Thursday, September 27, 2012

Never forget, never forgive

For recreational purposes only, from here:



How toxic is palmitate at any concentration from zero to 0.4mmol/l if glucose is held at 5mmol/l? It's not.

How toxic is glucose at 25mmol/l in the presence of increasing palmitate? Glucose at this concentration becomes progressively more toxic within increasing but still physiological levels of palmitate.

Glucose at 25mmol/l is UTTERLY non physiological.

There is potentially a huge amount to discuss from this paper, one day, maybe. Even though they never delve in to the ETC, which they should do. But anyway, someone commented that papers using 5mmol/l glucose in the culture medium were rare. This one is a hen's tooth.

Back to thread next.

Peter

45 comments:

donny said...

http://www.pnas.org/content/100/6/3077.full.pdf

No worries. Olive oil to the rescue. Or oleic acid, at least.
--------------------------

Triglyceride accumulation protects against fatty acid-induced lipotoxicity

Excess lipid accumulation in non-adipose tissues is associated with
insulin resistance, pancreatic -cell apoptosis and heart failure.
Here, we demonstrate in cultured cells that the relative toxicity of
two common dietary long chain fatty acids is related to channeling of these lipids to distinct cellular metabolic fates. Oleic acid supplementation
leads to triglyceride accumulation and is well tolerated, whereas excess palmitic acid is poorly incorporated into triglyceride and causes apoptosis. Unsaturated fatty acids rescue palmitate-induced apoptosis by channeling palmitate into triglyceride
pools and away from pathways leading to apoptosis. Moreover,
in the setting of impaired triglyceride synthesis, oleate
induces lipotoxicity. Our findings support a model of cellular lipid
metabolism in which unsaturated fatty acids serve a protective
function against lipotoxicity though promotion of triglyceride
accumulation.
----------------------------------

Eva said...

Yeah, interesting MUFA seemed to be the best deal IF in presence of high glucose.

Jane said...

So the glucose prevents fat oxidation in mitochondria, and fatty acids accumulate and are toxic? Why should they be toxic? Is it because they go to peroxisomes and produce H2O2?

RESULTS Only long-chain (>C14) saturated NEFAs were toxic to insulin-producing cells. Overexpression of catalase in the peroxisomes and in the cytosol, but not in the mitochondria, significantly reduced H2O2 formation and protected the cells against palmitic acid-induced toxicity.
http://diabetes.diabetesjournals.org/content/60/1/200.full

Eva said...

So at what point does glucose level become a problem for palmitic acid? Are such levels reached in diabetics?

O Numnos said...

@Eva

my thoughts exactly, the abstract indicates glucose tested at 5,11 & 20 nm/ml but the graph Peter published doesn't show 11, I assume it's intermediate. From Wikipedia(!) normal post prandial glucose is up to ~10nm/ml but obviously diabetics can go much higher.

I assume the graph is just indicating relative differences, the baseline ~10% cell death in 1-2 days sounds scary to me - I'm hoping that's an artefact of cells in culture and not reflective of in-vivo reality? what is the normal turn-over of pancreatic beta cells?

Also I'm not sure if it's just semantics/sarcasm but Peter's assertion that physiological levels of palmitate enhances the toxicity of supra-physiological levels of glucose doesn't ring true it reads like supra-physiologic glucose levels enhance FFA toxicity.

So I assume it was sarcasm? :-)

Eva said...

How you want to word it depends on how you want to spin it. Assuming high glucose but low palmitic shows no prob and high palmitic and low glucose shows no problem (in this experiment), then scientifically, if you are fingering blame on only one, you are showing a bias. Peter I think likes to wave his bias like a flag held high so all know where he stands, whereas in an official scientific paper you are technically not supposed to have a bias so having sneaky wording (and thought) bias is not supposed to be done. Likely that many scientists are so biased they don't even know they are biased. They likely assume it just is so obvious that it must be correct.

I think the main point of the post is that most in vitro research showing supposed dangers of palmitic are done in conditions of very high glucose, which may not be indicative of in vivo, and will likely not be indicative of in vivo in low carbers with normal blood sugars.

But yes, also good point, this was done in vitro. Those islet cells may have already been sick and hanging on the edge. It might take a lot more to kill them in vivo than in vitro. Might not be possible to correctly extrapolate those numbers to in vivo. I don't know much about natural cell death rates in vivo vs in vitro. I know they used to say that once our islet cells die, you can't get them back, although lately they have been backing off that claim to some extent. On the face of it, seems unlikely that 10% can be a normal death rate for islet cells.

