17.7.12

Enjoy Eating Saturated Fats: They're Good for You. Donald W. Miller, Jr....



Uploaded by on Aug 28, 2011
Dr. Miller is professor of surgery, cardiothoracic division, Univ. Washington, and writes frequently for http://www.Lewrockwell.com.

16.7.12

Food in Ireland 1600 - 1835

Food in Ireland 1600 - 1835




The potato has been around for a long time, and is one of the earliest ever cultivated foods, but only arrived in Europe in 1570, from South America. The Irish took to it quickly. It grew well in Irish conditions, provided bountiful harvests and, most importantly, could be easily stored and eaten during the winter months.

Its effect was nothing short of dramatic, but what seemed initially like the answer to a prayer would turn out to be a curse.

The Irish population, with access to this new staple food, began to grow, and extremely rapidly. When the potato arrived in 1580 there were fewer than 1 million people living in Ireland, by 1840 the population had exploded to more than 8 million, most of them poor.
The burgeoning population lived on a diet comprised mainly of potatoes and milk, which if eaten in sufficient quantity is a surprisingly nutritious, if monotonous, diet. It is also relatively tasty and easy to prepare.

It is estimated that by the late 1700s an average family of two adults and four children needed 5 tons of potatoes a year, or about 5lbs of potatoes each a day. Though this may seem a lot, even a poor farmer or farm labourer could readily grow this amount on just half an acre.

The Irish Diet before the Famine

By the early 19th century everyone ate potatoes, from rich to poor, and no meal was complete without them. For some this was almost all they ever ate.

What the Poor Ate

A report on the food given provided for inhabitants of workhouses in 1840 would have been an extreme, but not untypical, example of the diet of the poor.

Breakfast Dinner Supper
Kilrush
Men 4lbs potatoes, 1 pint skimmed milk. The same, with herring instead of milk in Winter. Not always provided.
Women 3 lbs potatoes, 1/2-1 pint skimmed milk The same.
Scarriff
Men 5lbs potatoes, 1 pint sour milk The same. Herring when milk cannot be had. The same
Women 3lbs potatoes, 1 pint milk The same The same
Milk was not always available and herring was a popular and cheap substitute, with oatmeal replacing or supplementing potatoes when they were scarce. They also ate what they could forage in the wild – berries, nuts, nettles, wild mushrooms and now and then a rabbit or bird. However these were all occasional rather than regularly eaten foodstuffs.

Poorer people either produced their own food or obtained it by forageing or hunting. Outside of cities, little or none was purchased in shops, even when these began to appear.

While the potato provided enough food to allow the poor to survive and grow in number, it also caused their diet to become very narrow and restricted, a massive change from the varied diet eaten in earlier times and, as would become clear, a very dangerous dependence.

What the Rich Ate



The better off had access to cultivated vegetables and regularly ate meat, primarily pork and mutton with rather less beef. However these foods were expensive and even in the homes of the well off tended to be ‘padded out’ with potato.

Many dishes looked on as being typically Irish – champ (potatoes and scallions, or spring onions), colcannon (potatoes and cabbage), Irish Stew (the poorer cuts of meat with potato and vegetables), boxty (fried potato cakes) – were developed at this time in an effort to eke out the food available and also, presumably, to provide some variety.

Another traditional Irish food, black pudding, which is made from ox blood and oatmeal, gave those who had a cow access to protein without killing their valuable animal – the blood came from occasional bleeding of live animals.

In towns, shops began to emerge from the early 1600s, primarily butchers and bakers, where before only open markets would have taken place. They had a ready clientรจle in the merchants who controlled the export trade, the administrators representing the English government, army garrisons and the agents of landlords. As well as locally produced food they sold imported delicacies, preserves, spices, sugar and tea.

Irish Farming Before the Famine

The vast majority of Ireland’s rapidly increasing population was engaged in agriculture – more than 75% of men and, at least seasonally, large numbers of women also.
Oats and barley were grown as cash crop rather than for consumption, cattle were reared and dairy herds developed, almost all of which went to satisfy the demand for food products in Ireland’s larger towns and cities and in the populous urban centres of England.

