One of the problems often pointed out about rice, and particularly about white rice, is that its nutrition content is fairly low. It is basically carbohydrates with some trace amounts of protein. A 100-g portion of cooked white rice will typically deliver 28 g of carbohydrates, with zero fiber, and 3 g of protein. The micronutrient content of such a portion leaves a lot to be desired when compared with fruits and vegetables, as you can see below (from Nutritiondata.com). Keep in mind that this is for 100 g of “enriched” white rice; the nutrients you see there, such as manganese, are added.
White rice is rice that has had its husk, bran, and germ removed. This prevents spoilage and thus significantly increases its shelf life. As it happens, it also significantly reduces both its nutrition and toxin content. White rice is one of the refined foods with the lowest toxin content.
Another interesting property of white rice is that it absorbs moisture to the tune of about 2.5 times its weight. That is, a 100-g portion of dry white rice will lead to a 250-g portion of edible white rice after cooking. This does not only dramatically decrease white rice’s glycemic load () compared with wheat-based products in general (with some exceptions, such as pasta), but also allows for white rice to be made into a highly nutritious dish.
If you slow cook almost anything in water, many of its nutrients will seep into the water. All you have to do is to then use that water (often called broth) to cook white rice in it, and you will end up with highly nutritious rice. Typically you will need twice as much broth as rice, cooked for about 15 minutes – e.g., 2 cups of broth for 1 cup of rice.
You can add meats to the white rice, such as pulled chicken or shrimp; add some tomato sauce to that and you’ll make it a chicken or shrimp risotto. You can also add vegetables to the rice. If you want your rice to have something like an al dente consistency, I recommend doing these after the rice is ready; i.e., after you cooked it in the broth.
For the white rice-based dish below I used a broth from about two hours of slow cooking of diced vegetables; namely red bell peppers, carrots, celery, onions, and cabbage. After cooking the rice for 15 minutes, and letting it "sit" for a while (another 15 minutes with the pan covered), I also added the vegetables to it.
As a side note, the cabbage and onion tend to completely dissolve after 1 h or so of slow cooking. The added vegetables give the dish quite a nutritional punch. For example, the cabbage alone seems to be a great source of vitamin C (which is not completely destroyed by the slow cooking), the anti-inflammatory amino acid glutamine, and the DNA repair-promoting substance known as indole-3-carbinol ().
The good folks over at the Highbrow Paleo group on Facebook () had a few other great ideas posted in response to my previous post on the low glycemic load of white rice (), such as cooking white rice in bone broth (thanks Derrick!).
Showing posts with label carbohydrates. Show all posts
Showing posts with label carbohydrates. Show all posts
How to make white rice nutritious
Labels:
carbohydrates,
glycemic load,
recipe,
refined carbs,
rice,
slow-cooking
Rice consumption and health
Carbohydrate-rich foods lead to the formation of blood sugars after digestion (e.g., glucose, fructose), which are then used by the liver to synthesize liver glycogen. Liver glycogen is essentially liver-stored sugar, which is in turn used to meet the glucose needs of the human brain – about 5 g/h for the average person.
When one thinks of the carbohydrate content of foods, there are two measures that often come to mind: the glycemic index and the glycemic load. Of these two, the first, the glycemic index, tends to get a lot more attention. Some would argue that the glycemic load is a lot more important, and that rice, as consumed in Asia, may provide a good illustration of that importance.
A 100-g portion of cooked rice will typically deliver 28 g of carbohydrates, with zero fiber, and 3 g of protein. By comparison, a 100-g portion of white Italian bread will contain 54 g of carbohydrates, with 4 g of fiber, and 10 g of protein – the latter in the form of gluten. A 100-g portion of baked white potato will have 21 g of carbohydrates, with 2 g of fiber, and 2 g of protein.
As you can see above, the amount of carbohydrate per gram in white rice is about half that of white bread. One of the reasons is that the water content in rice, as usually consumed, is comparable to that in fruits. Not surprisingly, rice’s glycemic load is 15 (medium), which is half the glycemic load of 30 (high) of white Italian bread. These refer to 100-g portions. The glycemic load of 100 g of baked white potato is 10 (low).
