As many of you know, I’m currently at the Ancestral Health Symposium at Harvard University. Yesterday I participated on a panel organized and moderated by Jimmy Moore called “Safe Starches: Are They Essential on an Ancestral Diet?” The panelists were myself and Paul Jaminet on the “pro-starch” side, and Dr. Ron Rosedale and Dr. Cate Shanahan on the “anti-starch” side (though Cate’s position is not quite as cut-and-dry as Ron’s).
I’m giving my talk on iron overload today, so I don’t have a lot of time, but I wanted to at least summarize the “anti-starch” side’s arguments and then list some bullet points of my arguments in favor of starch for those of you who aren’t here. I’m not sure if the panels will be made available after the fact (the talks will be).
Ron and Cate believe that glucose is toxic in any concentration, and it’s just a matter of scale. In fact, Ron is fond of saying that “everyone is diabetic”. Since starch breaks down into glucose, then by definition starch is toxic and should be avoided – by everyone. I’m a little less clear on Cate’s position, but she seemed to argue that glucose raises insulin, and insulin causes problems, so everyone should be on a low-carb diet ranging from 20 – 70 grams of carbohydrate a day, starch included.
My arguments in favor of starch
Let’s define the terms: are we debating whether starch is “safe” in healthy people or people with particular health conditions like diabetes or small-intestine bacterial overgrowth? These are very different conversations. People with hereditary hemochromatosis (a disorder that causes iron overload) should not eat iron-rich foods like liver and mussels; does that mean everyone should avoid these foods? Even if starch/glucose is “toxic” for diabetics, should everyone avoid starch/glucose?
If the argument is that starch is not safe for healthy people, I would say there’s little to no scientific or anthropological evidence to support that idea, and overwhelming evidence opposing it.
There are literally billions of people eating high-starch diets worldwide, and you can find many examples of cultures that consume a large percentage of calories from starch where obesity, metabolic problems and modern, inflammatory disease are rare or nonexistent. These include the Kitava in the Pacific Islands, Tukisenta in the Papa New Guinea Highlands and Okinawans in Japan among others. The Kitavan diet is 69% carb, 21% fat, and 10% protein. The Okinawan diet is even more carb-heavy, at 85% carb, 9% protein and 6% fat. The Tukisenta diet is astonishingly high in carbohydrate: 94.6% according to extensive studies in the 60s and 70s. All of these cultures are fit and lean with low and practically non-existent rates of heart disease and other modern chronic disease.
Amylase is thought to have played a key role in human evolution in allowing humans an alternative to fruit and protein. Compared with primates, humans have many more copies of a gene (AMY1) essential for breaking down calorie-rich starches. The ability to digest starch, along with the discovery of fire and cooking, gave humans a new food source that allowed us to thrive even in marginal environments. Some scientists have even argued that consumption of starch, along with meat, was primarily responsible for the increase in our brain size.
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Dr. Rosedale argues that evolution is optimized for fertility, not longevity, and that starch consumption decreases longevity. The evidence he cites from this come from studies of roundworm, C. Elegans. However, I am not aware of any evidence in humans showing that starch consumption decreases longevity, and some of the longest lived cultures in the world consume large amounts of starch. Okinawans over the age of 65 (who grew up eating a traditional diet) are a prime example. According to a study of the traditional Okinawan diet in 1949, they obtained 85% of calories from starch, mostly from sweet potato. Life expectancy was 86 years for women and 77.6 years for men. Life expectancy at age 65 is the highest in the world, at 24.1 years for females and 18.5 years for males. Finally, the Okinawan population has the highest prevalence of centenarians in the world. This is especially remarkable when you consider that Okinawans did not have access to modern medical care during the 40s & 50s and and higher rates of death due to infections like tuberculosis as a result. If glucose is toxic and promotes short lifespan, how do the Okinawans live so long?
There is no one-size-fits-all approach. The amount of starch (and carbohydrate in general) will depend upon genetic/epigenetic factors (like amylase production), existing health conditions and the volume and intensity of activity – among others.
If the argument is that starch isn’t safe for those with impaired glucose tolerance, I concede that may be true in many cases. However, I’d like to point out that there’s some evidence that suggests starch may be safe in this population as well. For example, low-fat diets also cause fat loss (even without deliberate calorie restriction), though to a lesser extent than low-carb diets. And there are documented cases of people losing significant amounts of weight and improving metabolic parameters by eating nothing but potatoes. For example, Chris Voigt lost 21 pounds over the course of two months by eating only potatoes and not deliberately restricting calories. Furthermore, his fasting glucose decreased by 10 mg/dL (104 to 94 mg/dL), his serum triglycerides dropped by nearly 50%, his HDL cholesterol increased slightly, and his calculated LDL cholesterol dropped by a stunning 41% (142 to 84 mg/dL).
There’s more, but I don’t think it’s necessary to go further. If Drs. Rosedale and Shanahan are going to advise us to avoid an entire class of food that has been eaten for a couple of million years by humans, the burden of proof is on them to tell us why that food isn’t safe. Evidence from roundworm experiments and biochemical/mechanistic speculation is not enough in the face of overwhelming evidence that starch and glucose are safe in the absence of certain existing health conditions.
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I work out every other day more or less. In addition to fatty meat, I add sweet potatoes on workout days, and on off days I add salad type vegetables instead of potatoes or occasional gluten-free grain.
I agree. One size does not fit all! Starch seems to work well for some people and not well for plenty of others.
The only thing I don’t understand is how anybody has the patience to argue with the lo carb crowd. Science has no role in religion, and a religion is really what they espouse. Further, people who have published books and based their reputations on lo carb can never admit error.
The best argument is your own success. If you’re trim, healthy, energetic, and have low levels of VLDL particles, are pain free and you are not deteriorating with age, then you win in your own world. The similarity to religion in Paleo comes primarily from the fact that they have been converted by their own success, overcome some obstacle after many failures, and they want to share the good news. You don’t see many of these people carrying a lot of extra weight and looking pasty and sickly – like my last 2 cardiologists. I count myself as a Paleo success – from 210 to 180 at 60 yrs and feeling better than I did at 40. I don’t try to convince anyone that they should go ultra low carb, I eat what I need to for my activity level, but a lot of family and friends have followed my example because the change was effortless for me and I eat more and better than I ever have.
Jon, On your pale example how low in carbs are you and did you moderate your carb intake after you reached you weight goal?
There seems to be a broad range in low carb. USDA was at 300 grams of carbs a day. 150 grams is half that so could that be considered low carb? I feel better at 125 to 150 grams of carbs a day.
Alec, I have never measured my carb intake by weight. I cut out all sugar, grains, beans/legumes. Basically eat a lot of veggies/salads, eggs, chicken and beef with some occasional bacon if I can find the uncured, sugar free kind. I eat as much as I’m hungry for of whatever I’m eating. If I’m getting hungry too quickly after meals, I up my saturated fat a bit or olive oil on salads. It is possible that I’m high carb, by weight – but it mostly comes from green veggies so I don’t worry about it. I moderate my intake of various foods based on my activity/exercise levels more than by any weight goal. 180 was not a goal, that is just where I stabilized after my diet change. Now I moderate my body composition (%fat) by activity. Dumbells and walking. I wish I liked sweet potatoes, but they taste bad to me, although I feel pretty good from eating them when I force myself. – Hope that helps.
