Saturday, October 01, 2011

HOW MANY bananas a day?

Our daughter eats everything. Her ultimate favourite food so far is a purée of pig heart casseroled in red wine. We tried her on a banana, head to head with 90% cocoa chocolate. My wife filmed the encounter.



The vocals at 19 seconds from the start sum it up.

Help was needed with the chocolate as it glues itself down to the tray, especially when well sucked!

Peter

24 comments:

Bill said...

She's hardcore on 90%!
I've been eating 100 grams of 85% a day for 2 years now.
Then Chris Kresser flags up high levels of phytic acid/phytates in cocoa powder and nutrient absorption issues. Recommends not being a staple and minimise.
Is this really an issue?

frankweir said...

I'm not a science guy and I can follow only about 15 percent of what you are saying on your blog BUT your daughter is gorgeous! And hysterically cute!

Peter said...

Bill, we all have our own ideas. Obviously plants hate us and use us. The cocoa bean bribes us with a rather pleasant hook. You also never mentioned the disgusting antioxidants in cocoa powder nor the prepoop. oops, I mean fibre. All nasties but hey ho... I'm no perfectionist!

frankweir, oh yes, that's how she is. Doesn't get it from me!

Peter

Olga said...

Hi Peter:

Have you seen this new study?

http://www.ncbi.nlm.nih.gov/pubmed/21943927

STG said...

What a great post--priceless! She looks like a very inquisitive child. Lucky parents!

Sam Knox said...

I love how she gets food everywhere but her bib.

Ellen said...

Peter, a little off subject, but wanted to see if you had any thoughts about this paper..

http://jcem.endojournals.org/content/89/4/1641.full.pdf+html

Why would the provision of polyunsaturated fats over saturated fats on a ketogenic diet result in better insulin sensitivity for the POLY group? I look at the food lists given and it seems to me it's real food over processed food, yet the processed food group had better IS scores. Wierd.

Stabby said...

Ha, I caught that yesterday in my youtube inbox, priceless. I think I see Jesus in the chocolate smears. Praise him! :)

Ellen, a quick objection is that the "saturated fat" diet was devoid of omega-3 fats. The history of bashing saturated fat is full of giving one group something like canola oil, and one group ultra-crappy industrial lard and then blaming "saturated fat" instead of lack of omega-3 fats.

Unknown said...

Peter, if you have time, I'm curious to hear your take on Stephan's new opus.

The Case for the Food Reward Hypothesis of Obesity

Jane said...

Bill, you asked whether phytic acid in cocoa powder is really an issue.

Have a look at this from the British Medical Journal (17th Sept 1977, p771)

'..The evidence incriminating phytic acid, based on relatively brief studies on humans and animals, is often at variance with epidemiological evidence, the principal exception being the experience in Iran. In South Africa Blacks in rural areas are accustomed to a relatively high intake of phytic acid. Yet our studies on groups on very high intakes compared with those on lower intakes have revealed no differences in mean haematological values, whether in children or adults. Observations on contrasting groups have revealed no differences in mean serum calcium levels, nor in the mean cortical thickness or other dimensions of the second metacarpal. Indeed, we have found satisfactory calcification even in groups of mothers who have had numerous pregnancies and long lactations. Nor in the groups mentioned have we found differences in the growth rate of children. In our appreciation, Third World experience does not support the view that phytic acid is significantly prejudicial to mineral metabolism or to health. ..'

It says 'the principal exception being the experience in Iran'. As I understand it, Iran's problems with mineral deficiency started during the Green Revolution, when Iranian farmers tried to grow high-yielding crops on mineral-poor soils. Teenagers were found with short stature and late puberty, which could be corrected by zinc supplementation.

From this observation, the entire zinc supplement industry was born, with Americans taking their zinc religiously when there is no evidence of zinc deficiency - no short stature, no late puberty, actually the opposite.

