Lab tests: high lipoprotein(a), any suggestions ?

Hello everyone. I just got some tests back. Any recommendations on how to deal with high lipoprotein (a) ?

I have also read the forum and found this: http://www.healthcentral.com/heart-disease/c/1435/44295/lipoprotein/

Have a great weekend !!

Le résultat de la prise de sang du 07/02/2014 :

ASPECT DU SERUM : Limpide ( )

------------------------ : HEMATOLOGIE ( )

------------------------ : ----------- ( )

GLOBULES ROUGES : 4.72 ( (4.40 - 6.50) )

HEMOGLOBINE : 15.0 ( (13.0 - 18.0) )

HEMATOCRITE : 42.7 ( (40.0 - 54.0) )

M C V : 90 ( (80 - 99) )

M C H : 32 ( (26 - 34) )

M C H C : 35 ( (30 - 36) )

GLOBULES BLANCS : 4550 ( (4000 -11000) )

FORMULE LEUCOCYTAIRE : . ( )

NEUTROPHILES : 45.7 ( (35 - 70) )

EOSINOPHILES : 1.8 ( (0.0 - 6.0) )

BASOPHILES : 0.4 ( (0.0 - 2.0) )

LYMPHOCYTES : 44.2 ( (20 - 45) )

MONOCYTES : 7.9 ( (2.0 - 13.0) )

COMPTAGE LEUCOCYTES : . ( )

NEUTROPHILES : 2079 ( (1400 - 6700) )

EOSINOPHILES : 81 ( (0 - 300) )

BASOPHILES : 18 ( (0 - 100) )

LYMPHOCYTES : 2011 ( (1200 - 3500) )

MONOCYTES : 359 ( (100 - 1000) )

PLAQUETTES : 2.10 ( (1.40 - 4.40) )

PLAQUETTES : 210 ( (140 - 440) )

FER : 106 ( (59 - 158) )

FERRITINE : 185 ( (30 - 400) )

VITAMINE B12 : 658 ( (191 - 663) )

ACIDE FOLIQUE : 19.3 ( (4.6 - 18.7) )

------------------------ : COAGULATION ( )

------------------------ : ----------- ( )

FIBRINOGENE : 249 ( (200 - 400) )

------------------------ : CHIMIE ( )

------------------------ : ------ ( )

CRP : < 0.1 ( (< 0.5) )

GLYCEMIE : 86 ( (74 - 109) )

PROTEINES TOTALES : 7.9 ( (6.6 - 8.7) )

CREATININE : 0.8 ( (< 1.2) )

CLEARANCE MDRD : 114 ( (> 60) )

GOT (AST) : 19 ( (< 40) )

GPT (ALT) : 20 ( (< 41) )

GAMMA-GT : 14 ( (8 - 61) )

SODIUM : 139 ( (136 - 145) )

POTASSIUM : 4.0 ( (3.5 - 5.1) )

CHLORURES : 101 ( (96 - 107) )

BICARBONATE : 28 ( (22 - 29) )

MAGNESIUM (ERYTHROC.) : 4.9 ( (2.8 - 6.6) )

CALCIUM : 10.0 ( (8.6 - 10.4) )

------------------------ : BILAN LIPIDIQUE ( )

------------------------ : --------------- ( )

LP(A) : 180 ( (< 30) )

------------------------ : VITAMINES ( )

------------------------ : ---------- ( )

25 OH VITAMINE D : 59 ( (30-100[VID]) )

------------------------ : SEROLOGIE INFECTIEUSE ( )

------------------------ : --------------------- ( )

HELICOBACTER PYLORI IGA : < 15 ( (<15:N;>20:P) )

------------------------ : !R!FONT 6;EXIT; ( )

------------------------ : ( )

------------------------ : Attention : changement de technique et de valeurs de référence ?partir d ( )

------------------------ : 01/09/2013 ( )

CHLAMYDIA TRACHOMATIS IGG : < 9.0 ( (<9=N;>11=P) )

CYTOMEGALOVIRUS IGG : < 1.0 ( (< 1.0) )

------------------------ : BILAN THYROIDIEN ( )

------------------------ : ---------------- ( )

TSH : 3.7 ( (0.27 - 4.20) )

A.C. ANTI-THYROIDIENS : . ( )

ANTI-TPO : 2 ( (1 - 16) )

------------------------ : HORMONES ( )

------------------------ : -------- ( )

CORTISOL 7-10H : 11.8 ( (6.2 - 19.4) )

------------------------ : Nouvelle technique et valeurs de référence ?partir du 11/12/2013 ( )

CORTISOL LIBRE : 0.3 ( (0.6 - 2.2) )

TRANSCORTINE (C.B.G) : 74.9 ( (33 - 46) )

IGF-1 : 174 ( (84 - 250) )

TESTOSTERONE TOTALE : 579 ( (250 - 840) )

TESTOSTERONE LIBRE : 13.2 ( (6 - 18) )

DHEA SULFATE : 397 ( (160 - 449) )

S H B G : 30 ( (18 - 54) )

OESTRADIOL : 35 ( (7.63 - 42.6) )

PROLACTINE : 6 ( (4 - 15) )

It's a good article on Lipoprotein(a). The only thing they left out is that tocotrienols are quite effective and it happens to help grow hair. I should also point out that the more aggressive the hair loss, the more likely the Lp(a) levels are higher than they should be.