Yay for sanity ! Obsessing about grams and percentages kills my joy in food ( and bores the pants off partner and family etc ). I have experimented , found what food suits my body and stick mainly to that and it happens to be the same as Jon’s ( except I adore sweet potatoes!) I still have some issues and am researching valuable resources like this site to see how others cope.
.I am another one who is a LC success story. I know starch is not a poison, so it is safe to eat, but when people age they seem benefit from eating less. Starch is the easiest thing to minimize in the diet.
I think that it is trial and error for each person. We are all individuals born with unique DNA. We have environmental differences, we have different food consumption/health histories, and we are of various ancestries. We are not all the same!
So I think that a higher-starch diet may work quite well for some and not for others.
Frankly I am sick of the idea that we all must eat exactly the same in order to achieve vibrant health and optimal weight.
I am overweight and I have a relatively sedentary job. I have tried all versions of Primal, Paleo, and Perfect Health, and a diet with lower carb consumption (which definitely includes limited portions of starchy fruits/tubers -bananas and sweet potatoes) works just fine for my general health and weight loss.
On the other hand, my very active husband does much better eating more starches, so he also consumes a moderate amount of white rice, and white potatoes occasionally.
If he cuts out the rice, he loses weight like crazy and has no energy. On the other hand, if I eat white rice and white potatoes, I feel tired all the time and don’t lose weight.
I don’t think there is a one-size-fits all approach to good health, though there are certain basic guidelines.
“According to a study of the traditional Okinawan diet in 1949, they obtained 85% of calories from starch, mostly from sweet potato”
Interesting that you refer to a study that was done just 4 years after the end of WWII, when the war’s effects on the local economy and diet would still be profound. This is around the same time that Ancel Keys was noting that Italians ate a lot of plain pasta with nothing but tomato sauce, also in large measure due to the dire effects of the war, an observation that helped lead to his diet/heart disease theories.
Yes, but the people that were born during this period and were eating this diet are still around. The longevity effect is due to caloric restriction, but if starch/glucose are “toxins” how is it possible for a culture that eats 85% of their diet from toxins to live so long? It’s highly unlikely that genetics could override such a powerful environmental influence.
But did they keep eating this diet after they became more prosperous? Any data on say, 1980s Okinawa diet?
The Okinawan diet: health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load.
http://www.ncbi.nlm.nih.gov/pubmed/20234038
From the paper:
“However, dietary change since World War II has been largely deleterious, with younger Okinawans developing a higher risk of obesity and other chronic disease risk factors [30,31] versus older Japanese.”
This demonstrates that Okinawan genetics are not the whole story regarding risk factors for chronic disease. But I did not find a reason to believe the Okinawan elders – the centenarians in good health – abandoned their traditional diet entirely. And even if they did, carbohydrate intake would STILL be quite high on the modern Okinawan diet:
“Despite the large increase in fat intake in Okinawa in recent decades, fat intake in the modern Okinawan diet is comparable to that of the DASH diet (at approximately 27% of total daily energy intake) and lower in fat than the traditional Mediterranean diet (42%). Saturated fat still only totals about 7% of total energy intake (versus 6% in DASH and 9% in Mediterranean). Carbohydrate intake (58%) of total calories remains highest (versus 55% for DASH and 42% for Mediterranean) and protein intake falls between the lower Mediterranean (13%) intake and the higher DASH (18%) intake.”
Either way, it seems that the Okinawan diet was always high in carbohydrates, even though carbohydrate consumption declined somewhat post-WWII.
I think as soon as you hear someone making statements that you should treat people as if “everyone is diabetic”, you should immediately discredit anything that makes it out of their mouths. It’s like telling everyone to reduce the intensity at which they can safely exercise because people who just had a myocardial infarction should—it makes no sense and puts people in a state of panic over nothing.
As a sidenote–the majority of people seem to be worried about weight loss but fail to notice that every traditional culture that displays extreme leanness is almost always on a high starch diet. The greenland inuit, which low carbers are so fond of citing, are probably the plumpest indigenous people i have seen. And I think it’s been made clear that the masai are not low carb at all.
Aren’t the Inuit obese because they all consume sugar, flour and alcohol now and have severe genetic intolerance of these foods? I’m confused by this claim since I’ve encountered quite a lot of examples of low-carb hunter-gatherer groups who had superb health… Also I thought the traditional staples of the Masai–nomadic herders, not farmers–were milk and blood? Is whole milk a ‘starch’?
Yes. They have an appallingly high consumption of refined flours, trans and other bad fats, soda pop, sugar, etc, and now make “Eskimo Ice Cream” with Crisco (!!!) instead of whale fat. The rates of T2, cancer and CVD are off the charts. And yes, they now have crappy teeth. This is true of all the Native populations here in Alaska, save those few individuals who are steadfastly eating a traditional diet.
Bananas, tubers, and honey were staples of the masai diet–milk and meat was not always available, and reserved for the ‘warriors’ mainly. My understanding in regards to the inuit is that they had rather pristine health. There was very little tooth decay, cardio problems…etc, but if you take a look at dated pictures from the 1960’s and earlier, you’ll notice they have plump faces and bigger bodies; Compared to tropical islanders, african tribes..etc.
*and whole milk, although it isn’t starchy (especially the super fatty stuff the masai drink), it does propel their carb intake to 100-200 grams/daily–which is no where near the low carb level that Rosedale or any other stringent low carbers are preaching.
The masai also have one of the highest protein %’s of any traditional culture~ 19%, which is at odds with another major tenant of Rosedale’s diet (i.e. reducing protein to reduce production of the evil glucose monster).
Even being a LCarber, I agree with you that we should immediately disregard whatever the person who said “you should treat people as if “everyone is diabetic” said.
Perhaps one of the most convincing arguments against starch consumption is Elaine Gotschal’s Breaking the Vicious Cycle. The theses being that poly saccharides are not an entity most of us can digest well, and the likelihood if leaky gut is exacerbated by consumption of poly saccharides. However, if we have attempted over a fair and long trail period to adhere to a standard low carb Paleo, and also, in an alternative effort, to supply carbs from fruit/fructose/honey while abstaining from poly saccharides, and have only experienced abysmally poor results in both dietary strategies, than it seems starch carbs as white rice may be our only satisfactory option. As a former triathlete, and later as a recreational active and fit person , I found it impossible to maintain leanness on either standard Paleo or Paleo plus fruit carbs. The low carb Paleo diet brought me insomnia, visceral fat, muscle deterioration, and the worst general health ever. Adding fruit carbs to the Paleo improved nothing and brought even more excess body fat. White rice proved to be my dietary salvation, to restore leanness, muscularity, and normal sleep.
This is only relevant for the particular population that has gut problems. I mentioned this in the article.
You need to differentiate between starch polysaccharide and non-starch polysaccharide. We are quite evolved and suited for the digestion of starch into glucose due to amylase production. Non-starch polysaccharide requires healthy gut flora to be dealt with in a beneficial way.
“the burden of proof is on them to TELL us WHY that food isn’t safe”
No, Chris, not quite.
