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Interventions for Preventative Heart Health
Table of Contents
Lowers Lp(a) as much as 46%.
Can cause constipation, and dangerous rebound effects.
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?
- Dietary fish oil enhances macrophage production of nitric oxide J Surg Res. 1994 Jul;57(1):65-8
Omega-3 fatty acids and coronary heart disease risk: Clinical and mechanistic perspectives
Effect of sex and genotype on cardiovascular biomarker response to fish oils: the FINGEN Study
- Beil FU, Terres W, Orgass M, Greten H. Dietary fish oil lowers
lipoprotein(a) in primary hypertriglyceridemia. Atherosclerosis
Omega-3 fatty acids -Their beneficial role in cardiovascular health
W, Biermann J, Kostner GM. Comparison of effects of N-3 to N-6 fatty
acids on serum level of lipoprotein(a) in patients with coronary artery
disease. Am J Cardiol 1995 Sep 1;76(7):459–462.
SM, Kennedy H, Bittolo Bon G et al. Fish intake, independent of apo(a)
size, accounts for lower plasma lipoprotein(a) levels in Bantu fishermen
of Tanzania: The Lugalawa Study. Arterioscler Thromb Vasc Biol 1999
- Possible side effects: Heartburn, indigestion. Nausea at
higher dosages and for some instead of reducing anxiety it increases it.
Insomnia. Rare cases - increase palpitations.
- Bleeding is not a problem.
of bleeding complications with omega-3 fatty acids + aspirin +
clopidogrel--versus--aspirin + clopidogrel in patients with
A Balanced Omega-6/Omega-3 Fatty Acid Ratio, Cholesterol and Coronary Heart Disease
Coco (cocoa powder)
polyphenols and procyanidins
My hunch is polyphenals are not really 'anti oxidants' but instead irritants that work via Hormesis.
of commercially available chocolate- and cocoa-containing products in
the United States. 2. Comparison of flavan-3-ol content with nonfat
cocoa solids, total polyphenols, and percent cacao.
activity and polyphenol and procyanidin contents of selected
commercially available cocoa-containing and chocolate products in the
Concentrations of Proanthocyanidins in Common Foods and Estimations of Normal Consumption
is a Powerful ex Vivo and in Vivo Antioxidant, an Antiatherosclerotic
Agent in an Animal Model, and a Signficant Contributor to Antioxidents
in the European and American Diets.
Cocoa-enriched diet enhances antioxidant enzyme activity and modulates lymphocyte composition in thymus from young rats.
(-)-Epicatechin mediates beneficial effects of flavanol-rich cocoa on vascular function in humans
Flavonoids from Theobroma cacao Down-Regulate Inflammatory Mediators
Dietary flavonoids: effects on endothelial function and blood pressure.
Consumption of flavonol-rich cocoa acutely increases microcirculation in human skin.
diet rich in dietary fiber from cocoa improves lipid profile and reduces malondialdehyde in hypercholesterolemic.
benefits in vascular function through flavanol-containing cocoa in
medicated diabetic patients a double-masked, randomized, controlled
Flavanol-rich cocoa a promising new dietary intervention to reduce cardiovascular risk in type 2 diabetes?
of cocoa flavanols and exercise on cardiometabolic risk factors in
overweight and obese subjects. International Journal of Obesity, vol.
32, p. 1289-1296, 2008. by K. Davison, A.M. Coates, J.D. Buckley and
P.R.C. Howe [PDF: 145 KB posted September 29 2008 (randomized, double-blind placebo controlled human trial)]
flavanols lower vascular arginase activity in human endothelial cells
in vitro and in erythrocytes in vivo. Archives of Biochemistry and
Biophysics, vol. 476, p.211-215, 2008 by O. Schnorr, T. Brossette, T.Y.
Momma, P. Kleinbongard, C.L. Keen, H. Schroeter and H. Sies. [PDF: 224
KB posted September 29 2008 (as the title indicates, this was a
hybrid study, involving both tissue samples, rats and human subjects)]
at heart: the anti-inflammatory impact of cocoa flavanols. Molecular
Nutrition & Food Research, vol. 52, p. 1340-1348, 2008. by C. Selmi;
C.A. Cocchi; M. Lanfredini; C.L. Keen and M.E. Gershwin. [PDF: 221KB posted December 29 2008 (review articles, including review of in vivo evidence).]
effect of a polyphenol-rich cocoa powder industrially processed to
preserve the original flavonoids of the cocoa beans. Journal of
Agricultural and Food Chemistry, vol. 57, p. 6156-62, 2009 by E.
Cienfuegos-Jovellanos, M. del Mar Quinones, B. Muguerza, L. Moulay, M.