The glycemic load of a portion of food allows for the estimation of how much that portion of food raises a person's blood glucose level; with one unit of glycemic load being equivalent to the blood glucose effect of consumption of one gram of glucose.
Two common denominators between hunter-gatherer groups that consume a lot of carbohydrates and Asian populations that also consume a lot of carbohydrates are that: (a) their carbohydrate consumption apparently has no negative health effects; and (b) they consume carbohydrates from relatively low glycemic load sources.
The carbohydrate-rich foods consumed by hunter-gatherers are predominantly fruits and starchy tubers. For various Asian populations, it is predominantly white rice. As noted above, the water content of white rice, as usually consumed by Asian populations, is comparable to that of fruits. It also happens to be similar to that of cooked starchy tubers.
An analysis of the China Study II dataset, previously discussed here, suggests that widespread replacement of rice with wheat flour may have been a major source of problems in China during the 1980s and beyond ().
Even though rice is an industrialized seed-based food, the difference between its glycemic load and those of most industrialized carbohydrate-rich foods is large (). This applies to rice as usually consumed – as a vehicle for moisture or sauces that would otherwise remain on the plate. White rice combines this utilitarian purpose with a very low anti-nutrient content.
It is often said that white rice’s nutrient content is very low, but this problem can be easily overcome – a topic for the next post.
(Source: Wikipedia)
When one thinks of the carbohydrate content of foods, there are two measures that often come to mind: the glycemic index and the glycemic load. Of these two, the first, the glycemic index, tends to get a lot more attention. Some would argue that the glycemic load is a lot more important, and that rice, as consumed in Asia, may provide a good illustration of that importance.
A 100-g portion of cooked rice will typically deliver 28 g of carbohydrates, with zero fiber, and 3 g of protein. By comparison, a 100-g portion of white Italian bread will contain 54 g of carbohydrates, with 4 g of fiber, and 10 g of protein – the latter in the form of gluten. A 100-g portion of baked white potato will have 21 g of carbohydrates, with 2 g of fiber, and 2 g of protein.
As you can see above, the amount of carbohydrate per gram in white rice is about half that of white bread. One of the reasons is that the water content in rice, as usually consumed, is comparable to that in fruits. Not surprisingly, rice’s glycemic load is 15 (medium), which is half the glycemic load of 30 (high) of white Italian bread. These refer to 100-g portions. The glycemic load of 100 g of baked white potato is 10 (low).
The glycemic load of a portion of food allows for the estimation of how much that portion of food raises a person's blood glucose level; with one unit of glycemic load being equivalent to the blood glucose effect of consumption of one gram of glucose.
Two common denominators between hunter-gatherer groups that consume a lot of carbohydrates and Asian populations that also consume a lot of carbohydrates are that: (a) their carbohydrate consumption apparently has no negative health effects; and (b) they consume carbohydrates from relatively low glycemic load sources.
The carbohydrate-rich foods consumed by hunter-gatherers are predominantly fruits and starchy tubers. For various Asian populations, it is predominantly white rice. As noted above, the water content of white rice, as usually consumed by Asian populations, is comparable to that of fruits. It also happens to be similar to that of cooked starchy tubers.
An analysis of the China Study II dataset, previously discussed here, suggests that widespread replacement of rice with wheat flour may have been a major source of problems in China during the 1980s and beyond ().
Even though rice is an industrialized seed-based food, the difference between its glycemic load and those of most industrialized carbohydrate-rich foods is large (). This applies to rice as usually consumed – as a vehicle for moisture or sauces that would otherwise remain on the plate. White rice combines this utilitarian purpose with a very low anti-nutrient content.
It is often said that white rice’s nutrient content is very low, but this problem can be easily overcome – a topic for the next post.
Labels:
carbohydrates,
glycemic index,
glycemic load,
glycogenesis,
refined carbs,
rice
Hunger is your best friend: It makes natural foods taste delicious and promotes optimal nutrient partitioning
One of the biggest problems with modern diets rich in industrial foods is that they promote unnatural hunger patterns. For example, hunger can be caused by hypoglycemic dips, coupled with force-storage of fat in adipocytes, after meals rich in refined carbohydrates. This is a double-edged post-meal pattern that is induced by, among other things, abnormally elevated insulin levels. The resulting hunger is a rather unnatural type of hunger.