From a larger perspective, I do wonder often about the diff between strategies to prevent breakage of the metabolism in vivo, vs strategies to help the metabolism after it's 'broke.' The best strategies for one vs the other may not be the same.

This stuff it sooo complicated. I think most researchers can't even begin to wrap their heads around all the variables. So biases tend to rule and each only looks at tiny pieces of the puzzle, mainly just trying to say that which yields more grant money. It may be eventually down the road we will need a very good computer program or ai to read all the research there is and sort it in an unbiased fashion.

Peter said...

Hi all,

There is no doubt that the toxicity of hyperglycaemia is mediated through lipid products, especially those of palmitate. NB this has nothing to do with beta oxidation, fatty acid oxidation is not happening under hyperglycaemic conditions. Because FFAs are rarely all palmitate I suspect 0.4mmol palmitate is actually supraphysiological and completely safe under normoglycaemia. My own line of thinking is how, on a basic level, does excess glucose stop the entry of fatty acids and their oxidation in mitochondria. At the moment I'm looking at glycerol 3-phosphate dehydrogenase as an input in to the CoQ couple under hyperglycaemia, limiting beta oxidation electons from from feeding in at this point. It would also generate reverse electron transport with a vengeance as the CoQ couple would be highly reduced and a ton of NADH available from glycolysis. I'm just looking at the logic here, not chased much in the way of papers.

Peter

blogblog said...

I've gone from a a VLC diet to around 30% carbs (mainly fruit and starches). I fast 23 hours per day and gulp down one large evening meal after exercising.

To be honest I feel FAR better on 200-300g carbs per day than I did on the VLC diet. No muscle cramps, no constipation and more energy.

Jane said...

Peter, are you sure high glucose prevents lipid oxidation in peroxisomes as well as in mitochondria? Glucose makes malonyl CoA of course which prevents entry of lipids into mitochondria. It also downregulates peroxisomes, or at least it downregulates PPAR alpha mRNA. But I don't see how it could completely eliminate peroxisomes. If there are enough left to oxidise the palmitate and produce H2O2, it would be toxic because beta cells have very little catalase.

M said...

http://www.wnyc.org/shows/heresthething/2012/jul/02/transcript/

Hello Peter, I thought you might find this interesting. It's an interview with Robert Lustig. It's nice to see that he is now much more down on carbs (not just sugar) and now he's saying a few things I remember reading in your blog, e.g. that the problems really start when you can no longer store fat in your body.

"Robert Lustig: Especially South Asians, Indians. They can’t carry as much subcutaneous fat and once you basically fill up your subcutaneous, your love handle fat stores, it starts building up in your liver and when that happens it’s all downhill after that."

Thank you for your blog.

karl said...

So the hypothesis is: High BG + palmitate that is doing the damage . And once the fat cells are fully loaded they leak palmitate. This damage may be what is further damaging the VMH making BG control even worse.

Do I have it right?

(This damage appears sadly permanent in MO (stem cell injections someday?))

Here is a link to the full paper:
http://endo.endojournals.org/content/144/9/4154.full

I'm wondering if it is just the consumption of BG raising sugars or if fructose containing sugars are key?

When you give someone a dose of fructose, we know it spikes Trygly, but what type of FA is it?

There is a flux of FA going into and out of adipose tissue - if tygly are high, could that increase the circulation of palmitic acid?

The general public has trygly averaging over 100. The medical people are telling people that it is OK to have levels up to 150.

http://en.wikipedia.org/wiki/Tryglycerides#Guidelines

I don't think that is really a healthy-normal level - having a will of steel, I've gone low carb for many years now and my trygly are now 45-50 - (Note that I eat lots of fat!)

Before people began enslaving others to grow sugar cane, it would have been quite difficult to have the average Trygly levels of today.

When the trygly from fructolysis is disassembled to enter adipose tissue what form is it - and inside the adipose tissue when trygly are again disassembled during weight loss - what form of FA do we have?

http://en.wikipedia.org/wiki/Fructolysis


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

M and Karl, the problem with fructose is that it causes copper deficiency. Lustig does not seem to have grasped this and somebody needs to tell him. Have a look at the titles of these papers.

