Friday, October 2, 2009

Cardio Controversies: Lp(a) Dangerous at ANY Value

What the heck...?

Can Lp(a) create more damage than we previously thought?

Dr. Hecht has apparently showed it with his examination of lipoprotein, cardiac and metabolic parameter comparisons with the real measure of heart disease risk: EBCT-determined plaque burden. Lp(a) was 3rd after HDL and LDL particle diameter in being highly associated with coronary calcifications. See below. Free PDF HERE. Normally at TrackYourPlaque we consider Lp(a) greater than 20 mg/dl as a high contributor toward accelerated plaque burden. When I look at Dr. Hecht's graphs, what I notice is that indeed this may not be true.

It appears to my observations that at ANY Lp(a) value, plaque burden is quite high reaching even 97th, 98th or 99th calcium percentile for CAD risk (of population norms) at severely low Lp(a) levels of 5 mg/dl or 10 mg/dl.



OK...what the heck?

I can make the same observations for my CAD (heart), PVD (peripheral), or CVD (stroke) patients and individuals with extensive diabetic complications. At any Lp(a), the extent of disease can still be quite pronounced.



What other factors are correlated to vascular damage?

1. Low HDL2b

2. High small dense LDL.

These THREE factors determine almost entirely the extent of disease. Both visionaries Dr. Davis and Dr. Hecht focus on these predominantly to control and halt the progression of calcifications.


How are these 3 metabolic parameters created in the first place?
--low fat SAD AHA low cholesterol low saturated fat diet
--saturated fat deficiency
--excessive carbs (>10 g/d, >20 g/d, >50 g/d, >100 g/d -- depending on a person's insulin and insulin sensitivity and pancreas/adipose/hormone status)
--inflammation (excessive omega-6 oils)


Not... necessarily... a Slo-niacin or Niaspan deficiency...




Saturated Fats Like Butter Beat the Cr*pola Out of Canola in Lowering Lp(a)

We've discussed Dr. Mozaffarian earlier in Part IV Benefits of High-Saturated Fat Diets where he showed higher sat fat (> 12.0%), lower n-6 PUFA and lower carb were associated with less coronary artery stenosis; in fact in the quartile of the highest sat fat dietary intake, regression of coronary artery stenosis was signficantly observed. No other parameter was correlated to regression. Right...! ONLY higher dietary saturated fat consumption... (this quartile also was found to smoke more and took less pharmaceuticals).

Is Krauss in the house?? OK, Dr. Mozaffarian at Harvard has come through again (sort of). He did the right study again (though... 'wrong' conclusions). In his most recent publication Mozaffarian showed that after switching human subjects off of various concentrations of dietary trans fats to different fats (saturated and n-6), dramatic changes in cardiac parameters were noticed (Mozaffarian D, Clarke R. Eur J Clin Nutr. 2009 May;63 Suppl 2:S22-33. Free PDF HERE. ) Butter and other saturated fats were shown to lower the baseline Lp(a) to greater degrees than n-6 PUFAs like soybean, cottonseed, or canola oil.

Butter, palm oil and lard beat canola and other n-6 PUFA oils by 3-4-fold.






Mechanism of Action of: B U T T E R

Butter is comprised of part monounsaturated fats and part saturated fatty acids with one of the predominant acids being BUTYRIC ACID, a 4-carbon chain entity. It turns out that ALL the saturated fatty acids behave much like the omega-3 PUFAs that we enjoy for their plaque-regression, lipoprotein improving, immunomodulating and anti-inflammatory properties. Omega-3 PUFAS bind the whole-pan-PPAR receptor family to shift to LDL larger particles and increase HDL2b. Saturated fats bind most strongly to PPAR-gamma which raises HDLs and and lowers both Lp(a) and Small Dense LDL (particularly LDL-IVb, the 'death band'). They bind weakly to PPAR-delta but sufficiently to paradoxically and P-O-T-E-N-T-L-Y lower inflammation (NFkB, TNF-alpha).

