Wednesday, March 03, 2010

Intimal wall volume reductions with weight loss

Thanks to Chris for the heads up on this one.

Just briefly: Low fat, Mediterranean and low carbohydrate: Statistically significant reductions in carotid vessel wall volume for all of them, with no significant differences between groups, so long as you lose weight:

"with no differences in the low-fat, Mediterranean, or low-carbohydrate groups (-60.69 mm(3), -37.69 mm(3), -84.33 mm(3), respectively; P=0.28"

But the LC group lost more intimal vessel wall volume than the other two groups, even if this wasn't statistically significant. I've also not got access the information about what they mean by low carbohydrate. As we know this could be anything up to 150g/d in some people's book!

2010 could be a good year for LC and honesty!

Peter

15 comments:

Chris D said...

"The low-carbohydrate, non–restricted-calorie diet aimed to provide 20 g of carbohydrates per day for the 2-month induction phase and immediately after religious holidays, with a gradual increase to a maximum of 120 g per day to maintain the weight loss"
http://content.nejm.org/cgi/content/full/359/3/229

The fulltext of the cirulation article (which i've uploaded here) does not seem to mention much about diet, only references the NEJM article. "Interventions were reported in detail previously. (11)"

Ned Kock said...

Hi Peter.

You may want to take a look at an interesting study (see post below) of various hormone levels (including adiponectin and tumor necrosis factor-alpha) after a high saturated fat meal. What makes this study interesting is that it is one of the first to look at the effect of dietary saturated fat on adiponectin; a health-promoting hormone secreted by body fat.

http://healthcorrelator.blogspot.com/2010/03/adiponectin-and-tumor-necrosis-factor.html

The conclusion contradicted the authors’ initial assumptions. Saturated fat had positive effects: an increase in adiponectin and decrease in tumor necrosis factor-alpha.

Interestingly, those effects were later messed up by three low fat meals rich in refined carbs and sugars, which were supposed to help the participants “recover” from the high fat meal.

donny said...

---------------------------------
The drug was withdrawn from the U.S. market in 1997 after reports of heart
valve disease,[2][3] and pulmonary hypertension, including a condition known as cardiac fibrosis. After the US withdrawal of fenfluramine, it was also withdrawn from other markets around the world.
The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendineae. One mechanisms used to explain this phenomenon involves heart valve serotonin receptors, which are thought to help regulate growth. Since fenfluramine and its active metabolite norfenfluramine stimulate serotonin receptors 5-hydroxytryptamine (5-HT) this may have led to the valvular abnormalities found in patients using fenfluramine. In particular norfenfluramine is a potent agonist of 5-HT2B receptors, which are plentiful in human cardiac valves. The suggested mechanism by which fenfluramine causes damage is through over or inappropriate stimulation of these receptors leading to inappropriate valve cell division. Supporting this idea, is the fact that this valve abnormality has also occurred in patients using other drugs that act on 5-HT2B receptors. [4]
--------------------------------

That's from wikipedia. Mis-regulation of serotonin, leaky artery akin to leaky gut at one end, over-growth at the other? I wrote some stuff in my blog today, inspired by Westie's comment about glutamine and its effects on glucose and fat metabolism. Mostly about how it relates to leptin.

http://naivenutrition.blogspot.com/2010/03/fellow-commenter-westie-on-peters.html

Less food, less serotonin signalling, right?

Or you could go this way;

"Inhibition of serotonin-induced mitogenesis, migration, and ERK MAPK nuclear translocation in vascular smooth muscle cells by atorvastatin."

http://www.ncbi.nlm.nih.gov/pubmed/17545489

Yeesh.

LeenaS said...

According to the fultext of the former NEJM article on the same group (given by Chris D in first comment) this "Atkins" was closer to 40% carbohydrates after the initial phase and it was not the induction carbs even at the beginning. This was not put into words in the text, but fortunately the authors did give out quite a bit of data in tables, so it can be calculated.

So, 150-200g seems plausible for this Atkins. But with more cholesterol (and more saturates) than in other groups or in their previous diet, it still worked better than the other plans :)

Regards,
LeenaS

JohnN said...

A more accurate observation could be made by replacing the term "weight loss" with its physiological equivalence "fat metabolism" as in:

"The effect is similar in low-fat, Mediterranean, or low-carbohydrate strategies and appears to be mediated mainly by the fat metabolism-induced decline in blood pressure."

Let the reader draw his own conclusion as to what diet to follow.

John

Peter said...

Hi All,

Thanks for access to the papers. The original study is not very clearly written and it seems unlikley that the limit of 120g/d was actually adhered to. The average carb intake was 40% of an unspecified amount of calories! At 1800kcal this is around 160g/d and that's the average and we have to guess at the 1800kcal. Weight rose after the initial dip so compliance probably dropped too, but this is not shown in the tables. It looks like some people made it in to the graphs but not the tables.....