Copper availability contributes to iron perturbations in human nonalcoholic fatty liver disease.
http://www.ncbi.nlm.nih.gov/pubmed/18505688

A role for low hepatic copper concentrations in nonalcoholic fatty liver disease.
http://www.ncbi.nlm.nih.gov/pubmed/20407430

High fructose feeding induces copper deficiency in Sprague-Dawley rats: a novel mechanism for obesity related fatty liver.
http://www.ncbi.nlm.nih.gov/pubmed/21781943

Copper is needed for all aspects of iron metabolism and in copper deficiency iron gets stuck, either in the liver or in other tissues including, terrifyingly, the brain. The people who work on copper say most of us have copper deficiency. Your government will tell you (as the UK government told me) that 'copper deficiency is rare'. Yes, gross copper deficiency is indeed rare. This does not mean that mild chronic copper deficiency is not a major cause of modern disease.

Eva said...

To clarify on the bias issue. My issue is that IF one actually writes a research paper, one should try to write it in an unbiased way. In order to do that, you must first at least understand your own bias. It also helps if you are not being paid to be biased (yeah right).

However, a blog is a whole different animal and a certain amount of bias and sarcasm from time to time is fairly standard and almost expected. I suspect everyone in the universe has bias about some things, but it's much better if you at least know your bias instead of being oblivious or in denial.

karl said...

@jane

The real problem with fructose is we never evolved to eat the quantities that the average westerner (and now most of the world ) is eating.

Small amounts don't seem to be a problem - I don't think we understand all the details yet, but I think the liver gets backed up with chronic exposure and not only do you see fatty-liver-disease, but my hunch is the liver can't pull the fructose out of the blood stream fast enough and even small amounts of circulating fructose can do bad things.

I don't think we understand the role of copper well enough http://wiki.xtronics.com/index.php/Interventions_for_Preventative_Heart_Health#Copper

First, there is no accepted definition of an antioxidant, (some measures use copper as the exposure). The proposed methods are are based on storage antioxidants, but some substances - copper included, look to have a reverse role invitro. (Vit C at high dosages may well be a pro-oxidant in vitro via the Fenton reaction involving iron) - The point is that I think we don't understand enough about copper - there may be some connection with hormones.

I know fructose spikes triglycerides - what I don't know is if it changes the type of FA in the triglycerides - I suspect it might as fructose is a 5 carbon sugar compared to glucose which has 6.


Peter said...

Jane, I've not been through the methods in any detail, the paper is really a side issue, but I can see ways in which glycolysis products might well inhibit beta oxidation. For the moment I'm willing to accept this from the paper.

M, good.

Karl, yes, I think that is what is happening. The fructose-trigs thing is interesting. Krauss has a paper suggesting that it is the lack of insulin drive from fructose which pushes it toward visceral rather than s/c fat. You could also argue that lack of insulin should produce highly saturated fat after fructolysis due to failure of insulin induced SCD1 activation, so palmitate should be produced. If there is a glucose load at the same time that might be rather a bad combination.....

Eva, I hope my biases are utterly clear and that if anyone thinks I am unbiased they had better stop reading the blog PDQ. Fake objectivity is for Guyenet. Someone has to argue the lipid corner! I keep working at it.

Peter

karl said...

@ Petro

Re: the fructose-trygly thing - I found the abstracts of couple of older papers that were looking at ethanol and FA production ( I didn't have a way to see the full text)

Ethanol and fructose share some of the same metabolic pathway.

I think you see what I'm poking around at. From the epidemiological papers, it appears that fructose is doing more harm than glucose ( from rice starch etc ) but I want to find some better evidence.

It could be that just the elevated Trygly messes with leptin sensitivity as Guyenet wrote about (without citing any paper that actually showed Trygly producing leptin-resistance!@#%&# and I couldn't find any on my own. (a floating abstraction?)).

If the sucrose dimer of glucose and fructose pumps BG and palmitate it might explain a bit of what is going on.


blogblog said...

Our immediate ape ancestors almost certainly consumed very large quantities of sugars including fructose. There are also many traditional societies (mainly in Southeast Asia) who consume very large quanties of sucrose and fructose. (In an extreme case dates are around 80% sucrose).

The problem isn't fructose per se. It is the high consumption of nutrient deficient refined fructose (particularly as beverages) combined with a sedentary lifestyle.

Pieter said...