By the way, I often read here and there, mostly in blogs, that “insulin suppresses hunger”. I frankly don’t know where this idea comes from. What actually happens is that insulin is co-secreted with a number of other hormones. One of those, like insulin also secreted by the beta-cells in the pancreas, is amylin – a powerful appetite suppressor. Amylin deficiency leads to hunger even after a large carbohydrate-rich meal, when insulin levels are elevated.
Abnormally high insulin levels – like those after a “healthy” breakfast of carbohydrate-rich cereals, pancakes etc. – lead to abnormal blood glucose dips soon after the meal. What I am talking about here is a fall in glucose levels that is considerable, and that also happens very fast – illustrated by the ratio between the lengths of the vertical and horizontal black lines on the figure below, from a previous post ().
Those hypoglycemic dips induce hunger, because the hormonal changes necessary to apply a break to the fall in glucose levels (which left unchecked would lead to death) leave us with a hormonal mix that ends up stimulating hunger, in an unnatural way. At the bottom of those dips, insulin levels are much lower than before. I am not talking about diabetics here. I am talking about normoglycemic folks, like the ones whose glucose levels are show on the figure above.
On a diet primarily of natural foods, or foods that are not heavily modified from their natural state, hunger patterns tend to be better synchronized with nutrient deficiencies. This is one of the main advantages of a natural foods diet. By nutrients, I do not mean only micronutrients such as vitamins and minerals, but also macronutrients such as amino and fatty acids.
On a natural diet, nutrient deficiencies should happen regularly. Our bodies are designed for sporadic nutrient intake, remaining most of the time in the fasted state. Human beings are unique in that they have very large brains in proportion to their overall body size, brains that run primarily on glucose – the average person’s brain consumes about 5 g/h of glucose. This latter characteristic makes it very difficult to extrapolate diet-based results based on other species to humans.
As hunger becomes better synchronized with nutrient deficiencies, it should promote optimal nutrient partitioning. This means that, among other things: (a) you should periodically feel hungry for different types of food, depending on your nutrient needs at that point in time; (b) if you do weight training, and fell hungry, some muscle gain should follow; and (c) if you let hunger drive food consumption, on a diet of predominantly natural foods, body fat levels should remain relatively low.
In this sense, hunger becomes your friend – and the best spice!
By the way, I often read here and there, mostly in blogs, that “insulin suppresses hunger”. I frankly don’t know where this idea comes from. What actually happens is that insulin is co-secreted with a number of other hormones. One of those, like insulin also secreted by the beta-cells in the pancreas, is amylin – a powerful appetite suppressor. Amylin deficiency leads to hunger even after a large carbohydrate-rich meal, when insulin levels are elevated.
Abnormally high insulin levels – like those after a “healthy” breakfast of carbohydrate-rich cereals, pancakes etc. – lead to abnormal blood glucose dips soon after the meal. What I am talking about here is a fall in glucose levels that is considerable, and that also happens very fast – illustrated by the ratio between the lengths of the vertical and horizontal black lines on the figure below, from a previous post ().
Those hypoglycemic dips induce hunger, because the hormonal changes necessary to apply a break to the fall in glucose levels (which left unchecked would lead to death) leave us with a hormonal mix that ends up stimulating hunger, in an unnatural way. At the bottom of those dips, insulin levels are much lower than before. I am not talking about diabetics here. I am talking about normoglycemic folks, like the ones whose glucose levels are show on the figure above.
On a diet primarily of natural foods, or foods that are not heavily modified from their natural state, hunger patterns tend to be better synchronized with nutrient deficiencies. This is one of the main advantages of a natural foods diet. By nutrients, I do not mean only micronutrients such as vitamins and minerals, but also macronutrients such as amino and fatty acids.
On a natural diet, nutrient deficiencies should happen regularly. Our bodies are designed for sporadic nutrient intake, remaining most of the time in the fasted state. Human beings are unique in that they have very large brains in proportion to their overall body size, brains that run primarily on glucose – the average person’s brain consumes about 5 g/h of glucose. This latter characteristic makes it very difficult to extrapolate diet-based results based on other species to humans.