Some of the native Irish were tenant farmers but most were cottiers or labourers, working not for money but in return for the right to a small plot of land, known as ‘conacre’, on which they could grow enough potatoes to feed their family.

A writer of the time, describes vividly the conditions in which they lived:
The master never fed a labourer…it was on the contrary a chief object with him to keep such a person as far away from his dwelling as possible. He therefore allowed him to occupy, at some remote corner of his farm, a miserable hut, a mere shell, formed of mud or sods, without loft, apartment or partition and sometimes without any other covering than that of straw or any chimney than the door. In one corner of this hovel was lodged his cow, while in the opposite were his wife, his children and himself.
The better off Irish who had land in excess of that needed to feed their families, such as the tenant farmers, sold almost everything they could produce to meet the demand for rent and to provide a modest income. As the population grew in cities like Dublin and larger towns, where there was the beginnings of industrial development, the market demand for grain, meat and dairy produce grew too.

Increasingly milk, for so long a vital part of the diet of the poor, was too valuable to drink whole and was either used to make butter or to fatten animals for sale. Poor families were left with the less nutritious whey. With milk less available, the state of nutrition of the poor population became ever more perilous and localised failures of the potato crop, which occurred sporadically from about 1800 on, saw many forced to leave their land and to forage or beg for survival.

It was, in every sense, a disaster waiting to happen. And then it happened.

Why I Don't Give a Crap What the Kitavans Eat - The Spark of Reason: Comment on Guyenet vs. Taubes

Comment on Guyenet vs. Taubes; or Why I Don't Give a Crap What the Kitavans Eat - The Spark of Reason

"So while carbs in general may not lead to metabolic syndrome, once you've arrived dumping carbohydrates on your broken carbohydrate metabolism is tantamount to doing jumping jacks on two broken legs. I believe the science (along with a massive stack of anecdotal evidence) is pretty clear here, in that the most successful treatment for metabolic syndrome is carbohydrate restriction." 
This post started as a comment to Stephan Guyenet's excellent post on the carbohydrate hypothesis of obesity, got too long, and so I'm putting it here. Do read Stephan's post, and keep an open mind. It's got loads of interesting and cutting-edge science, and this sort of debate and information exchange is how science progresses. If you find yourself experiencing cognitive dissonance, remember that absolute belief is antithetical to science. We always must update our beliefs as new information emerges.

Short summary of Stephan's blog post: the hypothesis that carbohydrates in general are fattening is probably over-simplified and does not reflect the most recent scientific understanding of metabolic regulation. It also leads one into a variety of paradoxes, a la the "French Paradox" of the diet-heart hypothesis.

I think part of what we're seeing here is the rather poor taxonomy of nutrition. We discuss things in terms of macronutrients, but those macronutrients come with (or without) all kinds of other metabolically relevant substances. And even within a given macronutrient group there can be significant metabolic differences, e.g. for fatty acids of different chain lengths, or between glucose and fructose (though Dr. Feinman might have something to say about the latter).

I've posted here before on my favorite example of this, and it seems like a good time to revisit (working from memory and about 4 hours of sleep, so please correct me if necessary). The Aztecs had a corn-based diet. They did experience obesity, but despite documenting a wide variety of health issues in detail never described diabetes. The Egyptians ate a wheat-based diet, also experienced obesity (along with heart disease, cancer, and the whole host of other fun "diseases of civilization"), and did document diabetes. Two high-carb diets, both resulting in some level of obesity, but from what we can tell (thousands of years later), both having radically different metabolic endpoints.

Two take-home points here. First is that we likely need to consider a broader dietary context than that imposed by our artificial macronutrient classification scheme, i.e. wheat and corn both provide primarily carbohydrates as energy, but probably do not have the same metabolic effects, particularly when considering over the timescale of a human life. Second, obesity is a symptom. A given symptom may result from multiple underlying conditions. We need to focus the discussion on more specific pathologies than just "obesity".