@karl

While I agree with

"Before people began enslaving others to grow sugar cane, it would have been quite difficult to have the average Trygly levels of today"

I notice we sometimes make the same mistake. You could also say

"Before people began enslaving cows to make butter and cream, it would have been quite difficult to have the average Cholesterol levels of today"

Jane said...

Hi Karl
Yes copper is confusing and we don't understand enough about it. One thing very difficult to understand is this: the RDA for copper in the US was recently set at 0.9 mg/day, a level found by Leslie Klevay to cause symptoms of heart disease in volunteers. Why was it set so low? Because of this, people think they don't have copper deficiency when they do.

It goes without saying that white flour, white rice and white sugar have had much (or all) of their copper removed. Here in the UK, the copper content of vegetables has fallen since 1940 by a staggering 76%. Meat, by 55%, and dairy by an almost unbelievable 97%. See Table 9 in this paper.
http://www.mineralresourcesint.co.uk/pdf/Mineral_Depletion_of_Foods_1940_2002.pdf

Here's what Leslie Klevay has to say about heart disease and copper.

'.. Copper deficiency is the only nutritional insult that elevates cholesterol (7), blood pressure (8), and uric acid; has adverse effects on electrocardiograms (7, 9); impairs glucose tolerance (10)... and which promotes thrombosis and oxidative damage. More than 75 anatomic, chemical, and physiologic similarities between animals deficient in copper and people with ischemic heart disease have been identified. ..'
http://ajcn.nutrition.org/content/71/5/1213.full

Theresa Slowik said...
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karl said...

@blogblog

The diet in Asia is something I'm quite aware of. I've heard this argument before but find it lacking. The sweet fruits are available at only certain times a year and I just didn't see the people eating huge amounts of them.

(Also - The sweetest fruits were not always as sweet as they are now - selective breeding has changed the fruits.)

( Traditional diets in the area also contained(s) quit a bit more insects than people realize.)

The reality today is that most of fructose consumed in Asia comes from sugarcane or HFSC. There is some in the fresh fruit, but it is eaten as fruit, not as a huge dose in soda pop.

What is interesting to me is that the prevalence of T2D in Asia ( my wife is from the Philippines) has gone up rapidly from when I was first there 27 years ago. When I was first there, soda pop was an expensive treat - it is no longer the case and the people that seemed less fat than Americans when I was first there are catching up.

The consumption of rice was always there - which gets digested to glucose, yet there wasn't a huge amount of T2D. People would cook fish in coconut oil, I used to see buckets of lard for sale.

The problem is, other things also changed - when I was first there, the meats were not refrigerated, now they are. The type of rice used to be much harder, but now they are eating the gooey rice. They are now eating more processed foods, more exposure to trans-fats, increased O-6 . We walked a huge amount of the time where we now ride. Exposure to plastics that might mimic estrogen, refined vegetable oils, a large increase in wheat based products, more dairy etc etc..

We are back to correlations don't show causation - yet I suspect fructose as I know it has a profound impact on trygly.
If we make a list of dietary and environmental changes in different populations as T2D increases, increased fructose consumption is one thing that is always there.

For the record, I don't think we know what is causing the pandemic of T2D - it is possibly a combination of things - but my short list of prime candidates includes fructose along with trans-fats, O-6.

So my observation of Asia is that T2D is following the trend in the USA with a time lag - if we could see data that correlated the time of the change with a specific food it would be really suggestive.


Theresa Slowik said...

fortune said...

@karl

"For the record, I don't think we know what is causing the pandemic of T2D - it is possibly a combination of things - but my short list of prime candidates includes fructose along with trans-fats, O-6."

It's not white sugar; Filipino consumption of which has actually declined somewhat recently. (http://www.ats-sea.agr.gc.ca/ase/5754-eng.htm)

It's Coke. Filipinos now drink 121 liters per capita per year. (http://www.brandchannel.com/features_effect.asp?pf_id=40)

George Henderson said...

@ Karl, you're right, it's O6 plus fructose
http://www.nature.com/oby/journal/v20/n10/full/oby201238a.html
Ever since the CSPI put seed oil in the friers at MacDonalds, Americans have craved more sodas (FRH).
More than they need in CICO terms, and enough to start the CIH ball rolling.
As processed food is also depleted in omega 3, there's nothing to stop it.
I call it the Unifying Theory of Obesity.

@ Peter, did you know DHA increases metabolic rate by increasing membrane permeability, meaning cells must work harder to maintain proton gradient?
Great book - "The Queen of Fats" by Susan Allport.