They have already TOLD us: instead we need facts – as in population and longevity data for Homo Elegans not C. Elegans.
In addition, we need a detailed biochemical/pathway explanation which provides the HOW – not WHY.
Stand-alone arguments are useless, scientific data alone convinces.
Slainte
With all respect Chris, the Okinawans are a terrible example. They could eat anything they like and still reach 100 – due to their particular genetics. Anyone can Google the many studies of their unique old-age genes. Particular alleles of the HLA II locus on chromosome 6 give them special longevity. Those of us without those genes can’t necessarily follow their example.
I wonder why they were engineered to live so long. Did the young ‘uns need a lot of instructions from the old folks to get be able to survive long enough to be old enough to breed?
Nutritional statistics is such a mess. Everyone wants to have an opinion. If I die an early death because I was eating sweet potatoes well I guess I gave it my best stab. I’ve killed sugar and grains and bad fats, am sub 10% body fat and people tell me I am unhealthy. I think people should be able to detect when things are happening CORRECTLY in their body. It’s not like we just wake up one day and say oh my God I got fat overnight. Eat the potatoes and if you put on 10 pounds of body weight in one day or you feel like crap then I would say you’ve gone a bit to far. Love your work Chris!
Like another commenter I ceased menstruation when I cut out starch. I kick myself now for being so quick to jump on that bandwagon, but there were so many compelling anti-starch arguments. For a long time I didn’t understand that I needed carbs, this was when paleo was all about the low carb. For me no starch was a terrible experiment, but great birth control. I wish so much that I had read something like this post before I screwed my hormones. Chris- you do a great service by questioning anti-starch/carb. There is not one diet for everyone!
Wow, Chris, I am impressed. For someone having so little time, this post is killer.
My position: PRO STARCH!
I had a very bad experience on a low carb diet. My hormones were out of whack from pregnancy and nursing. Low carb only made it worse.
Since I switched to a higher carb diet, I’m doing much, much better. I eat lots of whole grains and fruit every day now. My temperature is up from the low 97s on low carb to a steady 98.6.
I think instead of all these folks blaming starches and carbs for diabetes, they should look first to optimizing hormone function.
Thanks for this well written and informative article, there is no shoe that fits all sizes, and we all see around us people who eat a lot of carbs and have “perfect” blood tests and weight.
In my case I choose to avoid the starches, my carb intake comes from some fruits and any carb that comes with yogurt. I estimate my daily carb intake at less than 80g. I don’t feel the need to add the starches. On my days of “lifting heavy things” (two a week, 20 minutes sessions) I notice that an extra banana or two “feels” much better.
To me it is as clear as daylight. Insulin is mitogenic. Starch elevates insulin ergo it ages you faster no matter what short term kick you may gain from it. Clearly it does not fit into a longevity diet. All this talk of it being safe is misguided. And who cares what your okinawans eat? Talk of “studies” here is useless until you have had the luxuary of following a group of very low carbers for a life time, placebo controlled appropriately.
“Starch elevates insulin…”
Not necessarily. People who have insulin-sensitive livers can need less insulin to maintain normal blood glucose level when they eat some carbohydrate, as it suppresses hepatic glucose production.
People who have insulin-resistant livers which secrete too much glucose whatever quantity of carbohydrate is eaten are better-off eating less carbohydrate.
Who cares if starch elevates insulin in a healthy person? That is exactly what is supposed to happen. It is a NORMAL physiological response. The carb-insulin-fat hypothesis has been so thoroughly debunked I can’t believe it’s still discussed. No scientist that studies body fat regulation takes it seriously.
“No scientist that studies body fat regulation takes it seriously.”
I’m surprised and dissappointed in you, Chris. You have any data to back that statement up?
“The carb-insulin-fat hypothesis has been so thoroughly debunked I can’t believe it’s still discussed. No scientist that studies body fat regulation takes it seriously.”
Chris, If you are stating (indirectly) that Taube’s “Why people get Fat” and more recently, Wheat Belly, are just plain wrong – I’d appreciate it if you would point me to the information that counters it. For me, when I originally read Gary’s book, it made so much sense to me that I immediately changed diet and fat immediately started melting off me. I eat much more now, meat, fruit and veggies, and continue to maintain a trim weight. The only thing that explains that (to me) is the “Carb-insulin-fat” hypothesis.
I also have to admit being completely taken aback by reading that statement and I set it aside for future inquiry.
Any guidance appreciated.
Jon – I too have the same positive weight / fat response when maintaining a low-carb Paleo diet.
Chris, let me get this straight… I can eat a lot of carbs and not worry about the insulin response, or more importantly insulin insensitivity? And if I become metabolically deranged due to insulin insensitivity, I won’t get fat?
Unfortunately, you’ve just shot your credibility with me by saying that the “carb-insulin-fat hypothesis” has been so thoroughly debunked. There may be many factors playing a role and reasonable people disagree but insulin has a very definite role. To deny it is, well, very, very odd.
Just look at what insulin does when given to a person who is deficient in it:
http://wellcometrust.files.wordpress.com/2011/11/type-1-diabetes-patient.jpg
Taubes’ points out that carbohydrates spike insulin (absolutely not controversial, that’s what the glycemic index is based on) which shunts glucose into adipose tissue (also not controversial).
This is entirely consistent with our current knowledge of how insulin works in our body. To be more precise, here is a good explanation:
“The major function of insulin is to counter the concerted action of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels. Because there are numerous hyperglycemic hormones, untreated disorders associated with insulin generally lead to severe hyperglycemia and shortened life span.
In addition to its role in regulating glucose metabolism, insulin stimulates lipogenesis, diminishes lipolysis, and increases amino acid transport into cells.”
http://themedicalbiochemistrypage.org/insulin.php
“insulin stimulates lipogenesis” == creates fat
“diminishes lipolysis” == prevents fat from being burned
I could have used any number of biochemistry textbooks that say the very same thing.
As for why serious obesity researchers aren’t studying insulin more, isn’t Gary Taubes’ whole point that the obesity researchers *should* be paying more attention to insulin?
Or are you saying that if people eat plenty of refined grains, lots of high fructose corn syrup and potatoes as long as they don’t go above, say, 2000 calories a day they won’t gain weight?
I did not deny that insulin plays a role in obesity. I denied that the insulin hypothesis, as stated by Taubes et al., explains the obesity epidemic. That *has* been debunked, as anyone familiar with the literature on the topic will tell you.
Read this article for a good summary. If elevated insulin causes fat gain, then why do experiments that chronically elevate insulin levels in animals fail to cause them to gain fat? If anything, as Stephan points out, chronically elevated insulin seems to have the opposite effect: it opposes weight and fat accumulation in animal models.
Yes, insulin does all of the things you said it does. But that doesn’t prove that elevated insulin is the cause of fat gain in mammals, and when that has been tested experimentally it turns out to be false.
But of course you need extra insulin AND extra carbohydrate!
The insulin produced in response to carbs keeps fat from being burned and promotes glucose conversion to lipid.
