I have a Chinese friend that asked if Lp(a)is an inherited trait that Asians are known to have.  Are there races more likely to have Lp(a) than others?

Hi Dr D,

Thanks for the study, another very interesting one!

You also have to consider that the fish must be displacing something from the diet of the vegetarian Bantu. By definition that means that there MUST be a reduction in vegetable intake. We know from hard intervention studies that a low fat diet automatically increases Lp(a) by 7% and adding copious fruits, vegetables and nuts makes the situation slightly worse (9% increase). Conversely a high fat diet reduces Lp(a) by 11%. The high fat diet was only 60% calories from fat and allowed 13% of calories as carbohydrate, so there is ample scope for less vegetables as a really radical intervention to drop Lp(a).

Although not looking at Lp(a) the other hard intervention study looking at oxidative damage to lipids (and DNA and protein) found that near total elimination of all vegetables, without carbohydrate reduction, markedly reduced oxidative damage.

When replacing veggies with fish it shouldn't surprise anyone that Lp(a) drops.

Peter

I'd finger grains as the culprit before before vegetables any day.

Peter,
  The second study quoted has this logic:
"Since no long-term effects of GTE were observed, the study essentially served as a fruit and vegetables depletion study.The overall effect of the 10-week period without dietary fruits and vegetables was a decrease in oxidative damage to DNA, blood proteins, and plasma lipids, concomitantly with marked changes in antioxidative defence."
    But the study did not have a group of people who were on a proper(TYP style?) fruit & veg diet to compare. So it sounds like "there were no long-term effects of GTE, but the diet was meat, so it must be the fruits and veggies that is the culprit". Or am I missing something?
-neelesh

RE: racial differences in Lp(a). Yes, there are distinct differences in Lp(a) levels and apo(a) size. Africans have the highest level. There are also pockets of incrased Lp(a) in the British/Irish/Scottish, some of  Jewish descent, among others. I do not know about Asian.

zute, I'd blame grains for a host of problem but the low fat diet study doesn't give you menus, so who's to say. Except concluding that fruit, veg and nuts don't protect you from grains any more than they protect you from a reduced fat diet. Whichever. But the second study, which only looked at oxidative damage, was high in bread and cake. It's a pity they didn't look at Lp(a) in this one. I know which way I'd bet it went.

Neelesh, I'm not quite sure I understand you comment. Are you suggesting meat inclusion alters the finding that fruit and vegetable elimination reduces oxidative damage? On a basic low carbohydrate, HIGH meat diet blood antioxidant status improves within three days. Again, this is far off of the topic of Lp(a), but meat got the credit for improving antioxidant status. You could equally well argue it was the lack of vegetables.

I feel there is a massive difference between eating a steak on its own and eating that same steak with chips, peas, tomatoes, a bowl of green salad plus two bread rolls on the side. Intervention studies suggest one oxidises your lipids, the other doesn't. Epidemiological and observational studies are usually performed by people without this concept. In intervention studies veggies don't do so well. The authors are usually amazed. Very off topic (sorry) but there are very few intervention studies which measure Lp(a).

Peter

Hi Peter,

Interesting study.  Do you have any reason to attribute the increase in antioxidant defenses to increased meat consumption, rather than decreased carb?

Hmmmmm...    I take high doses (5-6 grams) of High Potency EPA/DHA Fish Oil daily.

I haven't seen any effect on my high Lp(a).

Maybe it has to be directly from the fish (and while I do eat fish - it's only once or twice a week).

Fruits and veggies - I eat a lot of those, too.

Sheesh - this is confusing.  I can't imagine eating less fruits and veggies.

Bonnie

Peter,
  What I mean is this. Without a group of people being subjected to a fruit+veg+GTE diet and another group to meat+GTE group, one cannot conclude that "meat+GTE= less oxidation damage" implies  "lack of veg/fruit = less oxidation damage" .
    Again, this does not mean that there is no credit to the observation that meat+GTE reduced oxidation damage. However, we cannot logically deduce from that observation  "hence it is because of lack of fruits and veggies".

High Lp(a) is one of the factors cited for the very high incidence of CVD in the South Asian population (India, Pakistan, Bangaldesh....).  Search Pubmed for work done by Dr. Enas Enas

Hi sasquatch,

I originally thought it was the lack of carbs rather than the high meat intake in the cyclist study, but the high carb vegetable washout study convinced me it was the lack of vegetables rather than carbs per se.

The persistent antioxidant effect of fruit and veggies appears to be largely an effect of uric acid produced by ourselves in response to fructose. I've got a paper on this somewhere. Certainly the body eliminates most plant based antioxidants as fast as it can, ref the green tea extract paper.