@ Blogblog, yup, I also use what starch I do eat, once a day, to feed my gut bacteria. I may not need it but it sure keeps the commensals happy.

Eva said...

"For the record, I don't think we know what is causing the pandemic of T2D - it is possibly a combination of things - but my short list of prime candidates includes fructose along with trans-fats, O-6."

I'd add wheat and excitotoxins (msg and aspartame) as also on that list. Diary (at least the way they make it now) may also be complicit but I am not sure on that one. Nutrient deficiencies are likely also an issue but if you got rid of all that other stuff, that might self correct to a large extent.

I also do not really think of it in terms of diabetes. Many don't have high blood sugar but still have major metabolic probs. If your pancreas can keep up, that helps but it doesn't mean you are fine. I think of diabetes as just one symptom. High blood pressure, weight gain, plaque buildup, gall bladder probs, IBS, alzhiemers, cancer, MS, hypothyroid, what a bunch of sick people we are! How many people actually don't take/need medicines anymore!?!

COuld well be that there is a whole symphony of causes. Fructose I think it likely fine in its natural form. How many apples do you feel like eating? One is usually enough. But cake or candy make you want to eat a lot more fructose than you would get naturally. So I think the prob is when unnatural foods short circuit the natural satiation systems. In the tropics, you can get fruit most of the year and some of it is naturally sweet. Plus humans are and were plenty smart enough to dry fruit and store it for year around use. Some populations likely had access to a lot of fruit. But imo, when things work naturally, desire for natural sugars follows need. You'd crave when glycogen stores were low but not so much if they were not low. There's a whole synergy with foods eaten in their natural state and many things we don't really understand about how it works. In comparison, our systems seems not to work so well when we make our artificial creations with completely different balances of nutrients and ingredients.

(btw, has anyone noticed these prove you are not a robot number reading tasks are sometimes close to impossible. What number is that fuzzy blob supposed to be LOL!!?!)

blogblog said...

@Karl and Eva,

Australians have ZERO trans fat and HFCS intake. We also have a reasonably low N6:N3 ratio. Total sugar consumption has also fallen considerably compared with a century ago. Yet australians are amongst the fattest people in the world.

blogblog said...

@karl,

most modern fruits have similar sugar content (10-12%) to their wild ancestors. They are sweeter because they are far less sour/bitter. Lemons and oranges have the same carbohydrate content (12%) but no one considers lemons to be sweet.

blogblog said...

The real problem with carbs is snacking. Until a few decades ago people only ate once very few hours. This helped stabilise metabolism.

Now many people constantly snack and consume sweetened drinks. This means blood glucose is elevated for up to 16 hours a day.

Many traditional societies (eg Kitavans) eat ONE main meal a day. They get ONE glucose surge per day and rely on fat metbolism for 12-16 hours per day. In turn they means they can eat as much carbohydrate as they like with few problems.

blogblog said...

Orange Juice or Fructose Intake Does Not Induce Oxidative and Inflammatory Response

Diabetes Care June 2007 vol. 30 no. 6 1406-1411

http://care.diabetesjournals.org/content/30/6/1406.short

CONCLUSIONS—Caloric intake in the form of orange juice or fructose does not induce either oxidative or inflammatory stress, possibly due to its flavonoids content and might, therefore, represent a potentially safe energy source.

This research was based on actual humans.

Breckenridge said...

Interesting link:
http://rdfeinman.wordpress.com/2012/10/02/suddenly-last-summer-part-ii/

George Henderson said...

@ Blog Blog, is the aussie 6:3 ratio as low as the Japanese at 2:1?
Or is it just lower than the US 10:1?
Aussies still eat sugar (not much HCFS which is the red herring) and drink fruit juice and alcohol.
It's what the fat people ate that counts.

George Henderson said...

http://www.ncbi.nlm.nih.gov/pubmed/17464520

Lipids. 2007 Sep;42(9):811-9. Epub 2007 Apr 27.
Membrane fatty acids as pacemakers of animal metabolism.
Hulbert AJ.