One needs to eat carbs regularly (as we are advised to do for our “blood sugar”, and as junk food eating and soda consumption promotes) otherwise the situation will reverse when fasting (unless we have diabetic gluconeogenesis going on)
one needs adequate thiamine status (unlike most high-carb Asian populations, or our own past)
but putting conditions on a rule does not disprove the rule.
Every scientific hypothesis that was correct has been modified over time.
You may be surprised to learn that de novo lipogenesis (glucose converted to fat) is not a major pathway in humans (contributing only about 5% to fat storage, if I recall correctly). So you cannot say that carbohydrates are easily converted to fat — they are not. See the work of Marc K Hellerstein for details.
Insulin reduces fat burning because it increases glucose burning by an equivalent amount. Just because insulin suppresses fat release temporarily does not mean total calorie burn is being reduced. This is where the confusion stems from.
Yes I am surprised.
It is easy to manipulate these studies by running them in weight loss or post-ketogenic states. See this paper:
http://www.lucastafur.com/2011/04/extra-glycogen-de-novo-lipogenesis-and_04.html
If you feed a starving person a high-carb, low-fat diet they will regain weight, won’t they?
In some contexts extra carbs turn to fats, in others they reduce the burning of dietary or stored fats. Fats can’t turn to extra fat or reduce the burning of fat.
The carbohydrate content of the diet controls the fate of dietary fats.
I found some time to examine the link you provided. It actually discussed 4 papers, but only the second paper really contradicted what I said about de novo lipogenesis.
Paper 2 only showed an increased rate of DNL in the context of caloric excess. To be clear, I’m not saying you can eat unlimited quantities of carbohydrate and stay lean.
What I’m saying is that DNL is not a major fat storage pathway in the context of caloric balance. But this is only true to a point. If you lower fat intake enough (while keeping calorie intake constant to maintain energy balance), then carbohydrate intake has to rise concomitantly to fill the gap. This excess carbohydrate WILL result in an increased rate of DNL. But this is not a problem – it’s only replacing the lipids that you would otherwise have otherwise obtained by eating fat anyway.
There’s nothing special about insulin here – the focus should be on caloric load. Insulin is a red herring, at least in the the sense that Taubes et al think it causes obesity.
You are right that insulin can help shunt _excess_ dietary carbohydrate into the fat cells. But one could similarly argue that ASP shunts excess dietary fat into fat cells.
ASP production is stimulated by chylomicrons, too. And chylomicrons come from – you guessed it – fat in the diet.
Do you accept both lines of reasoning?
That depends what ASP is. If it’s adipose set point, this is an abstract concept and can’t be “produced”.
It’s hard to fatten if you don’t eat carbs. It’s easier to lose weight if you cut them out.
It’s easier to restrict calories or do IF without carbs.
There has to be a reason for this – a mechanical explanation.
Even when only 5% of glucose carbon goes into DNL fat on a high-carb diet, there is also the ATP from more glucose being used to build it, and glucose being burned instead of fat.
And if you increased weight by only 1% a day, that’d be much more than most people gain.
“ASP” stands for acylation stimulating protein, not adipose setpoint. You can think of it as a hormone, even though it technically doesn’t quite meet the definition of one. CarbSane has written about ASP in the past.
The explanation for weight loss on ad-libitum low-carb diets (when it works, because there are definitely people for whom it doesn’t work) is that LC causes a spontaneous reduction in caloric intake. This is really the same as the way all diets work. One major explanation is that protein is highly satiating for most people, especially in the short-term. See this multi-part BBC documentary on the Atkins diet:
http://www.youtube.com/watch?v=2d_wxJageqw
I’m a bit confused as to what you are trying to say with this part: “Even when only 5% of glucose carbon goes into DNL fat on a high-carb diet, there is also the ATP from more glucose being used to build it, and glucose being burned instead of fat.” Why is it a problem that glucose is burned instead of fat? As long as net energy balance is negative, the fat will eventually get mobilized and burned.
But surely what happens in an energy deficient state is not directly relevant to cause and effect in obesity? What about studies of DNL during weight gain?
It is impossible to eat exactly isocalorically. What pushes weight and appetite to grow and increases the efficiency of storage mechanisms?
Even when weight is kept stable on a low-carb diet there is an improvement in fitness.
Less puffing and wheezing and sleep apnoea.
I don’t think any of the world’s fattest people got that way eating low-carb. Some people will overeat for reasons unconnected with energy. Some people will compulsively eat dirt or plastic for that matter. That doesn’t change the fact that carbohydrate is uniquely fattening for most people and fat in the absence of carbohydrate is not productive of pathological weight gain.
Why is it that so many people CAN eat more carbohydrate than they need AND store the energy as fat? This is a property of carbohydrate, not a quirk of some individuals.
“The discussion concluded with the vexed issue (once again) of carbohydrates versus calories – All agreed that significant calorie restriction is hard to achieve and restricting a single food class may be easier, and there was general consensus that carbohydrates probably have greater adverse metabolic effects than other food classes, and full consensus that this needs to be properly researched.” http://blogs.biomedcentral.com/bmcblog/2012/07/12/now-on-video-diet-cancer-and-obesity-emperors-clothes-and-elephants/
“But surely what happens in an energy deficient state is not directly relevant to cause and effect in obesity?”
Hmm? It’s directly relevant. Energy deficiency => weight loss. Energy surplus => weight gain. All I’m saying is that insulin’s temporary downregulation of fat oxidation (in favor of glucose oxidation) does not threaten this model.
Let’s look at it from another angle. Even if I were to allow that rates of DNL are highly significant, so what? This doesn’t explain the metabolic ward studies that fail to show a weight-loss advantage to low-carb diets at isocaloric intake.
“What pushes weight and appetite to grow and increases the efficiency of storage mechanisms?”
Food reward and palatability. The extent to which individuals are affected by highly rewarding food seems to be partially genetic, however.
Social factors could also play a role (i.e. you have been trained to finish everything on your plate, even if you are not hungry).
Regarding fitness and low-carb, you might be interested in Anthony Colpo’s post on the topic:
http://anthonycolpo.com/?p=1535
“I don’t think any of the world’s fattest people got that way eating low-carb.”
I don’t think any of the world’s fattest people got that way eating a high-carb vegan diet, either. That doesn’t tell us anything. The world’s fattest people probably ate incredibly calorie-dense, but unsatiating food. On a regular basis.
“That doesn’t change the fact that carbohydrate is uniquely fattening for most people and fat in the absence of carbohydrate is not productive of pathological weight gain.”
You haven’t provided a reason to believe carbohydrate is uniquely fattening (i.e. beyond its calorie content alone). Are you arguing that carbohydrates are less satiating (causing you to eat more), or that low-carb diets provide a metabolic advantage (insulin slowing down metabolic rate)? Or both? Neither is true, as far as I can tell.
And fat can surely induce weight gain (in the absence of carbohydrate!) if you ingest enough calories to produce a surplus. Do you deny this? It’s not any different from consuming too many calories as carbohydrate.
“Why is it that so many people CAN eat more carbohydrate than they need AND store the energy as fat?”
You can turn this argument around by substituting ‘dietary fat’ for ‘carbohydrate’, and it would still be accurate.
