Kurt Harris MD

An Archevore is someone who eats based on essential principles, and also someone who hungers for essential principles. Take your pick.

Exploring these principles is one of my interests, but not the only one.

So you may find commentary here about other issues in medicine, health, other sciences, or just about anything.

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Wednesday
Mar162011

Running Part I on Psychology Today

I'm doing some updating of the more popular posts I've written and migrating them to Psychology Today Online.

Click Here to help support my blog at no cost to you, and to see the re-write.

 

 

Wednesday
Mar162011

Help Japan

You could pray for Japan.

Or you could do something that might actually help them.

Here is a link to the American Red Cross website. You can click a button to direct funds to Japan relief.

I've just given $2000.00.

Tuesday
Mar152011

Chris Kresser Podcast

I will be interviewed by Chris Kresser of Healthy Skeptic this friday morning, March 18.

Submit any questions on his blog post here. I can't diagnose or treat you over the internet, but general questions are welcome.

Tuesday
Mar012011

A cartoon view of lipoprotein (a)

Reader Kelly asks about Lp (a) in the comments.

Dr. Harris, I'm just loving the last two posts and how you relate it to Stephan G.'s recent series.  
Slightly off topic, can you  (or others) elaborate on why zero Lp(a) is worse than low Lp(a)? I've seen Peter mention this too but cannot find details anywhere.  (My Lp(a) was nondetectable when tested last year).  Is it possible to raise or is it a gene that I carry and permanent?   My doctor said I'll likely never have a heart attack because of it...

thanks, Kelly

The first thing to understand is that Lp (a) is not something you can do much about, other than if its high you can reduce it a bit with increased saturated fat intake. (Yeah, I know about niacin...)
This is my cartoon version of Lp (a) and atherosclerosis/ coronary events:

Lp(a) is genetically determined in that some have the increased kringle repeats and some don't. Lp(a) seems to function as a repair molecule - including vascular repair, and may relate to infection control as well.
There are two reasons you could have high Lp (a) levels, and one that you could have zero. 

1) You could have lots of vascular damage going on, and the high levels would reflect lots of repair activity being required. You are the United States, with lots of crappy asphalt highways that are falling apart, so Lp (a) is the repair crews, and seeing a lot of them reflects high levels of road repair. You have repair crews and as many of them as you can muster are out fixing things because the roads are crap.

2) You could be born with a very high level, and if there is not much vascular damage going on, the high levels just mean you have a lot of Lp(a) available.  You are Germany, where the roads are well-engineered high quality concrete, and the high German taxes have funded plenty of DOT repair crews - all hanging around and waiting for something to fix, just in case.
 
3) You could be born with very little or undetectable Lp (a). As long as little vascular damage occurs you might not need much. As long as you have good roads and keep the overweight 18-wheelers off them, you might not need a lot of road repair crews. But having some Lp (a) or some road repair crews is going to be better than none, no matter how good condition your arteries or roads start out in.

This little cartoon and road metaphor for Lp (a) fits pretty well with what the epidemiologic data tell us and with the known genetics and putative actions of it in humans and hedgehogs. In humans, it's that j-curve again. On a population basis, the lowest mortality is in people with low but nonzero Lp (a), the highest is in those with very high levels, most of whom are doing a lot of vascular damage and repair, but not all!

If you have Lp (a) that is 0, you are in category 3. The evidence I have so far is that I am in category 2. I have Lp(a) of 85 but my calcium score at age 49 is 0, my CIMT is the same as a typical 30 year old and ancestors who don't smoke (and even some with up to 50 pack years or more) typically live to the 9th decade with no coronary events. It's worth mentioning that all my relatives eat the SAD and no one has ever been diagnosed with diabetes at any age, either.

Lp(a) is a good model for how something can be a statistical risk factor for coronary events, but be relatively meaningless when applied to single individual. Of course, in my model, it is not "causing" heart attacks or anything else.

 

Tuesday
Mar012011

Polyphenol Hormesis follow-up

 

Reader Joe has posted the following in the comments on "William Munny eats his vegetables".

It's kind of a dissertation, but has some very good questions, so I'll use it to expand on the original post.

Hi Dr. Harris,

I've read both of Stephan's posts and this one several times, and I had a couple of quick questions I was hoping to get your thoughts on.

First, I was wondering just how "strong" you consider the hormetic effect from plant compounds to really be. I've read Peter's "Fruits and Vegetables" series of posts, and he makes several good arguments that decreasing antioxidant consumption can sometimes be beneficial (such as the study (6) you quoted in this post), while increasing consumption probably doesn't have any significant effects (like (1), (2),and (3) above).

As I alluded to in the post, but maybe didn’t make explicit enough, I interpret Stephan’s idea to be good support for some veggies and fruits being better than none, but in no way support for “the more the better”. Think of the typical j-curve here, but with the ordinate representing harm, not benefit. Like for lipoprotein (a)- could be bad if high, but zero is worse than none. The attractive thing about the hormesis idea is exactly that it then makes no sense to think “the more the better”, anymore than it does for radiation or exercise or sunlight. Perhaps exercise is a bad example, as most people are deluded into thinking that relationship is both continuously linear, and positive! It’s might be fair to say that some of Peter’s posts argue that zero is the best level of polyphenols/antioxidants. If so, I am here speculating that some might well be better than none.