I take it at least once per day.

http://www.iherb.com/Jarrow-Formulas-Toco-Sorb-Mixed-Tocotrienols-and-Vitamin-E-60-Softgels/137

Thanks a lot Brian!

Study shows a positive effect of gingko biloba:

http://www.ncbi.nlm.nih.gov/pubmed/17397850

Niacin has also been used to lower LpA levels. However, there have been several reports here of niacin promoting greater hair loss, so that would be a component to look into.
But as far as the anti-atherosclerotic benefits, the management of LDL would be a benefit.

Overall, I think CS has got it right with the antioxidants. LpA is kind of like cholesterol in that high levels have been correlated to heart problems, but the actual function of LpA isn't truly known. Its kind of just a bystander who happens to be there and no one really understands how it actually contributes. The real issue is oxidized fats, so control over dietary fat types and taking stuff like vitamin E, gingko, EGCG, curcumin, vit C,   you name it...its all going to be protective.

This is what I gathered so far on the forum: Niacin (3000mg), vitamin C, krill oil, tocotrienols, L-carnitine, L arginine, ubiquinol CoQ10, L-Lysine and L-proline, alpha lipoid acid, and Ginko should all lower lipoprotein a.

Could it be that my lipoprotein is so high due to an infection, e.g. mononucleosis ?

And what about my free Corsisol, it's quite low: 0,3 !!

And also what about my Thyroid, do the tests show its slow ?

Thanks for the help guys!

Anyone tried omega 7 stuff ?

Like this:

http://www.iherb.com/SeaBuckWonders-Sea-Buckthorn-Oil-Blend-Omega-7-Complete-500-mg-120-Softgels/34922#p=1&oos=1&disc=0&lc=en-US&w=omega%207&rc=496&sr=null&ic=3

btw if I have anti-tpo does it mean I can have also hashimoto ?

Danny and Dr. Kharrazian seem to think is not good to supplement Iodine, and I'm currently supplementing...

http://www.dannyroddy.com/main/2010/10/25/iodine-supplements-suck-for-hair-loss-too.html

http://www.jlr.org/content/early/2004/04/21/jlr.R300019-JLR200.full.pdf

Infection, or any source of inflammation, can alter the lipid profile. Eliminating inflammation, in part by altering the fats in the diet, reducing infection, metals, managing blood sugar, etc - these will all correct lipid profiles.

So lipoprotein A levels aren't diagnostic for infection, but infection can lead to them. Mostly because the acute inflammatory response that occurs early on leads to altered fat metabolism.

There is a connection between elevated LpA and H Pylori, which could be worth checking for as its a more common one. Overall, your immune cell counts don't immediately point to infection, but that isn't always a sure-fire sign with some types of cryptic species.

Overall I'd look to correct every other possibility that was manageable: diet (particularly fats), control carb consumption, take some dedicated antioxidants (C, E, NAC), get some exercise, ensure adequate and quality sleep. See what happens to those levels. If things are persistent and don't respond to these lifestyle changes, then perhaps begin to look for some form of chronic infection. Again, disrupted stomach acid levels, GI histamine, altered bowel movements, fat in the stool, stomach/intestinal pain, can all be indicative of bad gut bacteria, including H Pylori if its present.

With the thyroid, the antibodies aren't high so I wouldn't be concerned with this. Most of us have some small amount of these antibodies. They'd be much higher if you had Hashi's.

radiance wrote:btw if I have anti-tpo does it mean I can have also hashimoto ?

Danny and Dr. Kharrazian seem to think is not good to supplement Iodine, and I'm currently supplementing...

http://www.dannyroddy.com/main/2010/10/25/iodine-supplements-suck-for-hair-loss-too.html

I wrote a comment on that article - It's junk science. Iodine is an essential element needed in all cells.
Dr. Kharazzian is dead wrong.

AS54 - There are many earlier posts in years past on this topic. Lipoprotein(a). There is an inverse association with iodine. I believe the "heart" of Lp(a) is both related thyroid hormones and possibly estrogen receptor modulation.