Excess zinc can cause copper deficiency. It's pretty clear that Americans DO have copper deficiency, see for example this paper linking it to fatty liver:
http://www.ncbi.nlm.nih.gov/pubmed/18505688

Chocolate is very high in copper. I think Chris Kresser should not be telling people to eat less chocolate because of the phytic acid.

Peter said...

Hi Olga,

Hadn't seen it but it certainly looks like there are protective pancreatic effects to parallel the CNS effects of ketogenic diets.

Ellen, corn oil has always been known to be more ketogenic than butter based diets. Extrapolating from 5 days to a lifeltime ignores the fact that safflower oil is one of the most effective generators of a fatty liver you can ask for. The cirrhosis literature is full of this information, omega threes in excess do the same.

Also palmitate induces insulin resistance better than PUFA. Under ketogenic conditions you are not supposed to be insulin sensitive. Combining fat burning and glucose burning at the same time seems an excellent way to kill your mitochondria.

Improved ISI would probably come from increased oxidation of omega 6s as the body really does not want a fatty liver or oxidatively unstable inner mitochondrial membranes. I've not got the mechanisms but the end results are old information.

The results of the current line of thinking will be that PUFA KDs are labelled as "best" and then all KDs will get trashed when people on 60% "healthy" PUFA KDs develop cirrhosis! Oh, and cancer too if lab rats are representative of humans.

I loved the word "imitation" as the first word of the Frankenfood list.

Duh.

Peter

Peter said...

Uknown,

I might get time to flick through it sometime. It's probably about as convincing as the critique of the carbohydrate hypothesis. These current posts are still in a large part pointing out why that carbohydrate critique is incorrect and the series is far from finished.

I have to say that Stephan will undoubtedly do very, very well in obesity research. He will undoubtedly convince many. It would be better if he were correct, but you can't have everything and obviously this has nothing to do with success in academia.

Peter

Olga said...

Hi Peter:

In your comment:
"Also palmitate induces insulin resistance better than PUFA. Under ketogenic conditions you are not supposed to be insulin sensitive. Combining fat burning and glucose burning at the same time seems an excellent way to kill your mitochondria."

Does this apply to insulin sensitive people? I understood that if you eat a reasonable amount glucose (just enough to stay out to ketosis) and saturated fatty acids, that your body will dispose of the glucose first and then you will switch to fat metabolism. Is this not correct?

nancan said...

How telling! Baby given non-sugary options will go for the gold.

john said...

Olga,

I think what you said is correct, but there's still more resistance with sat fat. It's pretty general: you see the same whether it's one mixed meal, 5 days of eating, or long term--though there are some conflicting results for each; Stephan has posted on long term sat fat & IR.

Peter said...

Olga,

I would assume that insulin sensitive people have, in general, normal metabolic responses to nutrients. A mixed meal should inhibit lipolysis and facilitate both glucose metabolism and fat storage. We certainly almost always run on a mix of fat and glucose if they are available, the rationing out should work fine if the fat is palmitate balanced by some monounsaturates. Insulin should never need to be very high and soon drops to allow lipolysis. Adequate mitochondria seem to be the essential requirement.

The current big experiment basing lipid intake on PUFA from bulk seed oils. Fatty liver will make the picking apart of exactly what is going on difficult, and somewhat pointless...

Peter

blogblog said...

@Jane,

deficiencies are only noted when obvious clinical symptoms appear. That doesn't mean that most people are getting adequate mineral intake.

blogblog said...

@Jane,

the mineral content of plants as determined by chemical analysis tells us absolutely nothing about how our bodies use those minerals.

If you want minerals eat meat or take a pill. Don't rely on plants.

ItsTheWooo2 said...

@Ellen

Looking at the diets, the poly group consumed far more glucose tolerance/insulin suppressing nutrients.


THe poly group is eating a lot of nuts (soy and walnuts), which are loaded with magnesium, which will suppress insulin levels (Greater lipolysis/ketones) and improve insulin sensitivity.


The poly group is eating more omega 3s as they are consuming walnuts and presumably fish; the sat diet is eating pepperoni sticks and ham rollups with cream cheese. Omega 3s are extremely important for glucose tolerance and insulin reduciton.