Recall: PPAR-Delta is the Dagger in the Heart of CAD


Saturated fatty acids in fact behave like hormones and bind like steroid nuclear hormones to the PPAR family of receptors (like vitamin-D-to-VDR, carotenoids-to-RXR, vitamin-A-to-RAR, thyroid-to-TR, estrogen-to-ER, etc). This research was done many years ago by Glaxo researchers Eric Xu and others (Molecular Cell, Vol. 3, 397–403, March, 1999). See below. Other researchers defined further the benefits of butyric acid (butyrate) by elucidating its binding activity of PPAR convincingly.


Our b*tt is made out of saturated fats and we eat saturated fats (almonds, coconuts, olives, fatty fish, grassfed beef, free-range eggs/fowl, wild duck, etc). Our body creates, metabolizes and burns saturated fats all day (recall: palmitic acid) esp when we are between meals, intermittent fasting, carb restricting, ketotic, exercising or starving.

Do we make butyrate??



Make Butter (Butyrate) In Your B*TT

Just kidding... North of the rectum (e.g. b*tt), in the colon , short-chain fatty acids like butyric acid (butyrate) one of the fatty acids found in butter, cream and cheeses is produced via anaerobic fermentation of dietary fiber. Our friendly happy gut flora actually produces butyrate (not us). We either consume it or we absorb it from our intestines from bacterial production.

Yes... *haaa* make BUTTER in your colon from vegetable fibers...



Butyrate Protects Against Colon Cancer by Lowering NFkB by Binding PPAR

Furthermore, butyrate has been shown in trials to be anti-inflammatory and immune-modulating. Deficiencies in luminal butyrate synthesis are associated with chronic bowel inflammation. Schwab M et al state:

"Previously, we have demonstrated that the nuclear hormone erceptors Peroxisome-Proliferator-Activated-Receptor (PPAR) and the vitamin D receptor (VDR), transcription factors with anti-inflammatory capacities, are up-regulated and activated by butyrate (Gaschott and Stein, 2003; Gaschott et al., 2001; Schwab et al., 2006;Wachtershauser et al., 2000). PPAR and VDR are highly expressed in the colonic epithelium indicating that both receptors are important agents in the physiology of the human colon (Desvergne and Wahli, 1999; Nagpal et al., 2005). Ligands for both receptors have been shown to interfere with the activity of NFkB and to influence the ability of olonocytes to express immune-modulatory cytokines (Segain et al., 2000; Sun et al., 2006)."

Independently in two labs in 2007, butyrate was found to control NFkB, one of the most potent pro-inflammatory cytokines of our immune system implicated in ALL chronic and acute diseases known to man, including colon cancer and coronary artery disease (Schwab M et al. Molecular Immunology 2007;44: 3625–3632.; Usame M et al. Nutr Res 2008;28:321–328. See end.) The anti-inflammatory power of lauric acid from coconut and palm oil and butyric acid from butter originates from their ability to bind and activiate PPAR-gamma as shown by these studies. PPAR, like the vitamin D receptor (VDR), is one of the master controllers of inflammation. Schwab shows in several publications that butyrate does in fact configure, bind, and activate PPAR receptors. Butyrate is like a DRUG. It binds the most potent receptor for energy balance, immunomodulation, control of lipids (Lp(a), HDL2b, sdLDL), and inflammation! End result... it knocks out NFkB. For the heart, this translates to kicking the cr*pola out of canola in terms of shifting to Pattern 'A', increasing HDL-2b, annihilating small dense LDL and Lp(a) and eradication of vascular atherosclersis.

See Prior Posts:
PPAR






Trying to Target Butter-Receptors: How About Grassfed GHEE??

"There is increasing evidence that the expression and activity of PPARg and VDR are under the control of butyrate implying that the receptors may participate in butyrate-mediated suppression of NFB activation (Gaschott and Stein, 2003; Gaschott et al., 2001; Schwab et al., 2006; Wachtershauser et al., 2000). PPARg and VDR are both ligand-activated transcription factors that belong to the nuclear hormone receptor family and participate in a variety of immune processes (Tirona and Kim, 2005). VDR is widely expressed in epithelial tissues, cells of the immune system and several cancer cell lines including colorectal cancer cells (Giuliano et al., 1991; Segaert and Bouillon, 1998). PPARg is activated by natural ligands such as fatty acids and eicosanoids and is highly expressed in colonic epithelium, indicating an important role of the receptor in the physiology of the human colon (Desvergne and Wahli, 1999). All these characteristics make both receptors potential targets in butyrate-mediated inhibition of NFkB signalling."