Also, it’s not just a binary choice between “carbs” or “no carbs.” By switching from refined carbs to whole food carbs, you still get an increase in satiety (and thus a spontaneous reduction in calorie intake) without having to cut out an entire macronutrient. This has numerous advantages, but I won’t enumerate them here because this comment is getting long 🙂
Will, no offense and I hope you’re not offended. I’ve enjoyed this debate and I always appreciate the chance to see where my own ideas are weakest.
I’ve followed the food rewards concept at Stephan Guyenet’s site and I remain a sceptic. I’ve seen it make sense for an instant, only to vanish like a mirage, and I can’t be bothered with its nebulosity. That said, I have a real appreciation of the good doctor’s Guyenet’s worth, and continue to read him with pleasure.
I don’t think food reward theory is incompatible with metabolism. Sweetness receptors stimulate insulin production. There’s no real dichotomy there. I’m a mechanical determinist by nature, but I think dieters have free will in their macronutrient choices.
This guy neatly reconciled Guyenet and Taubes a while ago. I don’t think its been said better.
http://sparkofreason.blogspot.co.nz/2011/08/comment-on-guyenet-vs-taubes-or-why-i.html
None taken. I guess I came off sounding more combative than intended.
I agree that food reward and the insulin hypothesis are not mutually exclusive. After all, Stephan didn’t say food reward was the _only_ factor, just a dominant one.
But the fact that they _could_ co-exist doesn’t change my view that the insulin hypothesis is wrong. Independently of this, I also think there is decent evidence for the food reward hypothesis.
Let’s put it another way.
If you store fat from carb and burn it later, no problems. Ditto fat.
But what if you can’t burn it readily because your high-carb diet is suppressing fat-burning genes? PPAR-alpha and the like?
Look at this guy who won a 100-mile marathon mostly on body fat reserves, when high-carb runners needed constant top-ups of glycogen:
http://www.meandmydiabetes.com/2012/08/11/western-states-100-low-carber-wins-ultramarathon-steve-phinney-and-jeff-volek-study/
If you are fat adapted you can burn fat; your appetite can decrease because you have round-the-clock access to anything stored.
You’re not actually burning fewer calories.
In some people insulin reduces fat burning, not temporarily, but overall. The switch becomes stuck in the “off” position, and their appetite tells them they need more carbs. Anything they can’t use goes into Fort Knox.
If PPAR-alpha and friends are a big problem, then why isn’t this evident in the controlled trials that compare macronutrient intakes?
Is Tim Olson first guy who has ever tried to compete in a marathon on low-carb? I’m skeptical. The vast majority of world-class endurance runners are fueled by high-carb diets, and more likely than not they have defeated many low-carb hopefuls in the past that we haven’t heard about. The fact that Olson is even news in the first place, speaks to the rarity of successful low-carb runners.
Furthermore, is Olson’s diet even low-carb? In the link provided, the researcher makes excuses about why they couldn’t reveal the details of his true diet. As Colpo described in my previous link, some “low-carb” athletes heralded by the LC community were not, upon closer examination, actually low-carb. To know for sure, Olson’s diet cannot be kept a secret.
“In some people insulin reduces fat burning, not temporarily, but overall. The switch becomes stuck in the “off” position, and their appetite tells them they need more carbs. Anything they can’t use goes into Fort Knox.”
Do you have a reference to back this up?
I am not saying that carb-adapted runners do badly. I am saying that Tim Olson, being fat-adapted. had ACCESS to many more stored calories than his competitors, thus needed to eat less.
What are two preconditions of obesity? Eating more, and burning less, calories.
What is the opposing view to mine? That everyone has equal access to stored energy, and its accumulation is always due to overeating and insufficient exercise?
Doesn’t that just beg the question WHY?
Now carbs are so beneficial that athletes are cheating to include them.
Someone better tell the IOC.
BTW I do eat “safe starches”. I actually have pretty much limitless respect for Paul Jaminet, Kurt Harris, and our host.
However, obesity, diabetes, and a host of inflammatory conditions are characterized by carbohydrate intolerance.
The diseases that can be made worse by increasing carbohydrate and cutting fat vastly outweigh, in terms of human suffering, the rare problems that can be eased or prevented by replacing fat with carbs.
If you are following current “healthy” guidelines you are snacking on high-carb foods 5 times a day. When does insulin become “temporary” if it is always “covered” with sugar?
Sorry if I offended you somewhere. I’ll keep it short this time:
“Doesn’t that just beg the question WHY?”
The answer, for the most part, is food reward.
“When does insulin become ‘temporary’ if it is always ‘covered’ with sugar?”
If most of your fuel is coming from carbs, then it makes sense that you should be spending more time burning carbs as opposed to fat.
High fasting insulin is a symptom of obesity & diabetes, rather than a cause. Allowing insulin to “cover” the entire day via snacking is not the same thing.
“The world’s fattest people probably ate incredibly calorie-dense, but unsatiating food. On a regular basis.”
Not necessarily calorie dense; soda isn’t calorie dense. Calorie density is probably not relevant, above a certain minimal dilution. In fact, if it was highly calorie dense, like pure lard or butter, it would be highly satiating.
But how does this conform with the food reward and palatibility idea?
Can’t a rewarding, palatable food also be satiating? Like a good cheese, or bacon and eggs with tomato relish? You are wandering into a subjective, aesthetic area of science. My daughter finds the music of Justin Bieber palatable, I do not.
Your mitochondria do not care whether calories come from dense food or soup, nor do they care much what it tasted like or how you felt about it emotionally. Those things might be involved in your choices, but at the energy level – e.g., whether you can readily burn stored fat – it only matters what the mix is; whether it came from your diet, or from your bodily reserves, is of little importance when the mix is the same.
Asking me for a reference, Will, gives a nice appearance of intellectual rigour, but this is unfortunately spoiled when you direct me to Anthony Colpo.
This is nice:
Despite an apparent absence of cardiovascular disease and the metabolic syndrome in the Kitavans, the relationship between TGs and HDL-C was similar to that observed in Caucasians, while neither of the variables was associated with markers of insulin sensitivity in the Kitavans. Whether the findings can be explained by normal physiology or partially reflect the high intake of carbohydrates *and saturated fat* in Kitava is uncertain.
http://www.ncbi.nlm.nih.gov/pubmed/12817903?dopt=AbstractPlus
Based on your commentary, I’m inclined to believe that you don’t properly understand the food reward concept. This is not meant to be spiteful; it is easily misunderstood. I’ll give a brief explanation, but I won’t comment further since I think you have already made up your mode about food reward.
Palatability and reward are often related, but they are technically distinct concepts, with different circuit systems in the brain. Your own examples show how palatability does not always travel with reward. Reward is a measure of how motivated you are to acquire and eat a given foodstuff again. Food that induces satiety has lower reward value than food which fuels hunger and craving.
If you read Whole Health Source, you know that Stephan has already attempted to defend food reward against claims that it is vague pseudoscience. I won’t try to rehash his arguments except to say that real scientists do take it seriously, and it is a frontier of modern obesity research. That’s good enough for me.
The reason I brought up food reward is to explain what drives us to eat more or less food. The mix of fuel seen by mitochondria is irrelevant. It may only _seem_ relevant if you believe the insulin hypothesis. If you don’t (as I don’t), then there’s no reason to invoke fuel types to explain overeating.