 I very much like Stephen's ideas on the hormesis model of how plant compounds may be beneficial, and I think it (along your thoughts in this post) explains a lot, not just about vegetables but about moderation in life in general: exercise, sunlight, fasting, etc... At the same time, though, I thought some of the beneficial results Stephan used to illustrate the effects of polyphenols in particular were actually rather small in the grand scheme of things - such as a slight reduction in blood pressure from drinking a half liter of OJ every day.

If you are looking for gross physiologic changes as evidence for hormesis in vivo, they are going to be small if even detectable almost by definition. The point is cumulative benefits from the whole suite of toxins you are exposed to in small quantities. The orange juice thing may even be a red herring and of course I would not recommend that. That is the whole point I am making, is not to pick and choose and then “load up” on particular compounds like hesperiden, even via food.

I thought the benefits in most of the examples Stephan used just didn't seem as large or as beneficial as some of Peter's examples in limiting antioxidants, making me wonder just how good hormesis from polyphenols can really be, relatively speaking.

So let’s imagine the j curve again. Here I am speculating, but the way I would synthesize Peter and Stephan is to guess (it is just a guess) is that the right hand side of the curve is steeper than the left. Reducing huge consumption of polyphenol containing plants down to reasonable -lets’ say 5 servings a day down to 5 a week- might be of more benefit than the jump from zero to one a day. The lack of benefit of plants in prospective trials may be confounding of actual harm from more plant compounds with benefits from eating less wheat and sugar – the displacement effect. The same is probably true in the observational data re: veg and meat consumption.

My question really boils down to the recommendation you make to "include a moderate variety of colorful plants". I definitely accept that this can be beneficial due to hormesis, and I would never argue to avoid vegetables; my question is about the phrase "moderate variety".

I meant moderate in variety, not quantity. Like all my recommendations, it is just meant as a reasonable guideline and it is not very quantitative on purpose as I hate to tell people what to eat (I’m more comfortable saying what not to eat and I limit that, too).

Is this mostly aimed towards those who would claim that all vegetables are poisonous and should be avoided, which is clearly unreasonable?

Yes, somewhat. You might say I am synthesizing Peter and Stephan to say that in addition to starchy vegetables as a staple, there may be positive benefit to including a variety of other less caloric vegetables and plant compounds in some quantity, but my intuitive skepticism of 3-5 servings a day and antioxidant supplementations seems to be well-founded.

Or is this a stronger recommendation - should someone like me, who regularly consumes only a small variety of polyphenols (from coffee, chocolate, tomatoes, and sweet potatoes, plus limited fruit and green leafy veggies) actually make a deliberate effort to include a wider range of plants, solely to induce hormetic effects?

I know if I say what I eat that there will be threads everywhere discussing my “new recommendation”. Let me be clear that I have no clue where the exact nadir of the polyphenol j-curve lies. It could be three Mark Sisson big-ass salads a day, or one a week. I have no idea. I just doubt it is either really high or zero. I would say that if you are a meat-and-water zero-carber, to start eating colorful tubers and root veggies with starch in them first. If you are getting a modicum of starch – my back of the envelope is 2K – twice the Kwasniewksi number of 10% of calories – 20%, then maybe add a few green salads a week. Personally, my polyphenol consumption sounds about like yours. I eat green salads and salsas and avocados, tomatoes, sweet and russet potatoes, green beans, etc. I also drink plenty of coffee and cold brewed white and green tea (just for the flavor) and dark chocolate makes the cut as well. I don’t plan to change or add to any of this, and if Stephan is wrong and Peter is right (no plants besides potatoes is best, e.g.) I would not change it anyway.

(Note: I am not representing Peter’s views here. I don’t know what his exact position is, I am just using his ideas to illustrate the left side of the plant spectrum.)

Is the question of polyphenol consumption, like the macronutrient ratio, just a wide spectrum of healthfulness - something like "it's healthier to eat at least some variety of plants than none at all, but stupid to take supplemental megadoses of plant compounds; anything in between is probably good". Would you agree with that sentiment, or am I off base?

Yes, I would basically agree.

Second, I would love to hear your thoughts on Stephan's "Second Mechanism", concerning the action of antioxidants consumed concurrently with fats to prevent oxidation of n-3 fatty acids during digestion. This caught my attention quickly, because it seems to be potentially significant; I remembered you stating that n-3 fatty acids are one of the least stable fats and are prone to oxidation in the gut. I try to eat high-GRAF (mostly from butter and cream), but most of the meat I eat is factory-farmed, bringing with it sometimes a fair amount of IRAF or NRAF as well, and I sometimes worry about getting enough n-3.

Grass fed butter and cream will give you plenty of n-3. You don’t need much. DHA levels in vivo are determined more by lack of excess n-6. I would worry more about the oxidation if you are eating too much n-3, not if you are eating very little.

 Will doing something as simple as drinking a glass of red wine with dinner increase the amount of n-3 that makes it through digestion? Do you think this effect is significant enough to keep it in mind when eating, or do you think it is relatively small and unimportant?

Whenever I eat grass-fed lambchops, with the very first first bite I always get the urge for a bottle of cabernet. Maybe that's instinctive behavior? What goes better with red meat than red wine?

But seriously, you can probably guess what I would think of obsessing over particular food combinations in order to protect your ingested n-3s.

Thanks again for writing a great blog and taking the time to participate in discussion!

-Joe

You’re welcome!