In Vivo (Live Humans) High Intake of Butter Associated with Reduced Colon Cancer

Of course Swedish researchers examined their nutrition data registry for the Swedish Mammagraphy Cohort and lo and behold found distinct correlations between high dairy intake and low colon cancer (Am J Clin Nutr. 2005 Oct;82(4):894-900.) Those in the upper 2 quartiles of CLA consumption and > 4 servings daily of high-fat dairy was highly associated with reduced colon cancer risk. The author's conclusions were: These prospective data suggest that high intakes of high-fat dairy foods and CLA may reduce the risk of colorectal cancer.



Diary Fat Potential Anti-Carcinogenic Agents

Parodi reviews the literature and reports that... "About one third of all milk triacylglycerols contain one molecule of butyric acid, a potent inhibitor of proliferation and inducer of differentiation and apoptosis in a wide range of neoplastic cell lines. Although butyrate produced by colonic fermentation is considered important for colon cancer protection, an animal study suggests dietary butyrate may inhibit mammary tumorigenesis. The dairy cow also has the ability to extract other potential anticarcinogenic agents such as beta-carotene, beta-ionone and gossypol from its feed and transfer them to milk (J Nutr. 1997 Jun;127(6):1055-60. Free PDF HERE). Grassfed cheese, cultured milk, yogurt, ghee, and butter also contain CLA. Parodi discusses that, "Recent research shows that milk fat contains a number of potential anticarcinogenic components including conjugated linoleic acid, sphingomyelin, butyric acid and ether lipids. Conjugated linoleic acid inhibited proliferation of human malignant melanoma, colorectal, breast and lung cancer cell lines. In animals, it reduced the incidence of chemically induced mouse epidermal tumors, mouse forestomach neoplasia and aberrant crypt foci in the rat colon. In a number of studies, conjugated linoleic acid, at near-physiological concentrations, inhibited mammary tumorigenesis independently of the amount and type of fat in the diet."




Beef Tallow SYNERGISTICALLY Beats the Cr*pola Out of Corn Oil (n-6 PUFA)

In another interesting animal study (mice), beef tallow (25% palmitic acid; 50% oleic acid) increased the potency of CLA in decreasing mouse mammary tumor metastasis. (J Nutr. 2006 Jan;136(1):88-93.) "Linoleic, oleic, stearic, and palmitic acids, either did not change or enhanced the cytolytic effects of CLA isomers on mouse mammary tumor cells in culture." The authors found that oleic + palmitic enhanced cytolytic CLA-derived tumor cell death, whereas n-6 PUFAs (linoleic acid) were associated with dose-dependent increases in tumorigenesis and blocking CLA-benefits.

See Prior Post:
Happy Cows and CLA (CLA is found in grassfed beef, dairy, lamb, pastured pork)




Rat Study: ONLY Olive Oil and n-6 PUFAs Associated with Cancer Model in High-Fat Diets

Rats are not humans but they have no gall bladders... so they are not unlike 80% of the individuals that I see who fail to have functioning gallbladders. Anyhow in this one study 4 high fat diets (corn, lard, beef tallow and coconut oil) and 1 low fat corn oil were used in 5 rat groups (Chan PC et al. Cancer Res. 1983 Mar;43(3):1079-83.). Mammary tumors were induced with N-nitrosomethylurea. Incidence of tumors in the high-fat groups was the lowest in the coconut oil group. Upon further analyses (these researchers were GOOD), they concluded, " the total oleic and linoleic acid intake in the five groups of rats correlated positively (r = 0.95) with mammary tumor incidence."




