32 replies to this topic

[woly]

Hey guys,

I am a 23 year old male and I have recently tested my LP(a) levels and found that they were in the High risk category (i dont have the numbers with me but ill post them later if anyone is interested), Now I know that Niacin seems to be pretty good at lowering these levels but I was wondering if anyone had any ideas of a more gentler approach? Or even better, foods that may have increased my LP(a) levels in the first place?

From what I have found so far, I plan to:
-Consistently drink some red wine each day- alcohol may reduce LP(a) levels
-Add coconut oil to my breakfast - short chain saturated fat may reduce LP(a) levels
-Eat more EPA/DHA?- I already consume ~1g EPA/DHA a day so I dont know if this is wise/make a difference
-Eat more almonds
-Eat more flax? - I read that it lowers LP(a) levels however I have also read of a possible prostate cancer risk. Does anyone have any data on this?

Apart from this, I haven't found much. Does anyone have any ideas about this? Any help would be greatly appreciated.

Thanks,
Woly

[woly]

Just to add to the list-
Tocotreinols and CoQ10 seem to help.
Correcting possible hypothyroidism also improves Lp(A).

[Lufega]

I've read L-lysine, proline and vitamin C help.

http://www.drkaslow....rotein__a_.html

[HighDesertWizard]

I've read L-lysine, proline and vitamin C help.

http://www.drkaslow....rotein__a_.html

forget the Pauling/Rath nonsense with no scientific study showing efficacy for Lp(a) reduction after decades of theory publication.

no one, i repeat, no one knows more about the reduction of cardiac event risk to virtual zero than the folks at the TrackYourPlaque.com forum.

IMO, Dr. William Davis, founder of TrackYourPlaque, is the world's leading expert on coronary plaque regression and cardiac event risk reduction.

There are incredible posts at that forum about Lp(a) reduction, including some written by me.

Edited by wccaguy, 08 January 2010 - 11:19 PM.

[DukeNukem]

Hey guys,

I am a 23 year old male and I have recently tested my LP(a) levels and found that they were in the High risk category (i dont have the numbers with me but ill post them later if anyone is interested), Now I know that Niacin seems to be pretty good at lowering these levels but I was wondering if anyone had any ideas of a more gentler approach? Or even better, foods that may have increased my LP(a) levels in the first place?

From what I have found so far, I plan to:
-Consistently drink some red wine each day- alcohol may reduce LP(a) levels
-Add coconut oil to my breakfast - short chain saturated fat may reduce LP(a) levels
-Eat more EPA/DHA?- I already consume ~1g EPA/DHA a day so I dont know if this is wise/make a difference
-Eat more almonds
-Eat more flax? - I read that it lowers LP(a) levels however I have also read of a possible prostate cancer risk. Does anyone have any data on this?

Apart from this, I haven't found much. Does anyone have any ideas about this? Any help would be greatly appreciated.

Thanks,
Woly

This one is DEAD EASY, and I've seen it help dozens of people: STOP EATING GLUTEN GRAINS AND FRUSTOSE. Boom. Done. Next.

[oehaut]

Hey guys,

I am a 23 year old male and I have recently tested my LP(a) levels and found that they were in the High risk category (i dont have the numbers with me but ill post them later if anyone is interested), Now I know that Niacin seems to be pretty good at lowering these levels but I was wondering if anyone had any ideas of a more gentler approach? Or even better, foods that may have increased my LP(a) levels in the first place?

From what I have found so far, I plan to:
-Consistently drink some red wine each day- alcohol may reduce LP(a) levels
-Add coconut oil to my breakfast - short chain saturated fat may reduce LP(a) levels
-Eat more EPA/DHA?- I already consume ~1g EPA/DHA a day so I dont know if this is wise/make a difference
-Eat more almonds
-Eat more flax? - I read that it lowers LP(a) levels however I have also read of a possible prostate cancer risk. Does anyone have any data on this?

Apart from this, I haven't found much. Does anyone have any ideas about this? Any help would be greatly appreciated.

Thanks,
Woly

I did not review much this, but seems like stearic acid (a saturated fatty acid) lower Lp(a). http://www.trackyour...et_update_3.asp

Here are a few papers :


Influence of n-6 versus n-3 polyunsaturated fatty acids in diets low in saturated fatty acids on plasma lipoproteins and hemostatic factors

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


Plasma lipoprotein (a) levels in men and women consuming diets enriched in saturated, cis-, or trans-monounsaturated fatty acids

Edited by oehaut, 09 January 2010 - 02:22 AM.