So a half baked, vegetarian biased and mildly reduced carbohydrate diet delivers the goods. You just have to wonder what a real food genuine LC diet might do!


Ned, That sounds very interesting. I do think there was an initial adiponectin dip after the high sat fat meal, it's just you can't make the baseline dot both colours. I was trying to see this in terms of MCTs (providing FFAs without storing fat) but can't get my head to fit the numbers believably!

Donny, just to tie this to the last picture posts. The other significant location of serotonin outside gut and brain is in platelets.... The classic degenerative valve disease in dogs is a mucopolysaccharide degeneration of the heart valves. Hmmmmmm

LeenaS, yes my math came out about the same... How do these papers get through the scrutineering process? So much for my hope for intellectual honesty in 2010!

Johnn, Yep!

Peter

Ned Kock said...

> I do think there was an initial adiponectin dip after the high sat fat meal, it's just you can't make the baseline dot both colours.

I thought that was the case too Peter, but when I looked at the table with the actual numbers, the values of adiponectin at 0 h were listed as 7.37 and 6.66. In any case, one wouldn’t expect two groups to have the exact same baseline mean level of circulating adiponectin. That would be an incredible coincidence! The zero on the vertical graph seems to be the overall mean.

Peter said...

Hmm, that's a bit bl00dy random! So there was no dip of 1mcg/ml in the sat fat group at the 1h mark, yet that's how they drew the graph??????????

Who does the scrutineering on these papers?

Peter

donny said...

So you eat carbs, and you're hungry until serotonin hits a certain level. Or you're a mouse, and they make you eat fructose, which causes all kinds of bad things to happen... unless you take glycine. Or you're a carb or alcohol addict, and you try to treat withdrawal with glutamine.
The glutamine and serotonin are intimately linked to glutamic acid, an excitatory neuro-thingy.
Excess leptin causes fat depletion in Sprague-Dawley rats. Once the fat is gone, the rats show an increased preference for protein vs carbohydrate. Our taste for protein is umami, specific to glutamic acid.
Maybe the basic appetite stimulus is glutamic acid; serotonin, glycine and glutamine would decrease hunger through competition with glutamic acid? The appetite for glucose becomes an artifact of the effect of serotonin on glutamic acid sensing. Glutamic acid itself is capable of becoming its own satiating neuro-protein in the form of glutamine.
Excitatory... that means a lot of calcium gets pumped into the cell, right? Excess leptin beats the crud out of bone mass. Only animals with skeletons have leptin.

Could serotonin-resistance be partial? Too much excitation (glutamic acid, calcium pulled into the cell), serotonin tries, but fails. But doesn't totally fail; promotes excess cell division, fails to regulate the calcium?

Ned Kock said...

Another possibility is that the zero on the vertical axis means different starting values for each group, which is something you see in a few articles (and that can be rather confusing for readers).

But the comments of the authors themselves in the results section tell a slightly different story. Even the discussion section, if read carefully, seems to support a view that SF has a positive effect on adiponectin at most time points.

One way or another, I am cautious about this study because of the small sample size. I am looking for other similar studies.

Adiponectin research seems to have become "hot" only recently.

karl said...

Similar results


http://journals.lww.com/americantherapeutics/pages/articleviewer.aspx?year=2009&issue=07000&article=00012&type=abstract

donny said...

I just read that vitamin c is necessary for conversion of tryptophan to serotonin. That study where carotid intimal wall thickening was associated with vitamin c supplementation comes to mind. Poor vitamin c status also seems to relate to intimal wall thickening, but there's more than one way to skin a cat. Does serotonin production use up vitamin c? (I would never skin a cat.)

Peter, that serotonin/platelet thing, what does that say about warfarin and other clot-preventative strategies? It sounds like what they prevent is healing. Gotta be a better way, eh?

http://www.pnas.org/content/71/7/2730.full.pdf

"Vitamin-k dependent modifications of glutamic acid residues in prothrombin"

There's that glutamic acid again.

blogblog said...
This comment has been removed by the author.
Bling said...

Hello, Read your bio. You've lost weight. Did you lose weight eating a high fat atkins? Any idea of your calorie intake when losing weight? I ak because I've followed this blog for a while and 6 months ago changed to eating low carb hyperlipid. Despite changing some things around slightly (different meats, lowering protein, cutting cheese, reintroducing cheese) nothing is changing. I have 5stone to lose and after 6 months of less than 50g of carb a day (typically 30g or less) I'm not losing. So with all your experience looking through these papers etc what is your hunch what the best foods and calorie intake to loose weight are? BTW I also checked my blood sugar and it was running a bit high but is looking more normal now, but still no weight loss. In fact I lost a few inches, put a couple of them back on and am actually heavier than when I started although I look less "puffy" - not so much a carb-face anymore if you know what I mean.
Thanks a million. I enjoy reading your blog.

Bling said...

Look at this for a laugh:
http://www.mayoclinic.com/health/low-carb-diet/NU00279/NSECTIONGROUP=2