In the US and many other Westernized countries, one can take a look around and do a "liver check". How many people do you see with a protruding pot belly as opposed to a general body-wide distribution of fat? Most people I see have the big belly, sometimes even being very lean elsewhere (particularly in the arms and legs); there are a few "Rubinesque" figures as well, but the pot bellies seem to be running away with the obesity stakes. The big belly is indicative of fatty liver. Considering how central the liver is in metabolic regulation, it should come as no surprise that an inflamed fatty liver could lead to a whole host of metabolic disturbances: obesity, abnormal lipid profile, elevated blood sugar, elevated insulin, etc. In other words, metabolic syndrome.

I would argue that the rapidly growing health problem is not simply obesity, but metabolic syndrome (remember obesity is only one symptom, and there are thin people with metabolic syndrome too). We want to understand both how we arrive at metabolic syndrome (so our children can avoid it), and also how to treat it for those who did not avoid it. It is clear "carbohydrates" across the board are not causal in the development of metabolic syndrome. Stephan provides several counter-examples; another is the Tarahumara, who like the old-school Pima subsist largely on corn, beans, and squash, but who have one of the lowest rates of Type 2 diabetes in the world.

But the cure is not necessarily the reverse of the cause when it comes to disease. Metabolic syndrome brings a whole host of issues, not the least of which is broken carbohydrate metabolism. So while carbs in general may not lead to metabolic syndrome, once you've arrived dumping carbohydrates on your broken carbohydrate metabolism is tantamount to doing jumping jacks on two broken legs. I believe the science (along with a massive stack of anecdotal evidence) is pretty clear here, in that the most successful treatment for metabolic syndrome is carbohydrate restriction.

So while yes, Virginia, the Kitavans eat a very high-carbohydrate diet and exhibit general metabolic health, for my personal dietary choices I don't really give a crap. The Kitavans have healthy carbohydrate metabolisms, but I don't (prior to going low carb I had a trophy beer gut, which in retrospect was my liver telling me "You're killing me slowly"). If you look down toward your feet and can see only your protruding liver, you might consider trading in the bagels for bacon (better yet, get yourself a blood glucose meter and check your post-bagel blood sugar - it might frighten you). It is important to remember that carbohydrate restriction is successful as a treatment for a disease, but it doesn't necessarily follow that all carbs are bad for everybody. We have several examples of cultures who thrive on diets of lean protein and whole food sources of carbohydrate, like starchy tubers and fruit. We also have examples of cultures thriving largely on protein and fat. 
Humans appear to have a remarkable ability to survive as omnivores eating whole foods, which in no small part explains why we are one of the most widely spread species on the planet. So if you have a healthy metabolism, you probably can choose from a wide variety of whole foods (and by "whole food" I mean something you could plausibly obtain from Nature without the aid of much more technology than fire and a sharp stick). Once your metabolism is broken, you will likely need to make some choices to avoid those things which, due to your disease state, have become effectively toxic. In other words, make your nutritional choices based on actual knowledge of metabolism and your own state of health rather than picking a buzz-phrase and applying it blindly.

And for God's sake, stop eating wheat ;-)

39 comments:

praguestepchild said...
Great stuff, and glad to see you are still alive and kicking. I've also been pondering the Taubes/Guyenet false dichotomy. It is an interesting dust up and it managed to pull you and Kurt Harris (at least in comments) back from The Fortress of Solitude, which is always a good thing. My thoughts on the food reward hypothesis are something like my thoughts on string theory. Deeply skeptical. But I know about as much about physics as I know about biochemistry.
Dave said...
@praguestepchild, Good to be back. I've been bubbling on a couple of posts for awhile, this being one of them. I dearly wish I had been at AHS to serve some this out in person. Food reward is likely part of the puzzle, as it clearly plays a part in metabolic regulation. I don't think it's the whole thing, but another potential area of malfunction, probably in concert with various other regulatory mechanisms. Successful organisms must have robust metabolic regulation, which generally means a lot of redundancy and intertwining feedback mechanisms. It also sounded like Stephan is suggesting that metabolic dysfunction is largely isolated in the brain - maybe I'm misreading (low on sleep). That seems backward to me, if you consider how multicellular organisms would have evolved from unicellular (indeed, this is the subject of another post I've been fiddling with). The brain is a pretty late arrival, evolutionarily speaking, while it's addition certainly helps in making overall regulation more robust, I'd be surprised if evolution had it take over the show and simultaneously devolved all of the mechanisms that existed before brains. What's wrong with string theory? It predicts everything - including everything that isn't observed ;-)
tk said...
Great post. Breaking down the science into common sense. My own carbohydrate metabolism is definitely broken. That I know for sure. I haven't looked down at my feet in a long time. (I hope they're still there!) :) For me, it doesn't matter if someone finds a group that is able to live to 150 with perfect health on a diet of only white bread and coca-cola. The fact is that I know that won't work for me. (I already tried that diet for years) Thanks.
Mrs. Ed said...
Great Post. The only one size fits all nutrtional advice I can figure out is that processed foods are bad for everyone. Beyond that it seems that it depends on the individual. I just focus on what works for our family, but I do like reading all the different takes on it. I have started to see more pop up about the role of gut bacteria and nutrition. Also that chemicals in our environment may play with our insulin.
Dave said...
Nice commentary by Dr. Andreas Eenfeldt: http://www.dietdoctor.com/guyenet-taubes-and-why-low-carb-works
Margaretrc said...
Very sane post! My sentiments exactly. When GCBC came out, I read it and thought "Wait a minute. what about the French? Thai? Greeks? Italians? etc. etc." Now I asked the same thing of Stephan re food reward. It doesn't fit a lot of traditional cultures outside of our own and it only fits our own in recent times, after we moved to a low fat, high carb diet laden with sugar, white flour, and vegetable oils. Hmmm. Whatever role food reward plays, if any, I agree that the underlying problem has to be a metabolism broken by eating a diet that is unbalanced and full of artificial, processed garbage. And that is the problem that has to be addressed. It will be interesting to see if eating bland pap will do it, but personally, I would rather eat LCHF, which both my husband and I do. And eating LCHF did get rid of the liver belly my hubby had, so we are sticking with that.
Dave said...
@Margaretrc I've been thinking a bit more on this, and I think one point the discussion is missing is the detailed nature of the "carbohydrate hypothesis", in particular necessity vs. sufficiency. Is Taubes claiming that that carbohydrate consumption *will* make you fat (which leads one to "paradoxes"), or that it is a necessary ingredient for obesity? I believe he's pushing necessary instead of sufficient, namely that carbohydrate consumption sets up the hormonal/metabolic environment to promote obesity, but that the actual manifestation may require other factors as well. I feel another blog post coming on...
Anonymous said...
do Kitavans eat breakfast, lunch & dinner? Looking at nutrient intake per day may be a misleading if we don't take into account meal frequency. And it's kind of funny that everybody seems to leave aside the idea that the Kitavans could be genetically adapted to their regional natural food supply. What may be valid for them may not apply to europeans or africans because they evolved in a different region. Duh.
Chris said...
I posted a few comments on Dr. Eenfeldt's blog about this (the good Dr's post on Guyenet referenced by Dave), and I think it fits in here. I think Dr. Eenfeldt's reference to the 'trees for the forest' phenomenon is a good metaphor for Guyenet's argument. I've been mulling it over, and I think I can certainly conceive of a bigger picture that included both insulin-driven, hunger-based food seeking behavior, in tandem with a reward feedback loop that is not unlike the reward response you get with addicitive substances, like cocaine or amphetamines. Let me just illustrate with my own n=1 observations: I went low-carb back in April of this year, and when I stick to it, I do not get that gnawing empty hunger feeling in the pit of my stomach that I used to get when I would, say, start my day with a blueberry muffin and a cup of coffee with sugar in it. The hunger on a LCHF diet, for me, is mild and far from desperate. I've read the comments of other folks at various blogs who say the same thing. Now, I would bet that many others who have struggled with their weight in the past have had the 'drug-like' experience that comes along with bingeing on ice cream or cake frosting or some other sugary treat - I mean, I literally would go into a trance-like mental state on such a binge, and engage in almost ritualistic