As hunger becomes better synchronized with nutrient deficiencies, it should promote optimal nutrient partitioning. This means that, among other things: (a) you should periodically feel hungry for different types of food, depending on your nutrient needs at that point in time; (b) if you do weight training, and fell hungry, some muscle gain should follow; and (c) if you let hunger drive food consumption, on a diet of predominantly natural foods, body fat levels should remain relatively low.
In this sense, hunger becomes your friend – and the best spice!
Labels:
body fat,
body fat loss,
carbohydrates,
hunger,
insulin,
refined carbs
Triglycerides, VLDL, and industrial carbohydrate-rich foods
Below are the coefficients of association calculated by HealthCorrelator for Excel (HCE) for user John Doe. The coefficients of association are calculated as linear correlations in HCE (). The focus here is on the associations between fasting triglycerides and various other variables. Take a look at the coefficient of association at the top, with VLDL cholesterol, indicated with a red arrow. It is a very high 0.999.
Whoa! What is this – 0.999! Is John Doe a unique case? No, this strong association between fasting triglycerides and VLDL cholesterol is a very common pattern among HCE users. The reason is simple. VLDL cholesterol is not normally measured directly, but typically calculated based on fasting triglycerides, by dividing the fasting triglycerides measurement by 5. And there is an underlying reason for that - fasting triglycerides and VLDL cholesterol are actually very highly correlated, based on direct measurements of these two variables.
But if VLDL cholesterol is calculated based on fasting triglycerides (VLDL cholesterol = fasting triglycerides / 5), how come the correlation is 0.999, and not a perfect 1? The reason is the rounding error in the measurements. Whenever you see a correlation this high (i.e., 0.999), it is reasonable to suspect that the source is an underlying linear relationship disturbed by rounding error.
Fasting triglycerides are probably the most useful measures on standard lipid panels. For example, fasting triglycerides below 70 mg/dl suggest a pattern of LDL particles that is predominantly of large and buoyant particles. This pattern is associated with a low incidence of cardiovascular disease (). Also, chronically high fasting triglycerides are a well known marker of the metabolic syndrome, and a harbinger of type 2 diabetes.
Where do large and buoyant LDL particles come from? They frequently start as "big" (relatively speaking) blobs of fat, which are actually VLDL particles. The photo is from the excellent book by Elliott & Elliott (); it shows, on the same scale: (a) VLDL particles, (b) chylomicrons, (c) LDL particles, and (d) HDL particles. The dark bar at the bottom of each shot is 1000 A in length, or 100 nm (A = angstrom; nm = nanometer; 1 nm = 10 A).
If you consume an excessive amount of carbohydrates, my theory is that your liver will produce an abnormally large number of small VLDL particles (also shown on the photo above), a proportion of which will end up as small and dense LDL particles. The liver will do that relatively quickly, probably as a short-term compensatory mechanism to avoid glucose toxicity. It will essentially turn excess glucose, from excess carbohydrates, into fat. The VLDL particles carrying that fat in the form of triglycerides will be small because the liver will be in a hurry to clear the excess glucose in circulation, and will have no time to produce large particles, which take longer to produce individually.
This will end up leading to excess triglycerides hanging around in circulation, long after they should have been used as sources of energy. High fasting triglycerides will be a reflection of that. The graphs below, also generated by HCE for John Doe, show how fasting triglycerides and VLDL cholesterol vary in relation to refined carbohydrate consumption. Again, the graphs are not identical in shape because of rounding error; the shapes are almost identical.
Small and dense LDL particles, in the presence of other factors such as systemic inflammation, will contribute to the formation of atherosclerotic plaques. Again, the main source of these particles would be an excessive amount of carbohydrates. What is an excessive amount of carbohydrates? Generally speaking, it is an amount beyond your liver’s capacity to convert the resulting digestion byproducts, fructose and glucose, into liver glycogen. This may come from spaced consumption throughout the day, or acute consumption in an unnatural form (a can of regular coke), or both.
Liver glycogen is sugar stored in the liver. This is the main source of sugar for your brain. If your blood sugar levels become too low, your brain will get angry. Eventually it will go from angry to dead, and you will finally find out what awaits you in the afterlife.