[Lufega]

My LP(a) was elevated last time I checked. I was kind of confused by this. My diet, although I always ate very little, was tight. My parents were both healthy people and choose their foods intelligently. I was taught at an early age that sugars, sodas, etc. were bad. We ate plenty of vegetables, etc. Even today I eat only good oils. The only thing that comes to mind is that I still eat grains. eWccaguy, could you give me a link to some of those posts? I have also been considering trying 4 weeks with no grains per the site. Maybe I'll try a little experiment.

Edited by Lufega, 09 January 2010 - 02:17 AM.

[Lufega]

If I were you eliminate grains for 4 weeks, maybe longer, what kind of blood markers, aside from LP(a) can I test before and after, to measure improvements?

edit: found my own answer, thanks!

o HDL
o triglycerides -- over 70 is bad, and is a clear sign of eating too many carbs, especially fructose
o Lp(a) -- a very bad type of LDL
o A1c (glycated hemoglobin) -- long-term blood glucose measurement
o C-reactive protein (C-RP) -- measures inflammation
o fasting glucose -- above 100 is way too high (probably long-term carb-over-consumption damage)
o fasting insulin
o serum D (vit D level) -- below 50 is too low
o Liver enzymes -- good test to make sure your liver is not under stress from food, alcohol, environmental toxins, illegal or OTC drugs.
o homocysteine -- strongly associated with risk of cardiovascular event

If you're over 35 (and I know you're not), then I also recommend testing thyroid hormones, IGF-1 and sex hormones.

Of course, any lipid panel will include total cholesterol and LDL, but these are basically unimportant. Although, I try to keep my total cholesterol around 220-230, but the key is the composition of your cholesterol, NOT the total. You want HDL to be at least 70 -- anything less is a strong indication of a less-than-optimal diet, IMO.

http://www.imminst.o...&...st&p=373187

Edited by Lufega, 09 January 2010 - 05:15 AM.

[Luna]

good luck keep us posted with your results!

[woly]

Thanks for the help everyone!
Duke: Do you know any good studies investigating the effects of wheat/fructose on lp(a)?
oehaut: thanks for that post! i was adding coconut oil as my source of saturated fat but after your post ive found that its actually pretty low in stearic acid. I think ill sweet to coco butter or animal sources.

[woly]

Just for future reference Animal Pharm blog has some pretty good information on LP(A) reduction. Its worth doing a search and checking out his posts on the subject.

Out of the posts, a few intersting points I found were:
IGF-1 lowers LP(A) - I found that interesting to note since there is a lot of talk about reducing IGF-1 for life extension.
Studies that examined fish oils effects on LP(A) used a dose of around 4grams EPA+DHA
A high carb diet raises LP(A) while saturated fat lowers it.

[woly]

A few extra things of note are:
Exercise does not seem to help LP(A) and intense exercise has been associated with higher lp(a), animal pharm notes that this may be due to the high carb intake in athletees
Coq10 and NAC have shown to lower lp(a) quite dramatically but evidence is very limited.

[woly]

ok so from what I have read, here are the effects of each saturated fatty acid on lp(a) levels:
Myristic acid- lowers lp(a) the most.
Lauric acid - lowers it less
Palmitic acid - lowers it slightly less than lauric
Stearic acid- this one surprised me but actually has been shown in a number of studies to *increase* lp(a)!

From this, it would seem that coconut oil would be a pretty good candidate for decreasing lp(a). A side note on this is: a study i read (ill try and get the link again) showed that while myristic and lauric acid increased LDL, it showed a stronger increase in HDL than palmitic.

[4eva]

I think pantethine might be work looking into.

[s123]

Resveratrol seems to decrease Lp(a) and ApoB.