eating. You even stop thinking about or noticing how your stomach feels and instead focus on the taste and texture and the immediate pleasure sensation of putting the spoonfuls of sugar-laden stuff in your mouth. Like others have said (Lustig, Taubes, etc.), sugar is addictive - it is a drug. So, I see a useful synthesis of Taube's recognition of an insulin-driven, hunger-based carb-seeking behavior, coupled with a reward-system based drive to just eat and eat and eat sugar in its various forms. The insulin traps the fatty acids in the fat cells, the other cells kick into starvation mode, send signals to your brain to go get some carbs, then, especially if you are sucking up the sugar, the reward system response (is it dopamine-based, in your pre-frontal cortex?) kicks in to drive the bingeing. The insulin response is literally a 'gut feeling'; the 'food reward' response is our dopamine/PFC system kicking in (like those cocaine addicited mice perpetually pressing the lever to get a hit ... until they starve to death).
Dave said...
@Chris, I'm right there with you. Metabolic regulation must be considered as a whole. Obviously the part that determines what and how much you eat can't be decoupled from the part that handles how energy is used/stored. These two subsystems necessarily communicate, and screwing up one probably throws the other one out of whack as well.
Dave said...
I don't think the Kitavans have had enough to time to undergo significant genetic adaptation. Anyway, I don't think they would have had to. See my point about necessary vs. sufficient above.
Margaretrc said...
Dave, I 100% agree that Taubes is pushing necessary, rather than sufficient, and he said as much in an interview I listened to today: http://audio.5by5.tv/broadcasts/paleo/2011/paleo-030.mp3 And I agree with both of you that, whatever the reasons for metabolic breakdown, it is carbohydrate restriction that is the key to a return to health. Not undoing the damage--I don't know if that can be done--but a return to normal weight, heart health and non-diabetic BG numbers.
Anonymous said...
Food reward. This confuses me. I am reading a book about African cultures, how they stew meat for days and days with spices, eat it with whatever they have access too (presumably pulses, grains, animal fat, etc). Now this is all whole food by your standards (okay, maybe not the grains--depends on prep I guess) but this all sounds pretty dang tasty and rewarding to me and I could eat and enjoy LOTS of it. And I could think of other wholesome food cultures where, yes, the food is not processed, but where they ate carbs and fat together to no metabolic demise. So I guess my question, perhaps more for Stephan than for you, is why are we making this food reward thing out to be such a novel 21st century concept? People had carbs and fat together in a pleasure-inducing recipe combination since forever ago! This is not new! Is it because they didn't have everlasting access to those combinations? Seasonality, drought, governments taking away ingredients?? Would love your insight. Thanks in advance! ~Discombobulated
Dave said...
Isolating food reward tends to lead to circular arguments. Food reward is a learned response, your body's way of figuring out what's good to eat, and making you eat more of that. Say you try some round red things hanging off a bush. They taste sweet, which registers in the primary taste cortex. The process of digestion causes a variety of signals to be detected and integrated by the secondary taste cortex. These include things like glucose and insulin, along with other hormones, and probably micronutrients as well. The secondary taste cortex deems this a good thing, and the next time you see round red things on a bush, you'll have the urge to eat them. On the other hand, if they give you a stomach-ache, that behavior is downgraded. But I don't think you can say "eating rewarding foods leads to hedonic dysregulation" or something like that. That basically boils down to "eating rewarding foods leads to eating rewarding foods", to which I would respond "no shit". What made it so rewarding in the first place? We're not born loving wheat, we learn it from the biological feedback created by eating wheat. My point is that food reward is necessarily integrated as part of metabolic regulation, both short and long term. Try eating a whole stick of butter, or 20 pieces of bacon. Starts off very rewarding, but will stop tasting good after awhile. So I think the question isn't whether it's insulin (or leptin or whatever) vs. food reward, but why/how the connection between them gets broken.
Jane said...
Hi Dave, remember me? Good to see you back, and talking your usual good sense. With one tiny exception, perhaps. Wheat-bashing is SO last year ...
Dave said...
Hi Jane. Actually, with publication of William Davis' "Wheat Belly", I would think wheat bashing is very much this year. ;-) It comes down to the cost-benefit analysis. Wheat might be harmless, or maybe not. The potential downside is fairly large. We have to emphasize "potential", but there certainly exists a significant fraction of the population (e.g. celiac sufferers) for which the downside is definite and painful. And the potential upside? Not much, and certainly nothing not easily obtained by substituting other foods. So why risk it?
Jane said...
Thanks, I hadn't seen Wheat Belly. Would I be right in thinking that the bad stuff all relates to white wheat flour? - which I agree is so toxic it shouldn't even be called food. But you're right, why risk it? If you've been brought up on white flour, you will have been sensitised to gluten and probably can never tolerate it. I must say in wheat's defense, though, that the evidence suggests that if you've always eaten only whole wheat, it's a good food. Those ancient Egyptians apparently ate white flour, as rich people though the ages have done.
Dave said...
