacin? And if it improves lipis and oxidized LDL at the same time

This is an issue.. They found that that betaine supplementation, while effective at lowering homocysteine, also increased LDL cholesterol and triacylglycerol.

This discounts the increased triacylglycerol effect: In our study phosphatidylcholine supplementation slightly increased triacylglycerol concentrations in healthy humans. Previous studies of phosphatidylcholine and blood lipids showed no clear effect. Thus the effect of phosphatidylcholine supplementation on blood lipids remains inconclusive, but is probably not large.

phosphatidylinositol (phosphatidyl-inositol?)

This study has shown that daily PI is well tolerated and will result in significant elevations in HDL-C and apoA-I and reductions in plasma triglycerides when administered at 5.6g per day. Changes in plasma lipid levels were evident after only a few days of treatment and did not reach a plateau by 2 weeks. The most significant effects were observed when PI was administered with food. The increase in HDL-C in fed high dose individuals reached 18% after only 2 weeks of administration. Since niacin can produce little change in HDL-C within 2 weeks, this result may suggest that PI could equal or surpass the efficacy of niacin in longer term studies.

May reduce cortisol?


1.25G BID Lp(a) reductions over 70% -- one small study. May be slight risk here - A human would have to take in 448,000 mg of NAC per day to = this level of mouse intake. - From:

NAC-treated mice developed pulmonary arterial hypertension (PAH) that mimicked the effects of chronic hypoxia.


400 mg - 800 mg FDA did, however give "qualified health claim" status to phosphatidylserine, stating that "Consumption of phosphatidylserine may reduce the risk of dementia in the elderly" and "Consumption of phosphatidylserine may reduce the risk of cognitive dysfunction in the elderly".

phosphatidylserine (PS) might be effective at helping to reduce the effects of cortisol (by lowering it?).

Things to Avoid


Avoid Carbohydrates

Avoid trans fats!

Yes, the AHA diet may be very bad if you have Lp(a)

Vitamin A - cod-liver oil


Exerts from the above paper Vitamin D Council's Dec 2008 News letter

Avoid excess Calcium

Despite the health friendly advise - taking supplemental calcium may not be good for us - I would use VitD3 to prevent osteoporosis instead - or first.


Pro-oxidant appears to make things worse

The next one seems to suggest the opposite

Avoid excess Iron

Pro-oxidant May well make things worse


PCSK9 inhibitors

This paper Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease was called early - twice as many deaths in the statin only group than was expected - the drug lowered LDL yet more heart deaths and more all-cause-mortality. ( do statins not work as well as they think? ) The companies stock dropped after this paper came out.

Thyroid hormone

Lp(a) reductions of up to 50%

Body makes T4:T3 4.22:1 - or about 20% T3 Replacing T4 with T3to achieve 20% T3

T3 +	T4 ≈	T4 equivalent dose μg
5	20	40
7.5	30	60
10	40	80
12.5	50 100
15 60 120
20 80 160
25 100 200
30 120 240
35 140 280
40 160 320
50 200 400
From annals of ???


May reduce Lp(a) up to 59%

Might reduce HDL-C

...BMI was the only predictor of HDL-C in multiple linear regression analysis in both sexes. In conclusion, the important decrease in HDL-C levels observed during puberty in boys in our study seemed to be related to both the testosterone-induced reduction in apo A-I and the reduction in HDL cholesterol content related to BMI.

Can Clomiphene citrate improve lipid numbers where Testosterone degrades ?


Ketamine ??

Ketamine’s anti-in-flammatory effects were discovered over a decade ago (see below) and appear to be mediated through an antagonism of nuclear factor-kappa B (NFKB) based on several lines of evidence: 1) NF-kappa B regulates the transcription of genes that encode the production of proinflammatory cytokines(8-10), and 2) Ketamine suppresses endotoxin induced NFKB expression(11-15).

Looks like it can be administered topically

Pletal (cilostazol)

Raise HDL (often up to 30% or more) It also reduces small LDL quite effectively. Not well studied

Zetia (Ezetimibe)

Not a recommended drug - the lack of CAD outcome improvement once again shows that the LDL theory of CAD is lacking.

Cholesterol Drug Lowers LDL-C Levels But Again Fails to Show Clinical Benefit

Blocks uptake of oxLDL by macrophages?

Blocks the intestines ability to absorb bile cholesterol. If you eventually take Zetia, you can then safely add phytosterols (or stanols = Benecol) to further increase your LDL lowering?

Statin Drugs

Not very effective - NNT says 1 in 83 helped (mortality) in 5 years. - they only LDL lowering drug that has positive mortality effect - the rest don't likely work  - may cuase diabetes or musle damage - memory problems.

Statins may up oxLDL while downregulating the receptor LOX-1

statins reduce inflammation by increasing Vitamin D? Expensive way to increase D - but it appears it reduces inflammation in more ways.

Here it suggests that statins lower oxLDL (I'm not buying this - as a percentage oxLDL can even go up)

It is well known that statins produce muscle damage via CQ10 depletion - but there are other side effects as well:

The above in spite of the fact it reduces depression for some people.

-- hmm from wikipedia IL-12 also has anti-angiogenic activity, which means it can block the formation of new blood vessels - so blocking would allow new blood vessels - could be good for a heart patient - bad for a cancer patient.

And promoting IL-4 induces B-cell class switching to IgE, and up-regulates MHC class II production. promoting of Interleukin-5 has long been associated with several allergic diseases including allergic rhinitis and asthma Promoting IL-10 is capable of inhibiting synthesis of pro-inflammatory cytokines like IFN-γ, IL-2, IL-3, TNFα and GM-CSF (this is a good effect.)

Statins - lowering of tryptophan availability and decreasing of serotonine levels This can be very bad for someone like me -

Methods that lower serum tryptophan are used to induce depression and has the side effect of increasing some inflammation markers. My hunch is that statins may improve mood in some people and cause problems in others. Statins appear to be a 'dirty drugs' - that is drugs that have many multiple actions - and not particularly selective in activity.

My review of the many effects leads me to think that there could be more surprises about statins down the road. My hunch is individual response may be quite varied due to the multiple actions - in other words YMMV!.

Statin drugs Seem to have little or no effect on:

Low HDL (Pitavawstatin? it is important to know which form of HDL is increased )
Small LDL
High triglycerides
Postprandial abnormalities
Statin Metabolic
Lipophilic Lp(a) HDL enodthelial
Smooth muscle
Neovascularization myocardial
Atorvastatin CYP3A4 1.00–1.25

Fluvastatin CYP2C9 1.00–1.25

Lovastatin CYP3A4

Mevastatin CYP3A4

Pitavastatin minimally CYP2C9 + Reduces? Raises Yes


Pravastatin NA -0.75–(-1.0)


Rosuvastatin CYP2C9 and CYP2C19 -0.25–(-0.50)


Simvastatin CYP3A4 1.50–1.75


In the pipeline

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