Role of Oliv-ola (Canola+Olive oil) Induced Colon Carcinogenesis:
Coconut Oil Beats the Cr*pola Out of OLIVOLA

Nair J et al in Germany have been conducting research in DNA damage associated with oils (Nair J et al. Mutat Res. 2007 Nov 1;624(1-2):71-9.) They tested LA (linoleic acid, n-6 PUFA), oleic acid and coconut oil in rats by lavaging them for 30day, sacrificing, then measuring etheno-DNA adducts in the organs. Etheno-DNA adducts are associated with j*cked up gene expression, mutations and carcinogenesis. They are produced by oxidative stress and lipid peroxidation. Their research showed that n-6 PUFAs have gender-specific toxicity and other surprising results. Not unlike the Israeli 'Paradox' (see below), female LA-treated rats showed increases in etheno-DNA adducts in the DNA of their circulating immune cells, the all important WBC (white blood cells). For both genders, colon was the target for stress-derived DNA-adducts in omega-6-PUFA treated rats, which supports the role for omega-6 induced colon cancer, the authors concluded.

'Unexpectedly, olive oil treatment enhanced entheno-adduct levels in prostate 3-9-fold' the researchers observed.

What... the... H E C K ?

So... olive oil (n-9 monounsaturated) is highly implicated in TWO studies with cancer: mammary and prostate. Is this only seen in certain situations?

Lame-o retard-o dietary fat composition?

Saturated fatty acid deficiencies?

Omega-3 deficiencies?

Most lab rats are vitamin D deficient as well...



Here is other provocative (ok, not really) research showing the same thing in more in vivo animal cancer model studies:
--coconut oil beats the cr*pola out of n-6 PUFAs
--MCT oil (50% of coconut oil) beats the cr*pola out of n-6 PUFAs
--the lower the rat cholesterol, the higher the incidence of mammary tumorogenesis... in other words (switch around), the larger the LDL particles induced by saturated fatty acids which results in a higher total cholesterol, the lower the risk of breast cancer in rats. Applies to humans too.

Dietary fat and mammary cancer. II. Modulation of serum and tumor lipid composition and tumor prostaglandins by different dietary fats: association with tumor incidence patterns.
Cohen LA, Thompson DO, Choi K, Karmali RA, Rose DP.
J Natl Cancer Inst. 1986 Jul;77(1):43-51.


Dietary fat and mammary cancer. I. Promoting effects of different dietary fats on N-nitrosomethylurea-induced rat mammary tumorigenesis.
Cohen LA, Thompson DO, Maeura Y, Choi K, Blank ME, Rose DP.
J Natl Cancer Inst. 1986 Jul;77(1):33-42.


Influence of dietary medium-chain triglycerides on the development of N-methylnitrosourea-induced rat mammary tumors.
Cohen LA, Thompson DO, Maeura Y, Weisburger JH.
Cancer Res. 1984 Nov;44(11):5023-8.
Medium chain triglycerides (MCT) in aging and arteriosclerosis.
Kaunitz H.
J Environ Pathol Toxicol Oncol. 1986 Mar-Apr;6(3-4):115-21.




So I've digressed... let's get back to the heart of the matter...


n-6 PUFAs Shrink LDL-Particles... To Pattern B (BAD)

Shrinkage... Not. Good. The rest of the Mozaffarian and Clarke's conclusions are not so justified by the medical literature. They further try to discuss the cardiac benefits of the n-6 vegetable oils without acknowledging the metabolic parameters that Drs. Hecht, Krauss, Superko and Davis support as the factors that are most highly correlated to plaque burden: LDL particle size, HDL2b and Lp(a). Unfortunately I find their so-called cardiac assertions kinda b-u-n-k-y. They employ parameters (TC/HDL ratio, apoB/AI ratio, CRP) that are not borne out to be associated with coronary calcium plaque burden or serial plaque progression according to Hecht's 2003 publication.

n-6 PUFA and olive oil are necessarily heart healthy?? No. In a study with rapeseed, olive oil or sunflower oil, LDL particles significantly (p=0.012) shifted to smaller, dense particles with all the oils tested, after a switch from a two-week saturated fat diet. BUNKY!!! See below.


Dietary mono- and polyunsaturated fatty acids similarly affect LDL size in healthy men and women.

Kratz M, et al. J Nutr. 2002 Apr;132(4):715-8.