The Bantu on the lake eat roughly half a kilo of fish a day (300-600g/d). That's about 100g of animal protein and 550 kcal animal calories. Assuming a 2000 kcal food intake that's an awful lot of displaced vegetables. Results speak for themselves. As far as you can talk about results in an observational study.

The paper linked to by Dr Davis provides this reference, which goes some way to explaining Bonnie's finding of no change in Lp(a) with fish oils. Unfortunately none of the fish (fish oil?) supportive refs have even abstracts on pubmed, so it's hard to see what's happening. BTW, I've got nothing against fish oils, 5g/d sounds like a very physiological intake. But it doesn't displace much in the way of vegetables.

Peter

Hi Neelesh,

I think that the study concluded that the GTE  had no lasting effect beyond its excretion in the urine, with an elimination 1/2 life of 2 hours.

There is no suggestion that meat plus GTE did any better than meat without GTE. It was a cross over study, so both groups got 3 weeks on GTE and 3 weeks off GTE.

Their conclusion was that GTE supplementation made no difference to any measured parameter.

As the GTE made no difference to antioxidant status (except transiently in the immediately post consumption period), the only hypothesis ultimately tested was whether fruit and veg elimination reduces oxidative stress.

So comparing a meat plus GTE diet with a veg plus GTE diet is a little pointless.

I would agree that you could argue that GTE does much more in the absence of meat, but I would want some logic as to how that might happen. I don't see why this should be the case.

In this study we had a group of people acting as their own controls, drop the veggies, oxidation reduces, reintroduce the veggies, oxidation increases. Forget the GTE. It looks very simple to me, but then I'm a simple person.

I as far as I can see the full text downloads for free. It does deserve careful reading. The EU was a major funder of the study and this funder was VERY unhappy with the results. From the EU's comments, linked to the asterisk at the end of the title, it looks to me as though the authors fought their funders tooth and nail to publish. It's a good study.

Peter

I am a 34 year old male South Asian, who recently had a mild MI (troponin returned a negative, but my doctors confirmed an MI). Subsequently, I had an angiography which revealed an occlusion in the right coronary artery (RCA). All other fields (leftmain, LAD) etc were normal. I underwent a PTCA (coronary angioplasty) which opened up the block. I was not administered any stents, as the doctor felt that the thrombus would clear on its own.

This was exactly 3 months ago. About 2 weeks ago, I went through a lipid profile test, along with some other tests the doctor prescribed (liver function test, Lp(a)). It was here that it was revealed that my Lp(a) was at 115 mg/dl. All along, all my risk factors were negative (blood pressure, blood sugar, lipids, and the only high figure was a marginally high cholesterol of 222). Finally, the doctor was able to put his finger on why this happened to me.

He has now put me on Niacin, alongwith my statin (Tonact 20) and Clopivas tablets. I understand that Lp(a) is largely genetic, and not really fixable through lifestyle changes. I must mention that my cholestrol has come down to 94 from a value of 222 after I have been on medication, a healthy diet, and exercise, all of which I am maintaining with some rigor.

I would like to know:

1. Where do I stand on the Lp(a) thing? Is there anything I can do to help my cause? Just how bad is it? Am I unlikely to live very long, or develop further complications?

2. Is it safe for me to have children? Will I be passing on this condition? What are the chances that my child will be unhealthy?

3. I like to have a drink of beer occasionally. I have got a green signal from my doc a month or so ago to have the odd drink. Is it ok if its beer, and not wine, as he has recommended? Is it ok if I have  2 pints (each pint 330 ml) about 2-3 times a week?

4. My Triglyceride levels are quite low (90). Also, my HDLC is currently at 30, and LDLC is 46, while VLDLC is 18. The LDLC/HDLC ratio is 1.53. Also CPK is 124 u/L. All other tests have returned normal values. F.B Sugar is 77 mg/dl. Fasting Urine Sugar is Nil. Blood Pressure is normal, I am not obese. There is no history of heart disease in the family known prior to this. I have quit smoking (I was a heavy smoker, about 20-30 cigerettes daily).

promit,
hope you've been reading this blog carefully! good luck

My mother had a serious problem of coronary plaque reversal, she now enjoys of great health but doctors lasted too much to diagnose the disease she was going through.

The Lugalawa Study opens the question of whether similar results can be obtained not by moving to Tanzania and fishing Nyasa Lake, but by mimicking their experience by supplementing high doses of omega-3 fatty acids.