Should you be a healthy athlete who severely depletes liver glycogen stores on a regular basis, you will probably have an above average liver glycogen storage and production capacity. That will be a result of long-term compensatory adaptation to glycogen depleting exercise (). As such, you may be able to consume large amounts of carbohydrates, and you will still not have high fasting triglycerides. You will not carry a lot of body fat either, because the carbohydrates will not be converted to fat and sent into circulation in VLDL particles. They will be used to make liver glycogen.
In fact, if you are a healthy athlete who severely depletes liver glycogen stores on a regular basis, excess calories will be just about the only thing that will contribute to body fat gain. Your threshold for “excess” carbohydrates will be so high that you will feel like the whole low carbohydrate community is not only misguided but also part of a conspiracy against people like you. If you are also an aggressive blog writer, you may feel compelled to tell the world something like this: “Here, I can eat 300 g of carbohydrates per day and maintain single-digit body fat levels! Take that you low carbohydrate idiots!”
Let us say you do not consume an excessive amount of carbohydrates; again, what is excessive or not varies, probably dramatically, from individual to individual. In this case your liver will produce a relatively small number of fat VLDL particles, which will end up as large and buoyant LDL particles. The fat in these large VLDL particles will likely not come primarily from conversion of glucose and/or fructose into fat (i.e., de novo lipogenesis), but from dietary sources of fat.
How do you avoid consuming excess carbohydrates? A good way of achieving that is to avoid man-made carbohydrate-rich foods. Another is adopting a low carbohydrate diet. Yet another is to become a healthy athlete who severely depletes liver glycogen stores on a regular basis; then you can eat a lot of bread, pasta, doughnuts and so on, and keep your fingers crossed for the future.
Either way, fasting triglycerides will be strongly correlated with VLDL cholesterol, because VLDL particles contain both triglycerides (“encapsulated” fat, not to be confused with “free” fatty acids) and cholesterol. If a large number of VLDL particles are produced by one’s liver, the person’s fasting triglycerides reading will be high. If a small number of VLDL particles are produced, even if they are fat particles, the fasting triglycerides reading will be relatively low. Neither VLDL cholesterol nor fasting triglycerides will be zero though.
Now, you may be wondering, how come a small number of fat VLDL particles will eventually lead to low fasting triglycerides? After all, they are fat particles, even though they occur in fewer numbers. My hypothesis is that having a large number of small-dense VLDL particles in circulation is an abnormal, unnatural state, and that our body is not well designed to deal with that state. Use of lipoprotein-bound fat as a source of energy in this state becomes somewhat less efficient, leading to high triglycerides in circulation; and also to hunger, as our mitochondria like fat.
This hypothesis, and the theory outlined above, fit well with the numbers I have been seeing for quite some time from HCE users. Note that it is a bit different from the more popular theory, particularly among low carbohydrate writers, that fat is force-stored in adipocytes (fat cells) by insulin and not released for use as energy, also leading to hunger. What I am saying here, which is compatible with this more popular theory, is that lipoproteins, like adipocytes, also end up holding more fat than they should if you consume excess carbohydrates, and for longer.
Want to improve your health? Consider replacing things like bread and cereal with butter and eggs in your diet (). And also go see you doctor (); if he disagrees with this recommendation, ask him to read this post and explain why he disagrees.
Whoa! What is this – 0.999! Is John Doe a unique case? No, this strong association between fasting triglycerides and VLDL cholesterol is a very common pattern among HCE users. The reason is simple. VLDL cholesterol is not normally measured directly, but typically calculated based on fasting triglycerides, by dividing the fasting triglycerides measurement by 5. And there is an underlying reason for that - fasting triglycerides and VLDL cholesterol are actually very highly correlated, based on direct measurements of these two variables.
But if VLDL cholesterol is calculated based on fasting triglycerides (VLDL cholesterol = fasting triglycerides / 5), how come the correlation is 0.999, and not a perfect 1? The reason is the rounding error in the measurements. Whenever you see a correlation this high (i.e., 0.999), it is reasonable to suspect that the source is an underlying linear relationship disturbed by rounding error.
Fasting triglycerides are probably the most useful measures on standard lipid panels. For example, fasting triglycerides below 70 mg/dl suggest a pattern of LDL particles that is predominantly of large and buoyant particles. This pattern is associated with a low incidence of cardiovascular disease (). Also, chronically high fasting triglycerides are a well known marker of the metabolic syndrome, and a harbinger of type 2 diabetes.