We investigated the hypolipidemic effect of resveratrol focused on the mRNA expression and hepatic HMG-CoA reductase (HMGR) activity in hamsters fed a high-fat diet. Male Syrian Golden hamsters were fed a high-fat diet containing 0.025% fenofibrate or 0.025% resveratrol for 8 weeks. The concentrations of serum total cholesterol and triglyceride were significantly lower in the resveratrol-fed group than in the control group. The resveratrol contained diet significantly decreased Apo B, Lp(a), and cholesterol–ester–transport protein (CETP) concentrations, but increased Apo A-I levels and the Apo A-I/Apo B ratio. The contents of cholesterol and triglyceride in hepatic tissue were significantly lower in the resveratrol group than in the control group. Real-time PCR analysis revealed that HMGR mRNA expression was significantly lower in the resveratrol group than in the control group. These results indicate that dietary resveratrol reduces serum cholesterol by down-regulating hepatic HMGR mRNA expression in hamsters fed a high-fat diet.

Cho et al. Resveratrol attenuates the expression of HMG-CoA reductase mRNA in hamsters. Biochemical and Biophysical Research Communications, 2008, 367, 1: 190-194.

[charlototo]

Resveratrol seems to decrease Lp(a) and ApoB.

We investigated the hypolipidemic effect of resveratrol focused on the mRNA expression and hepatic HMG-CoA reductase (HMGR) activity in hamsters fed a high-fat diet. Male Syrian Golden hamsters were fed a high-fat diet containing 0.025% fenofibrate or 0.025% resveratrol for 8 weeks. The concentrations of serum total cholesterol and triglyceride were significantly lower in the resveratrol-fed group than in the control group. The resveratrol contained diet significantly decreased Apo B, Lp(a), and cholesterol–ester–transport protein (CETP) concentrations, but increased Apo A-I levels and the Apo A-I/Apo B ratio. The contents of cholesterol and triglyceride in hepatic tissue were significantly lower in the resveratrol group than in the control group. Real-time PCR analysis revealed that HMGR mRNA expression was significantly lower in the resveratrol group than in the control group. These results indicate that dietary resveratrol reduces serum cholesterol by down-regulating hepatic HMGR mRNA expression in hamsters fed a high-fat diet.

Cho et al. Resveratrol attenuates the expression of HMG-CoA reductase mRNA in hamsters. Biochemical and Biophysical Research Communications, 2008, 367, 1: 190-194.

It's interresting if resveratrol can help to reduce Lipoprotein(a) but for coconut oil i never hear about that before, i think i will try this.

[Ames]

I've read L-lysine, proline and vitamin C help.

http://www.drkaslow....rotein__a_.html

forget the Pauling/Rath nonsense with no scientific study showing efficacy for Lp(a) reduction after decades of theory publication.

no one, i repeat, no one knows more about the reduction of cardiac event risk to virtual zero than the folks at the TrackYourPlaque.com forum.

IMO, Dr. William Davis, founder of TrackYourPlaque, is the world's leading expert on coronary plaque regression and cardiac event risk reduction.

There are incredible posts at that forum about Lp(a) reduction, including some written by me.

Okay, so give us the summary. That seems to be more rational than outright discounting the direction of Linus Pauling (you do know how qualified this man was, correct?) and then directing us to unnamed and unlinked to posts in a forum that few of us are likely familiar with.


So, respectfully, inform us.

Edited by golgi1, 08 February 2011 - 04:16 PM.

[JLL]

My LP(a) was elevated last time I checked. I was kind of confused by this. My diet, although I always ate very little, was tight. My parents were both healthy people and choose their foods intelligently. I was taught at an early age that sugars, sodas, etc. were bad. We ate plenty of vegetables, etc. Even today I eat only good oils. The only thing that comes to mind is that I still eat grains. eWccaguy, could you give me a link to some of those posts? I have also been considering trying 4 weeks with no grains per the site. Maybe I'll try a little experiment.

Following the official recommendations is a great way to increase Lp(a). That is, lots of fruit and veggies, whole grains, not too much fat, vegetable oils only.

[sthira]

ScienceDaily (Feb. 7, 2011) — In time for the chocolate-giving and chocolate-noshing fest on Valentine's Day, scientists are reporting discovery of how this treat boosts the body's production of high-density lipoprotein cholesterol (HDL) -- the "good" form of cholesterol that protects against heart disease. Just as those boxes of chocolates get hearts throbbing and mouths watering, polyphenols in chocolate rev up the activity of certain proteins, including proteins that attach to the genetic material DNA in ways that boost HDL levels.

Their report appears in the Journal of Agricultural and Food Chemistry, one of 39 peer-reviewed scientific journals published by the American Chemical Society.