"Wheat Belly" argues that wheat is bad across the board, white, whole, or whatever. Still not a lot of slam-dunk science here, but certainly many bits of evidence that all point in the same direction. Contains an interesting discussion of how modern "wheat" (dwarf varieties introduced in the 1980's) has significant genetic differences from the "ancient" wheat that drove the development of agriculture. How can gluten be bad in white flour but not in whole wheat flour?
Jane said...
Because the proper handling of gluten needs micronutrients that are removed from white flour. Gluten is not really a toxin, it's the plant's way of storing amino acids. When the grain germinates, gluten is broken down by enzymes that have counterparts in our own digestive systems, and require cofactors such as magnesium or manganese, which are almost completely removed from white flour. These metals are also needed by the gut immune system, which is normally instructed in a process called oral tolerance not to react to dietary proteins such as gluten. It's the failure of oral tolerance that causes celiac disease.
Dave said...
@Jane, Which enzymes? Do you have a reference showing this in humans? I don't see how the function of gluten for a plant is related to it's toxicity in humans. Cholesterol isn't a "toxin" per se, but is definitely toxic for rabbits. Here's they celiac hypothesis put forward in Wheat Belly (also the reference 24 pasted below): Regulating intestinal permeability is therefore a fundamental function of the cells lining the fragile intestinal wall. Recent research has fingered wheat gliadin as a trigger of intestinal release of a protein called zonulin, a regulator of intestinal permeability.24 Zonulins have the peculiar effect of disassembling tight junctions, the normally secure barrier between intestinal cells. When gliadin triggers zonulin release, intestinal tight junctions are disrupted, and unwanted proteins such as gliadin and other wheat protein fractions gain entry to the bloodstream. Immune-activating lymphocytes, such as T-cells, are then triggered to begin an inflammatory process against various “self” proteins, thus initiating wheat gluten- and gliadin-initiated conditions such as celiac disease, thyroid disease, joint diseases, and asthma. Gliadin wheat proteins are akin to being able to pick the lock on any door, allowing unwanted intruders to gain entry into places they don’t belong. Davis, William (2011). Wheat Belly: Lose the Wheat, Lose the Weight, and Find Your Path Back to Health (Kindle Locations 1289-1296). Rodale. Kindle Edition. 24. Drago S, El Asmar R, Di Pierro M et al. Gliadin, zonulin and gut permeability: effects on celiac and nonceliac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol 2006;41:408-19.
Jane said...
Have a look at 'The activation of intestinal peptidases by manganese', which is very short and says 'Since the intestinal enzymes that hydrolyse other peptides such as glycylglycine and prolylglycine are also activated by Mn, it becomes clear that there are in intestinal mucosa several metal-containing proteases.' The prolylglycine is important because peptide bonds involving proline are difficult to break, and there are lots of them in gluten. You could also try 'Metal activation of peptidases', or 'Alterations of pancreatic digestive enzyme content in the manganese-deficient rat'. I don't know of any paper addressing these questions specifically in humans. Some gluten breakdown occurs intracellularly in lysosomes, several of whose enzymes including the proton pump are glycosylated, which requires manganese. Manganese and magnesium activate the enzyme that makes glutamine, which is used as fuel by enterocytes. Everywhere you look, there are digestive processes dependent on these metals. About intestinal permeability. Gluten needs to open tight junctions to gain access to the gut immune system for establishment of oral tolerance. I had a quote about this from a textbook that I sent to some people and will try to find.
Jane said...
Here it is: Normally, a state of oral tolerance exists for gluten. In persons who do not have celiac disease, the peptide products of gluten digestion by pancreatic and brush border enzymes traverse the apical membrane into the enterocyte, where they are further processed by hydrolases to nonimmunogenic products. A tiny fraction of undigested gluten enters the lamina propria through tight junctions and generates oral tolerance. ...
Anonymous said...
WOW, Thank you for a sane sensible blog post. It's the best one I have read in quite a while.
montmorency said...
While the the phrase "great stuff" would apply to this and all of your posts Dave, I'm not sure it really applies to Stephan's IMHO. After supposedly deconstructing Taubes' major theses, even while admitting that low-carbing works for "some people" (I would say it works for everyone who tries it properly, but it may only work to a limited degree for quite a few of us), when at the end he is trying to describe how it works, he has to fall back on the old story "it works by reducing calories". Ah, so it was CICO all along! And I thought it was all so much more complicated, including leptin, ghrelin, other things ending in "-in", or "-ides", and lots of other things with ellipses in their names. Thank you for that insight Stephan. And I thought it was Taubes who was suppposed to be over-simplifying. What Stephan has failed to explain is why I and many other carbers, even if we haven't all quite got down to the 30-inch waists that we had as 20-year-olds, can reduce our calories (if that is indeed what we are doing) on a low-carb diet, without experiencing hunger in-between meals (even on only 2 meals a day for example, and without any form of snacking)? Gary Taubes would (I think) say that it's because of the newly liberated free-fatty-acids which are now available to supplement our now-reduced calorie intake. However, in what Stephan has written, he has eliminated that as a possibility (if you go along with him), but not put anything in its place. Non satis
Calorie Counter App said...