Where do large and buoyant LDL particles come from? They frequently start as "big" (relatively speaking) blobs of fat, which are actually VLDL particles. The photo is from the excellent book by Elliott & Elliott (); it shows, on the same scale: (a) VLDL particles, (b) chylomicrons, (c) LDL particles, and (d) HDL particles. The dark bar at the bottom of each shot is 1000 A in length, or 100 nm (A = angstrom; nm = nanometer; 1 nm = 10 A).
If you consume an excessive amount of carbohydrates, my theory is that your liver will produce an abnormally large number of small VLDL particles (also shown on the photo above), a proportion of which will end up as small and dense LDL particles. The liver will do that relatively quickly, probably as a short-term compensatory mechanism to avoid glucose toxicity. It will essentially turn excess glucose, from excess carbohydrates, into fat. The VLDL particles carrying that fat in the form of triglycerides will be small because the liver will be in a hurry to clear the excess glucose in circulation, and will have no time to produce large particles, which take longer to produce individually.
This will end up leading to excess triglycerides hanging around in circulation, long after they should have been used as sources of energy. High fasting triglycerides will be a reflection of that. The graphs below, also generated by HCE for John Doe, show how fasting triglycerides and VLDL cholesterol vary in relation to refined carbohydrate consumption. Again, the graphs are not identical in shape because of rounding error; the shapes are almost identical.
Small and dense LDL particles, in the presence of other factors such as systemic inflammation, will contribute to the formation of atherosclerotic plaques. Again, the main source of these particles would be an excessive amount of carbohydrates. What is an excessive amount of carbohydrates? Generally speaking, it is an amount beyond your liver’s capacity to convert the resulting digestion byproducts, fructose and glucose, into liver glycogen. This may come from spaced consumption throughout the day, or acute consumption in an unnatural form (a can of regular coke), or both.
Liver glycogen is sugar stored in the liver. This is the main source of sugar for your brain. If your blood sugar levels become too low, your brain will get angry. Eventually it will go from angry to dead, and you will finally find out what awaits you in the afterlife.
Should you be a healthy athlete who severely depletes liver glycogen stores on a regular basis, you will probably have an above average liver glycogen storage and production capacity. That will be a result of long-term compensatory adaptation to glycogen depleting exercise (). As such, you may be able to consume large amounts of carbohydrates, and you will still not have high fasting triglycerides. You will not carry a lot of body fat either, because the carbohydrates will not be converted to fat and sent into circulation in VLDL particles. They will be used to make liver glycogen.
In fact, if you are a healthy athlete who severely depletes liver glycogen stores on a regular basis, excess calories will be just about the only thing that will contribute to body fat gain. Your threshold for “excess” carbohydrates will be so high that you will feel like the whole low carbohydrate community is not only misguided but also part of a conspiracy against people like you. If you are also an aggressive blog writer, you may feel compelled to tell the world something like this: “Here, I can eat 300 g of carbohydrates per day and maintain single-digit body fat levels! Take that you low carbohydrate idiots!”
Let us say you do not consume an excessive amount of carbohydrates; again, what is excessive or not varies, probably dramatically, from individual to individual. In this case your liver will produce a relatively small number of fat VLDL particles, which will end up as large and buoyant LDL particles. The fat in these large VLDL particles will likely not come primarily from conversion of glucose and/or fructose into fat (i.e., de novo lipogenesis), but from dietary sources of fat.
How do you avoid consuming excess carbohydrates? A good way of achieving that is to avoid man-made carbohydrate-rich foods. Another is adopting a low carbohydrate diet. Yet another is to become a healthy athlete who severely depletes liver glycogen stores on a regular basis; then you can eat a lot of bread, pasta, doughnuts and so on, and keep your fingers crossed for the future.
Either way, fasting triglycerides will be strongly correlated with VLDL cholesterol, because VLDL particles contain both triglycerides (“encapsulated” fat, not to be confused with “free” fatty acids) and cholesterol. If a large number of VLDL particles are produced by one’s liver, the person’s fasting triglycerides reading will be high. If a small number of VLDL particles are produced, even if they are fat particles, the fasting triglycerides reading will be relatively low. Neither VLDL cholesterol nor fasting triglycerides will be zero though.