The goal of this study was to investigate the effect of the dietary fat composition on LDL peak particle diameter. Therefore, we measured LDL size by gradient gel electrophoresis in 56 (30 men, 26 women) healthy participants in a controlled dietary study. First, all participants received a baseline diet rich in saturated fat for 2 wk; they were then randomly assigned to one of three dietary treatments, which contained refined olive oil [rich in monounsaturated fatty acids (MUFA), n = 18], rapeseed oil [rich in MUFA and (n-3)-polyunsaturated fatty acids (PUFA), n = 18], or sunflower oil [rich in (n-6)-PUFA, n = 20] as the principal source of fat for 4 wk. Repeated-measures ANOVA revealed a small, but significant reduction in LDL size during the oil diet phase (-0.36 nm, P = 0.012), which did not differ significantly among the three groups (P = 0.384). Furthermore, affiliation with one of the three diet groups did not contribute significantly to the observed variation in LDL size (P = 0.690). In conclusion, our data indicate that dietary unsaturated fat similarly R E D U C E S LDL size relative to saturated fat. However, the small magnitude of this reduction also suggests that the composition of dietary fat is not a major factor affecting LDL size.
PMID: 11925466





n-6 PUFAs Cause Inflammation and Cancer: Israeli Experience

Shapiri discusses how changing from traditional oils (saturated fats like schmaltz (rendered goose or chicken fat w/onions) or beef tallow) to a high consumption of n-6 PUFA oil is postulated to have lead to the astronomic rise in cancer in Israeli Jewish women (Eur J Cancer Prev. 2007 Oct;16(5):486-94.)

It is discussed HERE as well.


Wanna CUPPA of CANCER? Increase your n-6 PUFAs, reduce your saturated fatty acids.





Small Dense LDL, OxLDL and Lp(a) SYNERGISTICALLY Grow Plaque

Why is Lp(a) so extremely toxic and an accelerant for all damage whether it is diabetic complications (microvascular: eyes - kidney - nerves - penile - brain (e.g. Type 3.0 Diabetes)) or atherosclerotic disease (macrovascular: heart, carotid, peripheral)? Apparently Lp(a) binds oxidized phospholipids of apoB 100 which is attached to all LDL, including Lp(a). What is Lp(a)? It is just LDL + apo(a) combined. Large LDL are rarely oxidized -- they are protected by size, buoyancy, high cholesterol content (yes, cholesterol is an 'antioxidant') and a high content of vitamins and fat-soluble antioxidants (ubiquinols, carotenoids, menaquinones (vitamin K2s), tocopherols, tocotrienols) and apo E (carriers of minerals and other vital micronutrients).



A novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma.

Bergmark C, et al. J Lipid Res. 2008 Oct;49(10):2230-9. Free PDF HERE.

Oxidized phospholipids (OxPLs) on apolipoprotein B-100 (apoB-100) particles are strongly associated with lipoprotein [a] (Lp[a]). In this study, we evaluated whether Lp[a] is preferentially the carrier of OxPL in human plasma. The content of OxPL on apoB-100 particles was measured with monoclonal antibody E06, which recognizes the phosphocholine (PC) headgroup of oxidized but not native phospholipids. To assess whether OxPLs were preferentially bound by Lp[a] as opposed to other lipoproteins, immunoprecipitation and ultracentrifugation experiments, in vitro transfer studies, and chemiluminescent ELISAs were performed. Immunoprecipitation of Lp[a] from human plasma with an apolipoprotein [a] (apo[a])-specific antibody demonstrated that more than 85% of E06 reactivity (i.e., OxPL) coimmunoprecipitated with Lp[a]. Ultracentrifugation experiments showed that nearly all OxPLs were found in fractions containing apo[a], as opposed to other apolipoproteins. In vitro transfer studies showed that oxidized LDL preferentially donates OxPLs to Lp[a], as opposed to LDL, in a time- and temperature-dependent manner, even in aqueous buffer. Approximately 50% of E06 immunoreactivity could be extracted from isolated Lp[a] following exposure of plasma to various lipid solvents. These data demonstrate that Lp[a] is the preferential carrier of PC-containing OxPL in human plasma. This unique property of Lp[a] suggests novel insights into its physiological function and mechanisms of atherogenicity.