CausticSymmetry wrote:

radiance wrote:btw if I have anti-tpo does it mean I can have also hashimoto ?

Danny and Dr. Kharrazian seem to think is not good to supplement Iodine, and I'm currently supplementing...

http://www.dannyroddy.com/main/2010/10/25/iodine-supplements-suck-for-hair-loss-too.html

I wrote a comment on that article - It's junk science. Iodine is an essential element needed in all cells.
Dr. Kharazzian is dead wrong.

and this guy sell an expensive book online.. Im wondering if you have an opinion regarding his "new version" since his book was debated here ?

I wrote this a few years ago, which explains away the false paradigm of "autoimmune" reaction over an essential mineral

Can Iodine cause Autoimmune Thyroid Diseases?

According to Dr. Guy Abraham, former professor of obstetrics, gynecology, and endocrinology at UCLA School of Medicine, the answer to this is "No." An autoimmune thyroid condition cannot be caused by inorganic iodide unless first combined with toxic halides (i.e. fluoride, bromide, chloride), which are goitrogenic substances that can exacerbate an iodine deficiency. Goitrogens are substances that suppress the function of the thyroid gland by interfering with iodine uptake.

The following is only a cursory explanation of how an autoimmune thyroid problem may manifest; a more thorough one can be found in Dr. David Brownstein's book, Iodine, why you need it, why you cannot live without it.

In order to create autoimmune thyroiditis in laboratory animals, anti-thyroid drugs and/or goitrogens must be administered along with iodine. The main problem is that insufficient dietary iodine allows these goitrogens to block iodine activity, and subsequently thyroid hormone which cannot be made without sufficient iodine.

When there is sufficient iodine in the body, it can produce iodinated lipids, which help protect against an autoimmune thyroid disorder. The problem today is that iodine consumption is so low, combined with our exposure to numerous toxic halides, that iodine may not be in adequate supply to produce iodinated lipids. In fact, it can require up to 100 times the RDA of iodine to produce these lipids. Some individuals with fibromyalgia require dosages of up to 100mg per day for benefits.

When there is an inadequate supply of iodine (iodide) for the thyroid gland, at the same time iodine binding sites are blocked (by competitive inhibition of iodine) by toxic halides (goitrogens), this is believed to activate the thyroid peroxydase (TPO) system through elevated TSH (Thyroid Stimulating Hormone). In turn, insufficient levels of iodinated lipids, combined with insufficient levels of magnesium can result in excess production of hydrogen peroxide.

Essentially the level of hydrogen peroxide is well above normal due to lack of a feedback system. When working properly, this feedback system acts as a "brake" to shut off excess hydrogen peroxide and keep it from causing damage to thyroid peroxydase (TPO) and thyroglobulin.

The damage to TPO and thyroglobulin elicits an autoimmune reaction via the production of antibodies, creating damage to thyroid cells and resulting in potential Hashimoto's or Grave's disease.

Thanks for all the answers!

I definitively feel better now

I'll stick to my regimen and report back with some other tests in 6 months from now!!

Have a great day!

CS,

Nice post on the iodine. And the thyroid connection to LpA makes total sense.

Here's something relevant. Since the Lancent published in 2000, the link between AGA and cardiovascular diseases. It was Lp(a) that was the distinguishing factor.

Here's an update:

Indian Dermatol Online J. 2013 Oct;4(4):283-7. doi: 10.4103/2229-5178.120638.
Androgenetic alopecia and risk of coronary artery disease.
Sharma L1, Dubey A1, Gupta PR2, Agrawal A3.

BACKGROUND:
Androgenetic alopecia (AGA) or male pattern baldness (MPB) has been found to be associated with the risk of coronary artery disease (CAD). The well-known risk factors are family history of CAD, hypertension, increased body mass index (BMI), central obesity, hyperglycemia, and dyslipidemia. The newer risk factors are serum lipoprotein-a (SL-a), serum homocysteine (SH), and serum adiponectin (SA).
AIM:
Identifying individuals at risk of CAD at an early age might help in preventing CAD and save life. Hence, a comparative study of CAD risk factors was planned in 100 males of AGA between the age of 25 and 40 years with equal number of age- and sex-matched controls.
MATERIALS AND METHODS:
Patients of AGA grade II or more of Hamilton and Norwood (HN) Scale and controls were examined clinically and advised blood test. The reports were available for fasting blood sugar (FBS), serum total serum cholesterol (SC) in 64 cases, 64 controls; lipoproteins (high, low, very low density, HDL, LDL, VLDL), serum triglycerides (ST) in 63 cases, 63 controls; SL-a in 63 cases, 74 controls; SH in 56 cases, 74 controls; and SA in 62 cases, 74 controls.
RESULTS:
In these cases family history (FH) of AGA and CAD was significantly high. The blood pressure (BP) was also found to be significantly high in the cases. The difference of mean serum HDL, LDL, VLDL, ST, SH, and SL-a in cases and controls were statistically significant and with increasing grade of AGA, the risk factors also increased.
CONCLUSION:
Patients with AGA appear to be at an increased risk of developing CAD, therefore, clinical evaluation of cases with AGA of grade II and above may be of help in preventing CAD in future.