Now, you may be wondering, how come a small number of fat VLDL particles will eventually lead to low fasting triglycerides? After all, they are fat particles, even though they occur in fewer numbers. My hypothesis is that having a large number of small-dense VLDL particles in circulation is an abnormal, unnatural state, and that our body is not well designed to deal with that state. Use of lipoprotein-bound fat as a source of energy in this state becomes somewhat less efficient, leading to high triglycerides in circulation; and also to hunger, as our mitochondria like fat.
This hypothesis, and the theory outlined above, fit well with the numbers I have been seeing for quite some time from HCE users. Note that it is a bit different from the more popular theory, particularly among low carbohydrate writers, that fat is force-stored in adipocytes (fat cells) by insulin and not released for use as energy, also leading to hunger. What I am saying here, which is compatible with this more popular theory, is that lipoproteins, like adipocytes, also end up holding more fat than they should if you consume excess carbohydrates, and for longer.
Want to improve your health? Consider replacing things like bread and cereal with butter and eggs in your diet (). And also go see you doctor (); if he disagrees with this recommendation, ask him to read this post and explain why he disagrees.
Labels:
carbohydrates,
Cardiovascular disease,
cholesterol,
HCE,
LDL,
low carb,
statistics,
triglyceride,
VLDL
There is no doubt that abnormally elevated insulin is associated with body fat accumulation
For as long as diets existed there have been influential proponents, or believers, who at some point had what they thought were epiphanies. From that point forward, they disavowed the diets that they formally endorsed. Low carbohydrate dieting seems to be in this situation now. Among other things, it has been recently “discovered” that the idea that insulin drives fat into body fat cells is “wrong”.
Based on some of the comments I have been receiving lately, apparently a few readers think that I am one of those “enlightened”. If you are interested in what I have been eating, for quite some time now, just click on the link at the top of this blog that refers to my transformation. It is essentially high in all macronutrients on days that I exercise, and low in carbohydrates and calories on days that I don’t. It is a cyclic approach that works for me; calorie surpluses on some days and calorie deficits on other days.
But let me set the record straight regarding what I think: there is no doubt that insulin is associated with body fat accumulation. I was told that an influential health blogger (whom I respect a lot) denied this recently, going to the extreme of saying that no professional metabolism or endocrinology researcher believes in it, but I couldn’t find any evidence of that statement. It is not hard at all to find professional metabolism and endocrinology researchers who have asserted that insulin is associated with body fat accumulation, based on very reliable evidence. Actually, this is Biochemistry 101.
What I think is truly unclear is whether insulin spikes associated with carbohydrate-rich foods in general are the cause of obesity. This idea is, indeed, probably wrong given the evidence we have from various human populations whose members consume plenty of non-industrialized carbohydrate-rich foods. On a related note, I particularly disagree with the notion that the pancreas gets tired over time due to having to secrete insulin in bursts, which seems to also be one of the foundations on which many low carbohydrate diet varieties rest.
As with almost everything related to health, the role of insulin in body fat gain is complex, and part of that complexity is due to the nonlinear relationship between body fat gain and postprandial insulin release. Industrial carbohydrate-rich foods have a much higher glycemic load than natural carbohydrate-rich foods, even though their glycemic index may be the same in some cases. In other words, the quantity of easily digestible carbohydrates per gram is much higher in industrial carbohydrate-rich foods.
In normoglycemic folks, this leads to an abnormally elevated insulin response, among other hormonal responses. For example, circulating growth hormone, which promotes body fat loss, is inversely correlated with circulating insulin. Insulin drives fat, typically from dietary sources of fat, into adipocytes. That fat may also come from excess carbohydrates, packaged into VLDL particles.
Under normal circumstances, that would be fine, since our body is designed to store fat and release it as needed. But the abnormal insulin response elicited by industrial carbohydrate-rich foods, together with other hormonal responses, leads to a little more body fat accumulation, and for longer, than it should. And I’m talking here about people without any metabolic damage. Saturated and monounsaturated fats are healthy when eaten, but when they are stored as excess body fat, they become pro-inflammatory.