Midori Natsume, Ph.D., and colleagues note that studies have shown that cocoa, the main ingredient in chocolate, appears to reduce the risk of heart disease by boosting levels of HDL, or "good" cholesterol, and decreasing levels of low-density lipoprotein (LDL), or "bad" cholesterol. Credit for those heart-healthy effects goes to a cadre of antioxidant compounds in cocoa called polyphenols, which are particularly abundant in dark chocolate. Until now, however, nobody knew exactly how the polyphenols in cocoa orchestrated those beneficial effects.

The scientists analyzed the effects of cocoa polyphenols on cholesterol using cultures of human liver and intestinal cells. They focused on the production of apolipoprotein A1 (ApoA1), a protein that is the major component of "good" cholesterol, and apolipoprotein B (ApoB), the main component of "bad" cholesterol. It turns out that cocoa polyphenols increased ApoA1 levels and decreased ApoB levels in both the liver and intestine.

Further, the scientists discovered that the polyphenols seem to work by enhancing the activity of so-called sterol regulatory element binding proteins (SREBPs). SREBPs attach to the genetic material DNA and activate genes that boost ApoA1 levels, increasing "good" cholesterol. The scientists also found that polyphenols appear to increase the activity of LDL receptors, proteins that help lower "bad" cholesterol levels.

[mikey]

I've read L-lysine, proline and vitamin C help.

http://www.drkaslow....rotein__a_.html

forget the Pauling/Rath nonsense with no scientific study showing efficacy for Lp(a) reduction after decades of theory publication.

no one, i repeat, no one knows more about the reduction of cardiac event risk to virtual zero than the folks at the TrackYourPlaque.com forum.

IMO, Dr. William Davis, founder of TrackYourPlaque, is the world's leading expert on coronary plaque regression and cardiac event risk reduction.

There are incredible posts at that forum about Lp(a) reduction, including some written by me.

Trackyourplaque requires that one pay a membership fee without telling anything about their program. I see commonly known nutrients that address cardiovascular health, but nothing unusual. Can you give me a sample post on Lp(a) reduction that would convince me to join?

[pamojja]

Trackyourplaque requires that one pay a membership fee without telling anything about their program. I see commonly known nutrients that address cardiovascular health, but nothing unusual. Can you give me a sample post on Lp(a) reduction that would convince me to join?

The 6the video on that page is Dr. Davis talking a bid:
http://ihda.ie/see-more/

Some information on his blogs:
http://blog.trackyourplaque.com/
http://www.wheatbellyblog.com/

And a forum by members free to sign up:
http://www.heartlifetalk.com/forums/

Edited by pamojja, 29 August 2013 - 09:37 PM.

[mikey]

Trackyourplaque requires that one pay a membership fee without telling anything about their program. I see commonly known nutrients that address cardiovascular health, but nothing unusual. Can you give me a sample post on Lp(a) reduction that would convince me to join?

The 6the video on that page is Dr. Davis talking a bid:
http://ihda.ie/see-more/

Some information on his blogs:
http://blog.trackyourplaque.com/
http://www.wheatbellyblog.com/

And a forum by members free to sign up:
http://www.heartlifetalk.com/forums/

Thank you. Looks very interesting.

[sthira]

... I have recently tested my LP(a) levels and found that they were in the High risk category..

Are you sure your premise is correct? I thought "Pattern A" LDL, the large fluffy type, is too big to get under endothelia cells and not a cause for concern. Shouldn't we rather be watching the small, dense "Pattern B" LDL? Or am I mistaken?

[niner]

... I have recently tested my LP(a) levels and found that they were in the High risk category..

Are you sure your premise is correct? I thought "Pattern A" LDL, the large fluffy type, is too big to get under endothelia cells and not a cause for concern. Shouldn't we rather be watching the small, dense "Pattern B" LDL? Or am I mistaken?

lp(a) is a different thing. It's a very atherogenic lipoprotein. I discovered that I had a dangerously high level a couple years ago, and have been using pharmacologic doses of niacin (1 gram/day, slow release) to bring it down. lp(a) is the reason that I am now able to use the phrase "my cardiologist"...

Edited by niner, 30 August 2013 - 09:03 PM.

[zorba990]

... I have recently tested my LP(a) levels and found that they were in the High risk category..