Butyrate NFkB References

Involvement of different nuclear hormone receptors in butyrate-mediated inhibition of inducible NF kappa B signalling.
Schwab M, Reynders V, Loitsch S, Steinhilber D, Stein J, Schröder O.
Mol Immunol. 2007 Jul;44(15):3625-32. Epub 2007 May 22.

Role of nuclear hormone receptors in butyrate-mediated up-regulation of the antimicrobial peptide cathelicidin in epithelial colorectal cells.
Schwab M, Reynders V, Shastri Y, Loitsch S, Stein J, Schröder O.
Mol Immunol. 2007 Mar;44(8):2107-14. Epub 2006 Oct 19.

PPARgamma is a key target of butyrate-induced caspase-3 activation in the colorectal cancer cell line Caco-2.
Schwab M, Reynders V, Ulrich S, Zahn N, Stein J, Schröder O.
Apoptosis. 2006 Oct;11(10):1801-11.

10 comments:

Stephan Guyenet said...

Hi G,

What do you think about the idea that Lp(a) is a marker of oxLDL? That seems to be one of the things I've come across in my reading. I've been enjoying your series.

Dr. B G said...

Hey Stephan,

Thank you!

I hadn't heard of that yet! It is definitely conceivable. (I'm kinda cheap*ss -- why pay for certain unvalidated tests when we already know the surrogates and the causes) That might be a great idea in this neolithic age. I do wonder though is Lp(a)/OxLDL just prevalent as a part of the normal standards b/c our normal population is sick? Not unlike thyroid , our lab values for TSH 'norms' have shifted but really it just that no one is truly euthyroid (incl me). Maybe that is the same case of Lp(a)/OxLDL. Everyone has it. Children w/MetS and obesity included. (I believe it starts in utero... I look forward to your facial structure series. n-6 PUFA in utero are TERRIBLE. Just TERRIBLE. Affects TSH and genetic expression which affects bone development *sigh*)

Interestingly, I don't know if you have come across this in your readings, Lp(a) is high in certain centenarians. It can be protective. Who? I dunno... maybe those with CETP SNPs associated with Pattern A, high HDL2b, and low LDLIVb like the Ashkenazi Jewish? Or other polymorphisms??

Also, to me, African Americans exhibit symmetrical apo (a) and Lp(a) particles. They also appear resistant (again just anectdotally to me) to certain diabetes complications, strokes and even heart attacks.

HHHMMMmm... it's all kinda fascinating. I'm trying to preserve my brain from OxLDL damage (though Dr. T argues the kidneys are more important *haaaa*).

As well as AGEs and ALEs.

It's all the same aint it.

-G

Mario Renato said...

Hi Doctors!

Dr. Stephan, the "thing" you've come across (Lp(a) x oxLDL), it's the supplement doc of "Changes in dietary fat intake alter plasma levels of oxidized low-density lipoprotein and lipoprotein(a)"????

http://www.ncbi.nlm.nih.gov/pubmed/14739118

That can be read here:
http://atvb.ahajournals.org/content/vol24/issue3/images/data/498/DC1/ATVB0794.DOC

Pretty strong association to me...

lightcan said...

Brilliant post.
It is fascinating for me too. I just met some people for whom it wasn't and I was surprised... They don't even know that LDL is not 'bad' and they don't care...
Please do continue to enlighten us with your musings on this amazing research.
re Lp(a) it's amazing how everything has its own role in the body. from Tsimikas et al 2005:
Possibly Lp(a) binds and detoxifies proinflammatory OxPL to provide protection from various oxidative stressors (wound healing); found in centenarians, may act as CRP, as an acute phase reactant.

Dr. B G said...

Mario,

Thanks for the link of the graph.

I have the PDF if anyone wants -- just email.



lightcan,

OxLDL and the ratio OxLDL/apoB are quite fascinating. Statins raise these. Either both or one. Both are associated and predict CAD events (Bruneck trial) as one might guess. Why? Coz oxidized anything, esp LDL is bad news. Oxidized Lp(a) is even WORSE.

Again at TYP, I have yet to see anyone have regression on coronary calcifications on a statin with Pattern B. It doesn't happen. There are many theories but I think is involves OxLDL and dense LDL.