Miguel and A. Aleixandre. [PDF: 771KB posted August 31 2009 (study in rats)]
chocolate or tomato extract for prehypertension: a randomised
controlled trial. BMC Complementary and Alternative Medicine, vol. 9, p.
22, 2009 by K. Ri ed, O.R. Frank and N.P. Stocks. [PDF: 355KB posted August 31 2009 (human clinical trial)]
Research Finds Flavanols in Cocoa May Help Treat Diabetes, Strokes and Dementia by Mars, Incorporated [PDF: 42 KB
(secondary source material, really a puff piece for a 2005 meeting of
experts convened by Mars to discuss their research for Cocoa-Via
products, which are no longer being manufactured....much of the research
though was in vivo).]
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?
- Selenium is a component of the enzyme that helps convert T4 to T3 peripherally
- But - excess intake of selenium may also depress T3 levels
- key issue - making sure to get enough, but not too much.
- selenium (deiodinases) allows for the recycling of iodide
- 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. It has been shown to act as an antioxidant in these
Iodine may have a relationship with selenium, and iodine
supplementation in selenium-deficient populations may pose risks for
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-
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..
we get this little tidbit:
Some population surveys have suggested an association between
lower antioxidant intake and a greater incidence of heart disease .
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 . 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??
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
75 mg/kg/d ??? * side effects?? -- Possible down sides?
- 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.
- Reduces aortic stiffness?
Vitamin D Inhibits Monocyte/Macrophage Proinflammatory Cytokine Production by Targeting MAPK Phosphatase-1
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
"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...
- Lowers blood pressure, reduce inflammation (CRP), regulation of calcification, raise HDL?
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."
- Below is a list of summary of actions of Vitamin D (Hormone D) from Nephrology Rounds. 2009; Volume 7, Issue 3:
- reduces cardiac hypertrophy (cardiac enlargement)
- reduces myocardial fibrosis (heart tissue scarring)
- protects against vascular calcifications
- lowers the risk of myocardial infarction
- suppresses renin production (this is the kidney hormone that stimulates angiotensin II leading to elevated blood pressures)
- increases intestinal calcium and phosphorus absorption
- enhances muscle mass/strength
- maintains normal bone formation
- increases insulin sensitivity
- prevents parathyroid gland hyperplasia (enlargement)
- suppresses parathyroid gland hormone (PTH) synthesis
- stimulates the Vitamin D Receptor (VDR) and the Calcium
Senseing Receptor (CaSR) in the parathyroid cells (see my previous
- reduces inflammation
- improves immune function
- reduces nephrosclerosis/glomerulosclerosis (kidney filter scarring)
- reduces the amount of protein in the urine
- slows down the progression of Chronic Kidney Disease (CKD)
- reduces mortality in patients with CKD and End Stage Renal Disease (ESRD)
- promotes cellular differentiation (cell type change)
- inhibits cellular proliferation
- reduces cancer risk and metastatic potential
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
- Persistent fatigue, nausea or anorexia may be a sign of hepatotoxicity.
- Nicotinic acid competes with uric acid for excretion by the
kidneys. Hyperuricemia associated with niacin appears to be more common
- Niacin has been shown to increase plasma homocysteine levels
- Nervous system side effects have included rare reports of
paresthesias, nervousness, dizziness, headache, fatigue, and insomnia.
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 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)
- High dosages of CoQ10 can induce restlessness and
insomnia. Long term side effects of high dose CoQ10 use are not clear at
- minor CoQ10 side effects have been reported, including insomnia, dizziness, Diarrhea, loss of appetite, nausea, stomach upset.
- - [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
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%.
- Fontana P, Mooser V, Bovet P et al. Dose-dependent inverse
relationship between alcohol consumption and serum Lp(a) levels in black
African males. Arterioscler Thromb Vasc Biol 1999 Apr;19(4):1075–1082.
- Marth E, Cazzolato G, Bittolo Bon G, Avogaro P, Kostner GM.
Serum concentration of Lp(a) and other lipoprotein parameters in heavy
alcohol consumers. Nutr Metab 1982;26:56–62.
- Välimeli M, Laithinen K, Ylikahri C, Ehnholm C, Jauhiainen M,
Bard JM, Fruchart JC, Taskinen MR. The effect of moderate alcohol intake
on serum apolipoprotein A-I-containing lipoproteins and lipoprotein(a).
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?
- Barnhart KT, Freeman E, Grisso JA et al. The effect of
dehydroepiandrosterone supplementation to symptomatic perimenopausal
women on serum endocrine profiles, lipid parameters, and health-related
quality of life. J Clin Endocrinol Metab. 1999 Nov;84(11):3896–3902.
reduces formation of oxLDL
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
Reduce blood pressure, amplify action of l-arginine
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
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
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?
of L-carnitine, a naturally occurring peripheral antagonist of thyroid
hormone action, in iatrogenic hyperthyroidism: a randomized,
double-blind, placebo-controlled clinical trial.