Feel free to look down on me for linking Colpo. I don’t much care if I look intellectually rigorous or not. But I am still interested in that reference, if you have one. To me, that reference would support the crux of your argument.
Thanks Will, the thiamine paper is very interesting. I am trying to find out where the study was done (fortified country or not?).
I don’t know whether the diets you mention would be as thiamine-replete as a western fortified diet. And I certainly don’t think thiamine can make everyone fat; taking multivitamins for years didn’t change my natural leanness. It is an observational hypothesis with some epidemiological support and a partially-understood mechanism.
It really depends on the extreme level of fortification seen in a country like the USA.
it is interesting that the GABA shunt appears to have a “food reward” type aspect.
I guess red meat might be bad if you eat it in a bun, remove its natural fat and cook it in oil, and wash it down with a coke.
No study I’ve ever seen measured those factors, and the correlations were not strong anyway (even in those “red meat kills you” studies, not eating meat killed almost as many people as eating it did, i.e. not many at all).
I liked this book: it approached all these issues from a novel and entertaining angle.
http://www.dailymail.co.uk/femail/article-2105132/Damn-low-fat-diet-How-reformed-vegan-John-Nicholson-gorges-foods-granny-enjoyed–felt-better.html
Apparently, he got fat and sick on a diet that was low in caloric density and palatability and anything but rewarding or satiating, and got better on the calorie dense diet he found most palatable, rewarding, and satiating.
Thanks Will, it’s been fun and stimulating.
I can see that to people still in the phase of food addiction or with complex emotional relationships to food, something like food reward gives a useful framework to step outside that.
This doesn’t mean that it has any more reality than the higher power postulates of 12 step programs.
Once you have moved on, and are no longer hooked, does it provide a useful knowledge base for what is happening to your body?
Does it explain exercise, or cancer, or circadian rhythm, or nutrition in the sense of being nourished?
What is the relationship between palatability, reward, satiety that is true for everyone?
Everyone can measure insulin, blood glucose, HDL/TG ratios, HbA1c and so on.
Their inter-relations can be shown on graphs, the patterns of gene expression and protein circuits behind them are being mapped.
What is the use of a medical theory with no diagnostic?
Here is a reference which relates to the Insulin hypothesis: http://www.ncbi.nlm.nih.gov/pubmed/21772313
however, referencing a hypothesis is not probative.
It only proves that people are thinking about it.
If you want a truly detailed and nuanced discussion of the insulin hypothesis, I recommend Hyperlipid’s blog
http://high-fat-nutrition.blogspot.co.nz/
Your concerns about food reward, as I understand them, have to do with the lack of concrete, verifiable, mechanisms behind it. But food reward has a very particular mechanism – activation of the hedonic and reward circuits in the brain. If an obesogenic mechanism does not activate these subsystems in the brain appropriately, then food reward is not at play. I will admit that I don’t know if all satiety factors influence these particular regions of the brain, but it wouldn’t surprise me if they did. Please see these blog posts for more info:
http://wholehealthsource.blogspot.com/2011/10/case-for-food-reward-hypothesis-of.html
http://wholehealthsource.blogspot.com/2011/10/case-for-food-reward-hypothesis-of_07.html
Now, back to the insulin hypothesis. 🙂
I agree that citing one reference wouldn’t “prove” the whole insulin hypothesis, but I was looking for something very specific. By what mechanism does insulin slow metabolic rate? And how important/relevant is this mechanism to general obesity?
The common low-carb answer (and the mechanism hinted at in your reference) is that insulin locks fat away via its action on LPL and HSL, so that overall energy expenditure must decrease. But as I said, metabolic ward studies show no significant metabolic advantage to calorie intake from carbohydrate vs fat. If there is an effect (by any mechanism whatsoever), it is likely quite small. Furthermore, those with high fasting insulin tend to have _greater_ resting energy expenditure, not less. Any plausible biological mechanism for supposedly “fattening” carbohydrates must bow to this evidence.
I’m familiar with with the insulin hypothesis and its most common arguments, having genuinely believed it myself in the past. I used to read Hyperlipid as well. In Peter’s response to Stephan’s famous critique of Taubes’ thesis, Peter writes:
“Starch based diets are not associated with obesity. They do not cause hyperinsulinaemia, post prandial or fasting. They do not cause insulin resistance. You can, with significant effort, become obese on starch but only if you force yourself to do so. I agree with this, in unacculturated people. I think it might even have applied to people in the USA of 1900. I disagree with this if applied to the current industrialised world, especially anyone who has become obese.”
Quite frankly, this surprised me at the time. Not because I didn’t believe it (I had already rejected the insulin hypothesis long before Stephan’s post), but because it was coming from Peter. Here, even Peter is admitting (with a couple of asterisks) that starch-based diets do not cause hyperinsulinemia, insulin resistance, or obesity.
I think you’ll find that the foods considered “most rewarding” are the foods that influence insulin the most. Sugars as well as starches.
http://www.ncbi.nlm.nih.gov/pubmed/19352508
For example, deep frying a starchy food impacts the insulin response compared to lower heat cooking at the same macronutrient amounts,
http://www.ajcn.org/content/91/5/1220.abstract
“Results: In comparison with the steamed diet, 1 mo of consuming the high-heat-treated diet induced significantly lower insulin sensitivity and plasma concentrations of long-chain n−3 (omega-3) fatty acids and vitamins C and E [−17% (P < 0.002), −13% (P < 0.0001), and −8% (P < 0.01), respectively]. However, concentrations of plasma cholesterol and triglycerides increased [+5% (P < 0.01) and +9% (P < 0.01), respectively].
Conclusions: A diet that is based on high-heat-treated foods increases markers associated with an enhanced risk of type 2 diabetes and cardiovascular diseases in healthy people. Replacing high-heat-treatment techniques by mild cooking techniques may help to positively modulate biomarkers associated with an increased risk of diabetes mellitus and cardiovascular diseases."
High heat treatment is part of what makes junk food "rewarding" (for some)
In what way does this contradict an insulin hypothesis?
It would make more sense to say that the food reward hypothesis adds another detail to the story of disordered insulin signalling, and that what we know about insulin offers a partial mechanism for food reward.
Again – I always discuss food reward separately and independently of the insulin hypothesis. Please stop claiming that I think they contradict each other. I do not. The insulin hypothesis is wrong, but NOT because food reward somehow conflicts with or invalidates it!
Your first reference says that the sweet taste receptor stimulates insulin secretion in a mouse model. It says nothing about the effect of insulin on the brain, the key player in food reward. If you knockout the insulin receptor in the brains of mice, they will increase their food intake: http://www.ncbi.nlm.nih.gov/pubmed/11000114
I’m not sure how the paper on deep frying contradicts anything I’ve said so far. As you noted, high heat treatment might make the food more palatable and rewarding. But the paper also stated “A 10% higher caloric intake was evidenced in the STD group as result of a higher overall food consumption and higher energy density, with a significantly higher intake of carbohydrates and fats…” (STD is the group that ate the deep fried diet).
I agree that insulin could have a role to play in food intake via it’s action on the brain. But that isn’t what Taubes is saying, and that’s not the version of the insulin hypothesis I disagree with.