WOW, Thank you for a sane sensible blog post. It's the best one I have read in quite a while. Thanks for sharing with us.
Johman said...
Amen to this post! In our society many are metabolically broken, perhaps from babyhood and have had constant exposure to processed foods. So what do we have in common with those primitive carb cultures metabolically? Not much. I'm tired of seeing "experts" putting obesity as the cause of the myriad of health problems that follow, rather than a symptom. That leads them to think that whatever skinnies up a person is healthy (bariatric surgery,anyone?).
montmorency said...
Dave, I hope you are going to post in 2012. I've been missing the Sparks of Reason, and I'm sure I'm not the only one. How about this to provoke you?: http://wholehealthsource.blogspot.com/2011/11/brief-response-to-taubess-food-rewad.html#more Regards, Mike
Dave said...
Thanks - lots of ideas, too little time. Been really busy lately, haven't even had a chance to read any of Taubes' replies to the initial argument.
Olga said...
Hi Dave: Could iodine be part of the reason some primitive societies tolerate carbohydrates so well? All the societies mentioned by Stephan Guyenet who eat primarily carbohydrates successfully live near the ocean. The Kitavan's, the Tokelauan's, the Okinawa. Perhpas they can eat carbohydrates, because they have healthy thyroids over their life times. The average Japanese consume about 12 mg of iodine per day. Far more than the RDI of 150 ug. It has been argued that 150 ug is merely the amount of iodine required to prevent goitre and that our actual needs are far greater for optimal health. Is it possible that the reason some people claim to experience a decrease in thyroid function when on a low carb diet, is because a low carb diet unmasks an iodine deficiency?
Jack C said...
Dave, In a 2010 post on the whole health website you discussed a problem that your infant son had with a caries. An internet friend from Montana has an infant son with several caries. She has been giving vitamin D and K2 but the caries have not healed. She is looking for advice if you have any to offer. Jack C. @ jandpc@bellsouth.net
Anonymous said...
Dave, I was looking at a comment that you made about tooth-recalification. My son has some "soft spots" that I would like to heal rather than fill. I would love to hear your experience. della.chad.spam@comcast.net Thanks. Della
George Henderson said...
@ jack, retinol is also required for remineralisation of teeth. I also suggest eating hard cheeses before bed. This is the best post I've read on this debate. Food reward is pseudo-scientific mysticism unless palatability is objectively measurable. A theory of addiction, mediated by exorphins and neurotransmitter modulators (MSG, fructose, etc) at least has the benefit of a measurable mechanism.
Reggie Dixon said...
I'm 47, Caucasian, Male, 6'3" and I have known for a long time that I eat a higher percentage of Carbohydrates in my diet than these Kitavans I had previously not heard of. I'm sure nobody "gives a crap" but I weigh 175 and have a 27" waist (as measured by a health professional). I know in advance the kind of adverse comments I am going to receive but my point is this. I would be willing to bet that I am absolutely the same in terms of internal chemistry as anyone else. There is a simple reason I am the weight I am, every morning I step on the scales, if the number is higher than the day before, I eat a little less, if it is lower I eat a little more.
Dave said...
@Reggie, And yet, animals, when eating the diet they evolved to eat, manage to avoid being overweight without scales or the ability to reason about the consequences of what they consume. Humans have obviously evolved to be special, where over the course of several million years our genes amazingly mutated such that the invention of the scale would save us from obesity.
Reggie Dixon said...
Sorry Dave, I should have been clearer that the scales were a device, I could equally have said that if I have overindulged one day I eat less the next. I have competitive (sporting) reasons for monitoring my weight.
Dave said...
@Reggie, Your internal biochemistry may be intrinsically the same as everyone else. But if you're a competitive athlete, the net result of that biochemistry is certainly different, since you are putting much different demands on your body. For instance, now that I've started training in power-lifting, I have to eat more carbohydrates to maintain muscle glycogen. Otherwise I literally run out of gas. The body is not a closed system, and the context in which it operates makes a big difference in the final outcome of its interactions with the environment. Interesting article, tangentially related: http://roarofwolverine.com/archives/1437
David said...
Hello Dave, My name is David Haskell - I am a co-producer on the new documentary "In Defense of Fat: Rethinking the Bad Science Eating at America's Health." The film is about obesity, health and the politics of nutrition, introducing the principles behind ancestral health and the paleo diet and encouraging a change in the way the culture talks about obesity. The film talks about this very issue and we would love to tell you more about. Please feel welcome to contact me at davidi.haskell@gmail.com. Thanks and keep up the great blogging. David
George Henderson said...
Not only in Kitava (et in Kitava ego?) but in pre-famine ireland, where the potato had supplanted wheat and buttermilk and spuds was the stable diet of the poor - who thrived on it while it lasted. Ireland on the potato, despite the worst poverty in Europe, had double the population growth rate of England and Wales on bread, and supplied most of the soldiers for the British army. http://www.dochara.com/the-irish/food-history/food-in-ireland-1600-1835/
Dave said...
@George, Interesting point, however I would counter that that reproductive success and "health" defined as quality-of-life don't seem to be closely related. The world is full of examples of individuals who created multiple children and dropped dead by 40.