Are you sure your premise is correct? I thought "Pattern A" LDL, the large fluffy type, is too big to get under endothelia cells and not a cause for concern. Shouldn't we rather be watching the small, dense "Pattern B" LDL? Or am I mistaken?

lp(a) is a different thing. It's a very atherogenic lipoprotein. I discovered that I had a dangerously high level a couple years ago, and have been using pharmacologic doses of niacin (1 gram/day, slow release) to bring it down. lp(a) is the reason that I am now able to use the phrase "my cardiologist"...

Do you take supplemental Lysine?
http://books.google.... lysine&f=false

[James Cain]

... I have recently tested my LP(a) levels and found that they were in the High risk category..

Are you sure your premise is correct? I thought "Pattern A" LDL, the large fluffy type, is too big to get under endothelia cells and not a cause for concern. Shouldn't we rather be watching the small, dense "Pattern B" LDL? Or am I mistaken?

Research fairly well shows that particle size loses statistical significance when controlled for particle number. The LDL-p (or ApoB as a surrogate marker) are independently associated with cardiac outcomes. Here's an example.

I'm not sure if I'm reading your post right, but it seems you may be mistaking Lp(a) for LDL-c pattern A.

http://en.wikipedia..../Lipoprotein(a)

http://en.wikipedia....ubtype_patterns

Edited by James Cain, 02 September 2013 - 06:33 PM.

[mikey]

... I have recently tested my LP(a) levels and found that they were in the High risk category..

Are you sure your premise is correct? I thought "Pattern A" LDL, the large fluffy type, is too big to get under endothelia cells and not a cause for concern. Shouldn't we rather be watching the small, dense "Pattern B" LDL? Or am I mistaken?

lp(a) is a different thing. It's a very atherogenic lipoprotein. I discovered that I had a dangerously high level a couple years ago, and have been using pharmacologic doses of niacin (1 gram/day, slow release) to bring it down. lp(a) is the reason that I am now able to use the phrase "my cardiologist"...

Do you take supplemental Lysine?
http://books.google.... lysine&f=false

Right. We want Pattern A, not B.

The lysine, proline, vitamin C notion is interesting.
Also worth considering is N-acetyl cysteine, although data is mixed on it.

From: Clinical Applications of N-acetylcysteine. By GS Kelly, p. 119
"Gavish and Breslow administered 2 grams NAC daily for
four weeks followed by 4 grams daily for four
weeks to two patients with elevated Lp(a).
They reported a 70 percent reduction of Lp(a)
in these individuals (reduction of plasma Lp(a)
from 58 to 20 mg/dl and from 59 to 18 mg/
dl).53 In cell cultures, NAC has been shown to
lower the intracellular accumulation of homocysteine.
54Wiklund et al showed administration
of NAC reduces plasma homocysteine
levels by 45 percent (P < 0.0001)). In their trial,
NAC had no effect on plasma Lp(a) levels.55

[albedo]

I am looking at this and resurrect this old thread just in case:

 

Do We Know When and How to Lower Lipoprotein(a)?

http://www.ncbi.nlm....pubmed/20842562

 

"Currently, there are significant data to support a link between lipoprotein(a) [Lp(a)] levels and cardiovascular risk. However, there has not been a clinical trial examining the effects of Lp(a) reduction on cardiovascular risk in a primary prevention population. Until such a trial is conducted, current consensus supports using an Lp(a) percentile greater than 75% for race and gender as a risk stratification tool to target more aggressive low-density lipoprotein cholesterol (LDL-C) or apolipoprotein B (apoB) goals. Therefore, Lp(a) measurements should be considered in the following patients: individuals with early-onset vascular disease determined by clinical presentation or subclinical imaging, intermediate and high Framingham risk patients with a family history of premature coronary disease, and low Framingham risk patients with a family history and low high-density lipoprotein cholesterol (HDL-C) levels. Once LDL-C goals are met, Lp(a) levels may be taken into account in selecting secondary agents to reach more aggressive secondary goals, including non-HDL-C and apoB. To achieve Lp(a) reduction, one evidence-based approach is to initiate therapy with low-dose aspirin and extended-release niacin, titrated from 0.5 g up to 2 g over several weeks. If higher doses of niacin are desired, crystalline niacin allows for titration to a dosage as high as 2 g three times a day; however, the flushing side effect usually is quite prominent. Although hormone replacement therapy (HRT) has been shown to lower Lp(a), there are no indications for using HRT for primary or secondary prevention; therefore, we do not advocate initiating it solely for Lp(a) reduction. LDL apheresis is an option to lower LDL-C levels in patients with homozygous familial hypercholesterolemia who are not responsive to medical therapy. Although it does lower Lp(a), there is no treatment indication for this. A recent study supports the cholesterol absorption inhibitor ezetimibe's ability to lower Lp(a), a finding that deserves further investigation as it has not been previously reported in multiple ezetimibe trials. Additionally, the apoB messenger RNA antisense therapy mipomersen currently is in phase 3 trials and may serve as a potential inhibitor of Lp(a) production. Ultimately, more trial evidence is needed to determine whether lowering Lp(a) actually reduces cardiovascular risk, although this may be difficult to isolate without a specific Lp(a)-lowering therapy." (bold mine)