Will, I disagree with the Food Reward theory because it doesn’t match my family experience or experiences of other immigrants I know who arrived to the US in a mature age. At the beginning we all got exited about new and convenient food, but after a year or two we returned to home cooking (who had time) or at liaest we prefer home cooking . Fast food is cheep and convenient, you don’t need to wash dishes and spent time cooking and cleaning kitchen afterwards, but we can’t eat it regularly, especially things like frozen prepared dinners.. My son couldn’t eat cafeteria food after he did it for one year in his university and started to cook his own food. If it was so carefully engineered to work almost like a drag, then the appeal has to be more universal. Not everybody reacts on starches with increased appetite, decreased energy and a weight gain, for some it is enough to reduce grains and sugar, but for more carb-sensitive people removing tubers from their diet is the next necessary step.
I also have a problem that WHS mostly discusses the obesity aspect of the food, which is reasonable because SG is the obesity researcher, but weight gain abnormalities are on the tip of an iceberg. I grew up in a fast-food-free society, and observed how people around me got various illnesses of a Western civilization without obesity being a problem in the population. One year ago I convinced my 75 yo mother to cut completely grains and tubers from her diet, and it normalized her GERD and blood pressure.
Starches are definitely not toxic, but it is not completely benign food for everyone. At the same time there are a lot of people around who are so little prone to obesity that they can eat only boiled potatoes or exchange normal coke for a diet one and loose weight because they need very little changes to drop weight. I needed to use a LC diet to loose weight, not just a slight change in my routine.Also, for the people who try to follow a diet after a weight-loss it is much more easy to manage when whole group of nutrients is minimized than trying to keep some sort of a balance. I have been doing LCarbing for around 5 years, cook food for my family. Limiting carbs makes a diet easy to comply. I just don’t put on my plate starches I made for my family, but we all eat the same meat and veggie dishes. I can go to any restaurant and most fast-food places and have a food appropriate for my diet (like a burger without a ban and minus french-fries). Following a food reward diet would be much more difficult undertaking.
So if you don’t replace the insulin hypothesis with food reward, what do you replace it with?
If someone eats rewarding, highly palatable food of low satiety and high calorie density, and gets more energy than they need, why doesn’t that energy make them energetic?
A food reward paradox; alcohol is very rewarding, palatable to those it rewards, of low satiety ditto, and calorie dense.
Yet an alcoholic who eats little other food will lose weight on a hypercaloric alcohol intake.
Why?
Because some of the alcohol is metabolized to heat, H2O and CO2 alone in peroxisomal oxidation. Like part of the energy from long-chain fats – call it metabolic advantage if you will, though I fail to see the advantage.
And alcohol depletes thiamine, which eventually means the body’s ability to metabolize glucose is reduced.
No doubt there are other mechanisms.
A further point is that carbohydrate is associated with other diseases, from cancer to diabetes to GERD to gout and arthritis, which are more-or-less amenable to its restriction. Insulin is known to be a significant factor here. There are many more experts researching the links between insulin and degenerative disease than there are researching food reward. And of course, obesity is a risk factor for those diseases. Go figure.
Galina,
Thanks for your comment. It was very interesting. I can’t argue with personal experience, of course. And I’m not arguing that starches are fine for every single person on the planet. I appreciate the efficacy of ketogenic diets in treating epileptic seizures, for example. In my view, low-carb is also useful if it winds up being the easiest trick for someone to maintain long-term weight loss. But the insulin hypothesis is an unlikely explanation, and the diet simply can’t be sustained for many people.
You mentioned grain elimination and blood pressure a couple of times. Please realize that grains, in particular bread and flour products, are a major vehicle for salt in Western diets. This alone could be the explanation. Moreover, displacing grains with more potassium-rich food sources like fruits and vegetables would also help improve blood pressure. I don’t think it’s grains per se unless you can rule out the influence of sodium and potassium.
George,
Excess calories => higher circulating leptin => appetite suppression & increased energy expenditure. Leptin’s appetite suppression effect occurs in the brain. Leptin resistance may occur via inflammation in the brain. Hope that clears up your confusion.
I’ve gotta say, I’m skeptical of your claims about alcohol. Drinking to caloric excess, coming mostly from alcoholic beverages? Is that even an ethical experiment? Please cite a reference; this one I’d love to see! But even if it were true, I don’t see the practicality. There is no significant effect for dietary carbohydrate or fat, and no sane person would recommend consuming lots of calories from alcohol for weight loss.
I read your blog post on thiamine. While interesting, there isn’t enough evidence to be convincing. Are there any controlled studies on thiamine supplementation by itself and weight gain? What about The Rice Diet (http://www.ricediet.com/page/view/nutrition)? The all-potato diet (http://20potatoesaday.com/)? Durianrider’s fruitarian diet (http://paleozonenutrition.com/2011/03/05/30-bananas-a-day-durianrider-an-analysis-of-his-paleo-vegan-diet/)? All of these diets are thiamine-replete because they come from whole food carbohydrates, and they did not cause weight gain.
In this report (http://www.food.gov.uk/multimedia/pdfs/evm_thiamin.pdf), the authors found a relationship between thiamine/calorie and BMI, where thiamine/calorie explained roughly 8% of the variation in BMI. But this correlation was inverted for women; the higher their thiamine/calorie ratio, the lower the BMI. Looking at the thiamine/%carb ratio makes the data even less compelling. What’s more, the effect with protein appeared to be 2X that seen with carbohydrates.
Are carbohydrates really associated with the other diseases? Look at the populations in good health today, or a few centuries ago. Almost all of them get the bulk of their calories from starch, except for perhaps a few scattered tribes living at the extremes of the environment. This is incontrovertible stuff.
And consider this. Red meat is associated with cancer, cardiovascular disease, stroke, type 2 diabetes, obesity, hypertension, gout, and arthritis. Beef scores just as high as pasta on the insulin index. Do you therefore avoid red meat? If you are being consistent with your own logic, you would. For that matter, do you avoid all protein sources that rank high on the insulin index?
This will be my final reply. I’ve enjoyed the debate, George. I will let you have the final word.
George,
Sorry, I linked the wrong report on thiamine. I meant to link this:
http://www.krepublishers.com/06-Special%20Volume-Journal/JHE-00-Special%20Volumes/JHE-15-Hum-Body-Comp-Web/JHE-SI-15-03-017-022-Chen-S/JHE-SI-15-03-017-022-Chen-S-Tt.pdf
It looks like my previous reply had enough links to get caught in Chris Kresser’s moderation queue. You’ll know what I’m referring to once it is approved 🙂
Will,
I have also problems with migraines which look like an epilepsy on an electroencephalogram, and ketosis is very beneficial for managing all that. I personally have unbelievable health improvements after I changed my diet on LC, like I am off asthma meds, didn’t have a single seasonal flue or infection since I started almost 5 years ago, list is so long I am afraid ii I continue it may sounds like I am selling a snake oil. I lost about 50 lb at 27 yo and around 40, and didn’t have similar health improvements back then . I don’t agree that bread carries salt into a diet. I cook since 10 years old (all my married life I cook every meal in my house), and according to my experience, soups , dishes with tomato paste and vinegar, cured meats and salads are major salt carriers. In my household it is probably a self-made fermented cabbage I have in my fridge all the time because sour taste lowers the perception of saltiness. Salt in ample amounts is necessary for many treasured food preparations like bone broth, fermented veggies, cured raw fish and salted fish eggs, pates, meat jellies (aspics). My mom continued eat big amount of sauerkraut and got her blood pressure to be normalized on a LC diet.