- Sirtori CR, Calabresi L, Ferrara S, Pazzucconi F, Bondioli A,
Baldassarre D, Birreci A, Koverech A. L-carnitine reduces plasma
lipoprotein(a) levels in patients with hyper Lp(a). Nutr Metab
Cardiovasc Dis 2000;10:247–251.
Hypertension and Insulin Resistance
Could tryptophan be a link in the depression/inflammation axis of CAD?
- Possible side-effects (mostly in bipolar people?)
- Signs of serotonin syndrome, such as:
- 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%).
- .. mild dehydration side effect symptoms. These include: dry
mouth, gas, weight gain, nausea, dizziness, upset stomach, bloating,
diarrhea and weakness.
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
Possible 5-Lipoxygenase Inflammatory Pathway inhibitor
May be increase PON-1 activity.
- MOLECULAR PROFILING OF GENE REGULATION REVEALS A POTENTIAL LINK BETWEEN NICOTINIC ACID AND SIRTUINS
- 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 email@example.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.
- 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. 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
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
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
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
This is an issue..
They found that that betaine supplementation, while effective at
lowering homocysteine, also increased LDL cholesterol and
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.
- 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?
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
phosphatidylserine (PS) might be effective at helping to reduce the effects of cortisol (by lowering it?).
Things to Avoid
- Kiortsis DN, Tzotzas T, Giral P et al. Changes in
lipoprotein(a) levels and hormonal correlations during a weight
reduction program. Nutr Metab Cardiovasc Dis 2001 Jun(3):153157.
- Müller H, Lindman AS, Blomfeldt et al. A diet rich in coconut
oil reduces diurnal postprandial variations in circulating tissue
plasminogen activator antigen and fasting lipoprotein(a) compared with a
diet rich in unsaturated fat in women. J Nutr 2003;133:3422–3427.
Avoid trans fats!
Yes, the AHA diet may be very bad if you have Lp(a)
- Shin MJ, Blanche PJ, Rawlings RS, Fernstrom HS, Krauss RM.
Increased plasma concentrations of lipoprotein(a) during a low-fat,
high-carbohydrate diet are associated with increased plasma
concentrations of apolipoprotein C-III bound to apolipoprotein
B-containing lipoproteins. Am J Clin Nutr 2007 Jun;85(6):1527–1532.
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 -
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
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.
Lp(a) reductions of up to 50%
- Dullaart RP, van Doormaal JJ, Hoogenberg K, Sluiter WJ.
Triiodothyronine rapidly lowers plasma lipoprotein (a) in hypothyroid
subjects. Neth J Med 1995 Apr;46(4):179–184.
- Martinez-Triguero ML, Hernandez-Mijares A, Nguyen TT et al.
Effect of thyroid hormone replacement on lipoprotein(a), lipids, and
apolipoproteins in subjects with hypothyroidism. Mayo Clin Proc 1998
- Milionis HJ, Efstathiadou Z, Tselepis AD et al. Lipoprotein
(a) levels and apolipoprotein (a) isoform size in patients with
subclinical hypothyroidism: effect of treatment with levothyroxine.
Thyroid 2003 Apr;13(4):365–369.
Cleveland Clinic Foundation in Ohio
have released new findings showing that correcting an underactive
thyroid gland normalizes elevated homocysteine levels in the blood. Even
more amazing is that the researchers were able to normalize
homocysteine levels without having to administer any of the B vitamins.
In other words, correcting the thyroid problem in turn corrected the
vitamin deficiency. (Ann Intern Med 99;131(5):348-51)
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
- SEX HORMONES (TESTOSTERONE, ESTRADIOL, SEX HORMONE-BINDING GLOBULIN) AND HDL-CHOLESTEROL LEVELS IN PUBERTAL SPANISH CHILDREN
- ...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’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
Raise HDL (often up to 30% or more) It also reduces small LDL quite effectively. Not well studied
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?
- side effects seem to include the muscle problems similar to satins..
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?
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 -
Statins may up oxLDL while downregulating the receptor LOX-1
Inhibition of LOX-1 by Statins May Relate to Upregulation of eNOS
- Which says "High concentration of statins (10 μM) was more
potent than the low concentration (1 μM)" Is this effect happening at
the blood levels achieved? (not convinced that t1uM represents a normal
serum level).. If statins up oxLDL - then down regulate the receptor -
is the result a wash?
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
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
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
||CYP2C9 and CYP2C19
In the pipeline