Full study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853891/

"A significant elevation in SL-a was found in cases as compared to controls which has also been reported earlier.[21] Increased level of SL-a is said to be associated with endothelial dysfunction and heart disease as it has a structure similar to LDL but is attached to a glycoprotein called apolipoprotein-a. It has sticky adhesive nature and can easily attach to LDL, calcium, and other components in an atherosclerotic plaque on the blood vessel wall. Due to its similarity with plasminogen, it competes for binding with fibrin inhibiting its breakdown and may promote blood clot formation. It also activates immune cells including monocytes and macrophages which help in inducing inflammation. These effects may help in inducing plaque formation and promote clot formation after the plaque is ruptured.[14]"

Acta Derm Venereol. 2010 Sep;90(5):485-7. doi: 10.2340/00015555-0926.
A comparative study of dyslipidaemia in men and woman with androgenic alopecia.
Arias-Santiago S1, Gutiérrez-Salmerón MT, Buendía-Eisman A, Girón-Prieto MS, Naranjo-Sintes R.

Several studies have analyzed the relationship between androgenetic alopecia and cardiovascular disease (mainly heart disease). However few studies have analyzed lipid values in men and women separately. This case-control study included 300 patients consecutively admitted to an outpatient clinic, 150 with early onset androgenetic alopecia (80 males and 70 females) and 150 controls (80 males and 70 females) with other skin diseases. Female patients with androgenic alopecia showed significant higher triglycerides values (123.8 vs 89.43 mg/dl, p = 0.006), total cholesterol values (196.1 vs 182.3 mg/dl, p = 0.014), LDL-C values (114.1 vs 98.8 mg/dl, p = 0.0006) and lower HDL-C values (56.8 vs 67.7 mg/dl, p <0.0001) versus controls respectively. Men with androgenic alopecia showed significant higher triglycerides values (159.7 vs 128.7 mg/dl, p = 0.04) total cholesterol values (198.3 vs 181.4 mg/dl, p = 0.006) and LDL-C values (124.3 vs 106.2, p = 0.0013) versus non-alopecic men. A higher prevalence of dyslipidemia in women and men with androgenic alopecia has been found. The elevated lipid values in these patients may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia.

Full study: http://www.medicaljournals.se/acta/content/?doi=10.2340/00015555-0926&html=1

CS you spoked about danny roddy pseudo science. In this link http://www.hairlikeafox.com/chapterseven/ he explain:

"More specifically, the case will be made that the current darling of the nutrition industry, the polyunsaturated fats (including omega-3s) are uniquely harmful for hair growth, and may even be a prerequisite for pattern baldness."

But I dont see any logical explanation.. There is no reference study, nothing, just a kind of conclusion.. What do you think about that ?

Shinobi - Yes, unfortunately, I completely disagree with DR's stance on this. I'll mention a brief history for what it is worth. It was DR's idea for me to start this forum. We used to participate on another forum before this. He was new to the hair loss world then and between the research I provided then helped him diagnose his thyroid problem. However, sometime later he branched off and started to form his own opinions looking into Ray Peat, Dr. Kharrazian and others.

Eventually DR wrote a book and helped digest some of this information in a more friendly, readable format.

That being said, I just don't agree with some of their views.

To split hairs a little, I think some of what was stated was too generalized.

Ray Peat recommends limited consumption of PUFA's (not exceeding 4 grams per day). His rational for this small amount
is to limit oxidation products and to spare the thyroid of "burning out." However, to me it doesn't add up on all PUFA's or EFA products. Trans-fats, hydrogenated oils yes, that would be a problem, or refined Omega-6 fatty acids that are heated...then yes.

I think that Omega-3 fatty acids are essential in any MPB regimen, because it helps reduce
PGD2. Here are some articles on wrote about them.

http://hairevo.com/shop/content/12-how-prostaglandins-affect-hair-growth
http://longevitypost.com/the-omega-6-myth/

Also I mentioned Dr. Kharrazian, because this is where he got the idea that iodine is 'bad.' This is another area I completely disagree with. I adhere to the research found in the iodine project, which has involved over 35,000 patients who have been tested before and after iodine therapy (high-dose), it is clear to me that iodine is necessary in every cell of the human body.