The recent discovery that the fatty acid composition of tissue phospholipids varies in a systematic manner among species has lead to the proposal that membrane fatty acid composition is an important determinant of the metabolic rate characteristic for each species. Endotherms (mammals and birds) have a basal metabolic rate (BMR) that is several times that of ectotherms and have more polyunsaturated membranes. In both birds and mammals, as species size increases there is a decrease in mass-specific BMR and a decrease in membrane polyunsaturation. Membrane-associated processes are significant components of BMR and important membrane proteins operate at much faster rates in species with high BMR than in those with low BMR. A series of "species-crossover" experiments show that the rate of this molecular activity is largely due to the nature of the membrane bilayer surrounding these membrane proteins such that polyunsaturated membranes are associated with fast membrane-associated processes. It is suggested that this influence is due to the physical properties that such polyunsaturated membranes possess. This has been called the membrane pacemaker theory of metabolism and provides a framework to understand factors such as the influence of diet on metabolism. It is noted that in the rat membrane fatty acid composition is a regulated parameter being more influenced by the balance between n-3 and n-6 polyunsaturates in the diet than it is by general diet content of saturated, monounsaturated and total polyunsaturated fats.

George Henderson said...

@ blogblog,
a single drink in healthy volunteers isn't proof of anything.
If someone wants to drink 300 cal of sugar once in their life, I say go ahead, it won't do you any harm. If it contains fructose, the uric acid elevation will cancel out the oxidation at first.
Next question.

Kindke said...

@blogblog,

I do agree that frequency of eating is a genuine problem. Especially with carbs as it seems to lead to over-expression of ChREBP in the liver. Im pretty sure thats where the fatty liver is coming from, atleast on a high carb diet. Whether or not ChREBP is also responsible for hepatic IR is another issue.

Ive been on warrior diet ( essentially 23/1 IF ) for over 2 weeks now and I absolutely love it. In the past ive tried it but always fell off because of poor willpower but after being on it for 1 week the daytime hunger completely vanishes, I have more energy during the day. Pigging out at 1 meal at night allows me to finally experience a "food orgasm" where complete satisfaction is met and my attention naturally turns away from food.

karl said...


@blogblog said...
blogblog said...
"Australians have ZERO trans fat ..."

Uh.. that is impossible - there are several sources of transfats besides hydrogenated vegetable oils.

And I'm not sure it matters if they get their fructose from cane-sugar or HFCS.
They would not have the import tariffs that the US has on cane-sugar - and as Australia imports a lot of food, I would be doubtful that the statistics are valid.

Re - frequency of eating - If I eat a little all day of carb foods - I would have constantly elevated insulin which would keep the fat locked into the adipose tissue. I think our evolved biology was for surviving frequent fasting - that doesn't prove it is necessary. (I also think we are evolved to eat more insects than the paleo dieters assume ).



@fortune

I would not have much faith in the survey statistics from the Philippines - not everyone even gets a death certificate there. I know they drink a lot of soda-pop - the sugar cane is locally grown. I have little faith in any statistics about the Philippines - lots of business is off the books.


George Henderson said...

@ Karl and Bloblog:

transfat levels in NZ are very low indeed compared to US and almost all from dairy, but some people eating certain foods that still contain artificial transfats would get more.
Artificial transfats are preferentially made from the alpha-linolenic acid in oils, therefore they are a marker for an omega-3 deficient diet.

blogblog said...

@karl,

total Australian sugar consumption has fallen 8% in the past 4 years and 23% since 1980. This is a fact not an opinion.

Austalian trans fat intake is miniscule.

There are societies in West Africa that live almost entirely on bananas. Other West Africans eat vast amounts of peanuts and have N6:N3 ratios greater than 100:1. Yet they have negligible obesity.

George Henderson said...

@ Blogblog, with african examples we are getting into FADS mutations that maximize EFA conversions.
It takes high 6:3 plus fructose to promote obesity; high 6:3 alone just generates disease. These populations are usually protein-deprived too.
HIV might help offset a more obesigenic modern food supply.

J said...

http://www.nytimes.com/2012/09/23/opinion/sunday/the-optimal-diet.html?_r=1&fb_source=message

Opinions?

jojopig.com said...

thanks for the posts. good blog.

Renaud said...
This comment has been removed by the author.
Bill said...

From this week’s Archives of Internal Medicine: http://annals.org/article.aspx?articleid=1379773
Poor sleep = 30% reduction in adipose tissue insulin sensitivity, but 16% reduction in systemic insulin sensitivity. Thoughts?

Renaud said...

We are all doomed :
http://www.sciencedaily.com/releases/2012/10/121030062007.htm

ROTFL!

Peter said...

As my work colleague would say (broad Italian accent) "Dig tha hole, choose tha coffin...

Peter