The poly group is eating no dairy, which is known to augment insulin. Whey protein is highly insulinotropic as are dairy products in general.
The sat group is eating tons of dairy.


The poly group consumed far more vinegar which is well observed, easily replicatable, to suppress insulin release after meals leading to inhibited feeding/weight loss/stable blood sugar.


I am not at all surprised that a ketogenic diet full of nuts/magnesium and vinegar and minimal dairy was superior in ketone levels and parameters indicating lower insulin levels (cholesterol). The satfat aspect was not the reason why; the reason why is that the poly group is more glucose tolerance nutrient rich whereas the sat fat diet was more insulinotropic.


The difference in insulin levels (sat fat diet required more of it due to being full of cheese and less magnesium/vinegar) would easily explain the changes in ketones and cholesterol between these diets.


If you gave the SAT dieters this supplement coctail:
-some flax seed oil + EPA/DHA in numerous grams per day
-magnesium citrate tablets,
-chromium picolinate/GTF,
-acetl-l-carnitine (ever so useful for CPT1, normal dopamine function, normal tesotsterone function in men, required to reduce insulin levels/not be a fatso)
-myo-inositol (required to have your insulin /serotonin/numerous other receptors work properly, depleted by hyperinsulinism)
-Lots of vinegar

I would bet a years pay that the "sat fat diet" would no longer show to be inferior to the poly diet, in fact you would probably observe the sat fat dieters to have far superior metabolic parameters and weight loss.


FYI, I discovered all of these tweaks and tips over the years of experience with inferior glucose tolerance and symptomatic hypoglycemia and obesity; only later did I find my practices validated by commonly replicatable research. But oh ya, n=1 so it's not valid, let's all go to WHS and listen to the real reasons people are obese/I am able to be 115 pounds for years and years, because I'm sure it is true that magnesium/vinegar/acetllcarnitine/inositol/lack of dietary carb just work via food reward reduction.

ItsTheWooo2 said...

Oh and ditto Peter's response. PUFAs do not cause as much insulin resistance as sat fat, but this is not always a bad thing, some insulin resistance is physiological.

The body can constrict or dilate blood vessels depending on numerous environmental variables such as position (sitting vs standing), temperature (warm vs cold environment), or blood volume (high or low fluid in the intravascular space).

Saying that a cold room where you are rising from your chair leads to vasoconstriction is the same thing as pathological hypertension, is just like analyzing whether high or low sat fat diets lead to greater or poorer insulin resistance. The transient change in insulin sensitivity from saturated fat while on an almost dietary glucose free diet is not the same as being a diseased type II diabetic with like 3 poorly functioning mitochondria left and a viscera full of fat (when white fat insulin resistance reaches a severe point, hyperplasia is no longer/never was possible for genetic reasons, onward and forward to severe metabolic disease!)

The ironic thing is, as Peter points out, the physiologic insulin resistance may be the very thing that prevents you from developing the pathological form.

Anon said...

It's the Woo, thank you for your posts.

Ellen said...

Thanks Peter, Woo and Stabby for your comments, I have a much better understanding now.

William said...

Our 25 week old son also loves himself some 85% cocoa. Here is a picture after a soft boiled egg yolk and sucking on a square of 85%: https://fbcdn-sphotos-a.akamaihd.net/hphotos-ak-snc7/387935_2644620598362_1341046999_33068634_605908967_n.jpg

trinkwasser said...

"I have to say that Stephan will undoubtedly do very, very well in obesity research. He will undoubtedly convince many. It would be better if he were correct, but you can't have everything and obviously this has nothing to do with success in academia."

What's noticeable to me is the severe difference in the comments and commenters on his blog pre and post Revelation.

Comments are the exact opposite to LDL. Small dense comments good. Large fluffy comments cause slumber.

Banning Woo while letting Randy back in under his new identity of Frank says a lot. Petulantly crossing your blog off his recommended list too, though I'm surpised he isn't (yet) adding Carb(in)sane.