Now Lp(a)... quite dangerous at any level. Just like FRUCTOSE.

I agree - I think Lp(a) is quite powerful and can actually detoxify. What circumstances??

Apo(a) has a promoter area in the DNA encoding region for estrogen to bind. Studies show that estrogen controls and lowers apo(a) and Lp(a) (in men and women -- any kind of estrogen -- horsey, synthetic, natural, phytoestrogen, etc ALL WORK).

Insulin and adiponectin -- they oppose each other. Low carb lowers insulin AND Lp(a). High fat/low carb raises adiponectin and lowers Lp(a).

All the above (estrogen, low insulin, high adiponecting) subsequently lead to high HDL, low TG and low dense LDLs/Pattern A.

You have neat thoughts!

-G

lightcan said...

Well, I have to get my act together with such high LDL (if you remember I said my LDL was 319) and I can't count on my doctor who wants me on high dose statin, so I have to do my own pathetic research. What better place there is than your blog?
Thanks.

Dr. B G said...

lightcan,

You are on the definitely the RIGHT TRACK!

What is your heartscan? Positive or negative? Family history of event?

If either are positive, yes I would choose an aggressive approach the first 24-36 months of your program. If the knuckleheads at the HATS trial (4g/day niacin) and in the case studies I am presenting can achieve regression (again, niacin 4g/day), then absolutely, so you can. It takes 3 yrs in the trials to achieve nice labs.

Our TYP advanced members (statin-less, or on the way to becoming statin-less) achieve it in 1-3 months.

I have this obscene confidence that anyone can achieve regression. Like a cancer, maximal lifespan can be achieved once the growth is arrested and halted.

-G

lightcan said...

I don't know what my heart scan is, you mean calcium score? My father had a heart attack at 71 so it doesn't count does it? His parents lived very long (88, 96), my grand parents on the other side not so much.
I read your most recent post with your recommendations for that particular case and it seems like a heck of a lot of supplements but I'll see what I can do. I liked the 'drop the olive oil' bit and the real age is your blood vessels' age.

Dr. B G said...

lightcan,

Did you inherit the lipoprotein pattern from your father's side? Hopefully the longevity genes as well!!

YES. Supplements are GREAT. I've actually tried them ALL except the hormones (I'm too young).

Our nutrition no matter how wonderful just cannot support life extension to the maximum - max quality, max quantity. Currently we live in a world overpolluted with depleted soils and excessive chemicals. Are you familiar with Bruce Ames work? He found that even one essential nutrient deficiency leads to DNA damage equivalent to radiation damage. No part of the world contains ALL the nutrients that humans require for 'optimal' health and biochemical reactions. Perhaps that is how certain genetic conditions evolved (like insulin resistance, thalessemia, hemachromatosis, etc).

Actually... many of supps prevent wrinkles *haa*. Niacin has a few nice trials that shows it improves skin (that's WHY I take it intermittently).

Now you know my secret.

-G

lightcan said...

Well, I think that low T3 gives me wrinkles and dry, saggy skin and after all that effort of losing fat I just look marginally better ... from behind. Talk about premature ageing at 40! I'm taking about 1 g of vit C and glucosamine sometimes MSM, Se, Zn and carotenoids from algae to help with the collagen production, it seems that it's not enough though. I should definitely take Coq10 100 mg or ubiquinol 50 mg for my gums. I have to find a good source.
It's hard to know what lipid profile I've inherited now that my parents are both sick. My father was told by his doctor that he had hypercholesterolemia, but that's nonsense, he had TC 230 and as we know that means nothing. He was told that because he didn't have any other of the risk factors (that they know about) for heart attack being a skinny nonsmoker vegetarian.
My grand father died at 96 because he started eating sugar from the bag with the spoon, maybe because he had dementia or some form of brain damage (maybe Alzheimer's, I wasn't at home for the last 17 years) After my grandmother died he used to fight stubbornly with everybody and he used to go out on his own, with people on the street bringing him home after he fell, in the end my father had to be his nurse and it was hard for both of them. See, no vitamin D, no social life, no exercise, no good diet, the end.