9.7.12

Insulin-like growth factor 1

Insulin-like growth factor 1


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Insulin-like growth factor 1 (IGF-1), also called somatomedin C, is a protein that in humans is encoded by the IGF1 gene.[1][2] IGF-1 has also been referred to as a "sulfation factor"[3] and its effects were termed "nonsuppressible insulin-like activity" (NSILA) in the 1970s.

IGF-1 is a hormone similar in molecular structure to insulin. It plays an important role in childhood growth and continues to have anabolic effects in adults. A synthetic analog of IGF-1, mecasermin is used for the treatment of growth failure.[4]

IGF-1 consists of 70 amino acids in a single chain with three intramolecular disulfide bridges. IGF-1 has a molecular weight of 7649 daltons.

Contents


Insulin-like growth factor 1 (somatomedin C)

PDB rendering based on 1bqt.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols IGF1; IGF-I; IGF1A; IGFI
External IDs OMIM147440 MGI96432 HomoloGene515 GeneCards: IGF1 Gene
RNA expression pattern
PBB GE IGF1 209541 at.png
PBB GE IGF1 209540 at.png
PBB GE IGF1 209542 x at.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 3479 16000
Ensembl ENSG00000017427 ENSMUSG00000020053
UniProt P05019 P05017
RefSeq (mRNA) NM_000618.3 NM_001111274.1
RefSeq (protein) NP_000609.1 NP_001104744.1
Location (UCSC) Chr 12:
102.79 – 102.87 Mb
Chr 10:
87.32 – 87.4 Mb

PubMed search [1] [2]