[albedo]

Very interesting: LP(a) as a proxy of IL-6?

 

Müller N, Schulte DM, Türk K, et al. IL-6 blockade by monoclonal antibodies inhibits apolipoprotein (a) expression and lipoprotein (a) synthesis in humans. J Lipid Res. 2015;56(5):1034-42.

 

Lipoprotein (a) [Lp(a)] is a highly atherogenic lipid particle. Although earlier reports suggested that Lp(a) levels are mostly determined by genetic factors, several recent studies have revealed that Lp(a) induction is also caused by chronic inflammation. Therefore, we aimed to examine whether cytokine blockade by monoclonal antibodies may inhibit Lp(a) metabolism. We found that interleukin 6 (IL-6) blockade by tocilizumab (TCZ) reduced Lp(a) while TNF-α-inhibition by adalimumab in humans had no effect. The specificity of IL-6 in regulating Lp(a) was further demonstrated by serological measurements of human subjects (n = 1,153) revealing that Lp(a) levels are increased in individuals with elevated serum IL-6. Transcriptomic analysis of human liver biopsies (n = 57) revealed typical IL-6 response genes being correlated with the LPA gene expression in vivo. On a molecular level, we found that TCZ inhibited IL-6-induced LPA mRNA and protein expression in human hepatocytes. Furthermore, examination of IL-6-responsive signal transducer and activator of transcription 3 binding sites within the LPA promoter by reporter gene assays, promoter deletion experiments, and electrophoretic mobility shift assay analysis showed that the Lp(a)-lowering effect of TCZ is specifically mediated via a responsive element at −46 to −40. Therefore, IL-6 blockade might be a potential therapeutic option to treat elevated Lp(a) serum concentrations in humans and might be a noninvasive alternative to lipid apheresis in the future.

[Phoebus]

 

Pak J Biol Sci. 2011 Aug 1;14(15):775-9.

 

The effect of hydro alcoholic Nettle (Urtica dioica) extracts on insulin sensitivity and some inflammatory indicators in patients with type 2 diabetes: a randomized double-blind control trial.

 

 

Abstract

 

Type 2 diabetes is a metabolic disorder that is strongly associated with cardiovascular risk. Inflammation is a potential risk factor for cardiovascular disease. In this study, hydro alcoholic extract of Nettle (Urtica dioica) on insulin sensitivity and some inflammatory indicators in type 2 diabetic patients were studied. A randomized double-blind clinical trial on 50 men and women with type 2 diabetes was done for 8 weeks. Patients were adjusted by age, sex and duration of diabetes, then randomly divided into two groups, an intervention and control group. They received, 100 mg kg-1nettle extract or placebo in three portions a day for 8 weeks. Interleukin 6 (IL-6), Tumor Necrosis Factor-alpha (TNF-alpha), High Sensitive C-Reactive protein (hs-CRP) and Fasting Insulin concentration were measured. Insulin Sensitivity was calculated, at the beginning and the end of the study. The data were analyzed by SPSS version 18, p<0.05 was considered significant for all variables. After 8 weeks, IL-6 and hs-CRP showed a significant decrease in the intervention group compared to the control group (p<0.05). The findings showed that the hydro alcoholic extract of nettle has decreasing effects on IL-6 and hs-CRP in patients with type 2 diabetes after eight weeks intervention.