I understand it is awkward to accept somebodies anecdotal experience, but I am also feel often uneasy when I read about some research which contradicts my own experience.There are individual differences. It looks like you don’t need to keep carbs really low. My son and husband are like that, but after looking at me , my son goes low-carb when he feels like he is getting a flue, so far it worked every time.
People often think that the insulin theory of obesity doesn’t make sense partially because they associate it only with a carbohydrate consumption. But insulin also get secreted when people eat any food (I think it is the reason why IF is helpful for a weight loss), any calories restriction lowers insulin. Insulin theory explains for me individual variations like why I can’t eat the same food as my husband and stay slim like him. I used to be abnormally hungry between meals, now I am hardly hungry at all even after more than 4hours between meals.
I enjoyed WHS blog much more before that “food reward” fixation occurred with Stephan. Nowadays he seems to think that because of the FR people get fat and then sick as a result, he even said that diabetes was caused by the weight gaining. All that seriously contradicts to what I see around. Weight gain is just the tip of an iceberg.
I absolutely agree. There are factors that modify the insulin hypothesis, and some researchers want to focus on those, but the “fattening carbohydrate” and basic metabolism are still the parsimonious explanation.
If you factor in, for example, the modifying effect of thiamine status, apparent anomalies between East and West, past and present, become consistent.
http://hopefulgeranium.blogspot.co.nz/2012/08/some-footnotes-in-support-of-thiamine.html
It is still carbohydrate driving obesity – and beri-beri as well.
>Amylase is thought to have played a key role in human evolution
>in allowing humans an alternative to fruit and protein.
You wanted to say “FAT and protein”?!
And what about tooth decay and dental degeneration caused by CH consumption? The studies of Weston A. Price? They seem to be a counterargument for me if we try to determine (high) starch/CH consumption to be “natural” or something we are well adapted to.
Cheers, Chantal
With modern dental hygiene and the use of fluoride (eek, I’m getting into controversial territory here…), cavities are not as big of a problem as they used to be – even in the face of increasing refined carbohydrate consumption.
Price himself advocated properly prepared whole grains and beans, by the way. He was not anti-carbohydrate by any means.
I am going to try out rice since it doesn’t contain fructose, just glucose and see if I am able to add that into a boring meat only diet. Not tons of it but in moderation. I was thinking of doing this just yesterday and found out you gave a speech about this at the AHS with considerable push back on this.
I can not tolerate sweet potatoes and avoid regular potatoes based on the whole argument Cordain and others make about avoiding these for autoimmune conditions. That got me thinking….is it the high lectins or saponins or is it the fructose that bothers us or maybe both?
Candidly it is hard to take arguments based on studies of earthworms extrapolated as to humans seriously. Even if some similarities exist, it is prima facie evidence of reaching.
Personally, while I felt great on a low carb diet, I feel even better on a diet with ample starch. As Chris (and other posters) discuss, however, the source of the starch matters (potatoes, sweet potatoes, and rice are my staples).
First, I appreciate and enjoy food much more when I eat starches. Maybe this shouldn’t be surprising. After all, starch is a staple in virtually all cuisine. As such, when I include starch, my diet instantly goes from types of food (meat, fruits, and vegetables) to types of cuisine. Note the fundamental distinction.
Second, there are real physiological benefits from eating starch. Serotonin, thyroid hormones, leptin, insulin, and glycogen status, among many others, are all implicated. Without pretending to understand the intricacies here (dare I say nobody does?), suffice it to say they are all interrelated and, for many people, myself included, the ability to handle stress (personal, work, exercise, etc.) and otherwise thrive and enjoy life is, for whatever reason(s), enhanced due to bio-chemical benefits sourced from dietary starch.
The key here is experimentation and patience. There are no magic bullets. All we can do is dedicate blocks of time to new ideas and test their applicability to our unique situations. This is the very essence of science.
Best of luck to all and a big thank you to Chris!
I am now pro-carb, starch, whatever. After tinkering with low carb, veggie + meat only for years, I discovered that my amenorrhea was due to lack of concentrated carb source in my diet. After introducing a very modest amount (less than 70 grams or so) of fruit/starch I immediately resumed my cycles.
I have read the longevity arguments, however I cannot for the life of me understand why eating a diet that causes hormonal imbalance for me is supposedly ideal. Doesn’t amenorrhea lead to bone loss in reproductive women? I’d hate to be the 120 year old lady who can’t stand up straight!
Another argument I didn’t include in the debate or this article due to time/space considerations is that there’s often a trade-off between longevity, health and performance. Certain interventions that improve one of these areas will sometimes cause a decline in others. For example, anabolic steroids may very well improve performance for certain athletes, but they will decrease both health and longevity.
If there was an intervention that could increase your lifespan by one year, but it meant your health and performance (mental and physical) would suffer, would you do it? Or would you prefer to optimize your performance and health and live on year less? Most would choose the latter.
I think that’s a straw man argument in this case, though, because there’s no credible human evidence that starch/glucose decreases longevity.
Definitely on the pro-starch side. I had a similar situation as commenter Tracy above, I went Paleo and VLC for quite some time and ended up being diagnosed with hypothyroidism. My doctor wanted me to get on thyroid medication but I decided to do my own thing…and that very thing was to get those safe staches back in my diet. Most of us live “always on the go” type lifestyles and when you combine that with lots of stressful workouts and such you cannot expect your body to produce its own glucose and do everything else it is designed to do. Give your body a rest and eat some carbs, don’t fear them!
From the blog the Scribble pad
” the problem is not food; the problem is hormones: insulin, leptin. The configuration of hormones, nervous system, determines how you feel and how your body works. Food merely affects these. The thing of concern when it comes to diet-related hypothyroid and infertility is negative fat tissue energy balance i.e. when more FAT is leaving your fat tissue than is coming in. When fat cells are shrinking, or you are trying to. This will always lead to low thyroid and decreased fertility unless the person in question is a million pounds and hasn’t lost much if any weight. IN OTHER WORDS, losing weight causes these problems. Not lack of carbs.”
http://itsthewooo.blogspot.com/2012/03/why-low-carb-does-not-explodes-thyroid.html
I would say one might lead to the other…it is not fair to say that a lack of carbs is the sole reason for low thyroid or decreased fertility…but when initially starting a VLC diet THAT is what causes a negative fat tissue energy balance (over some time.) Some say that a significant drop in body fat will lead to hormonal issues especially in women, and in this circle I believe it’s going VLC that brings on that fat loss. I believe another commenter mentioned this article, but it’s worth a read in my opinion:
http://www.paleoforwomen.com/carbohydrates-for-fertility-and-health/
Thanks Chris! That was highly informative. I’m 17 months Paleo and for the most part have avoided starches. Time for some sweet potato frys!