Body fat is like an organ, secreting many hormones into the bloodstream, several of which are pro-inflammatory. One of those pro-inflammatory hormones, which I believe is closely linked with many diseases of civilization, is tumor necrosis factor. (The acronym is now TNF. Apparently the “-alpha” after its name and acronym has been dropped recently.) Dietary fat, particularly saturated fat, seems to be anti-inflammatory. In other words, body fat accumulation is the problem. You only need 30 g/d of excess body fat accumulation to gain around 24 lbs of fat per year. Over three years, that will add up to over 70 lbs of body fat.
In my view, ultimately it is excess inflammation (which is, in essence, a vascular response) that is at the source of most of the diseases of civilization.
That is where the nonlinearity comes in. Insulin is healthy up to a point. Beyond that, it starts causing health problems, over time. And one of the main mechanisms by which it does so is via excessive body fat accumulation, with different damage threshold levels for different people. Insulin may decrease appetite as it goes up, but it increases it if goes down too much. If it goes up abnormally, typically it will go down too much. As it reaches a trough it induces hypoglycemia, even if mildly.
Take a look at the graph below, from this post showing the glucose variations in normoglycemic individuals. There is a lot of variation among different individuals, but it is clear that the magnitude of the hypoglycemic dips is inversely correlated with the magnitude of the glucose spikes. That inverse correlation is due primarily to the effect of insulin. Under normal circumstances, a decrease in circulating insulin would promote an increase in free fatty acids in circulation, which would normally have a suppressing effect on hunger in the hours after a meal. But industrial carbohydrate-rich foods lead to increases and decreases in glucose and insulin that are too steep, causing the opposite effect.
You may ask: why do you keep talking about industrial carbohydrate-rich foods? Why not talk about industrial protein- or fat-rich foods as well? The reason is that the food industry has not been very successful at producing industrial protein- or fat-rich foods that are palatable without adding a lot of carbohydrate to them.
More often than not they need enough carbohydrate added in the form of sugar to become truly addictive.
Based on some of the comments I have been receiving lately, apparently a few readers think that I am one of those “enlightened”. If you are interested in what I have been eating, for quite some time now, just click on the link at the top of this blog that refers to my transformation. It is essentially high in all macronutrients on days that I exercise, and low in carbohydrates and calories on days that I don’t. It is a cyclic approach that works for me; calorie surpluses on some days and calorie deficits on other days.
But let me set the record straight regarding what I think: there is no doubt that insulin is associated with body fat accumulation. I was told that an influential health blogger (whom I respect a lot) denied this recently, going to the extreme of saying that no professional metabolism or endocrinology researcher believes in it, but I couldn’t find any evidence of that statement. It is not hard at all to find professional metabolism and endocrinology researchers who have asserted that insulin is associated with body fat accumulation, based on very reliable evidence. Actually, this is Biochemistry 101.
What I think is truly unclear is whether insulin spikes associated with carbohydrate-rich foods in general are the cause of obesity. This idea is, indeed, probably wrong given the evidence we have from various human populations whose members consume plenty of non-industrialized carbohydrate-rich foods. On a related note, I particularly disagree with the notion that the pancreas gets tired over time due to having to secrete insulin in bursts, which seems to also be one of the foundations on which many low carbohydrate diet varieties rest.
As with almost everything related to health, the role of insulin in body fat gain is complex, and part of that complexity is due to the nonlinear relationship between body fat gain and postprandial insulin release. Industrial carbohydrate-rich foods have a much higher glycemic load than natural carbohydrate-rich foods, even though their glycemic index may be the same in some cases. In other words, the quantity of easily digestible carbohydrates per gram is much higher in industrial carbohydrate-rich foods.
In normoglycemic folks, this leads to an abnormally elevated insulin response, among other hormonal responses. For example, circulating growth hormone, which promotes body fat loss, is inversely correlated with circulating insulin. Insulin drives fat, typically from dietary sources of fat, into adipocytes. That fat may also come from excess carbohydrates, packaged into VLDL particles.
Under normal circumstances, that would be fine, since our body is designed to store fat and release it as needed. But the abnormal insulin response elicited by industrial carbohydrate-rich foods, together with other hormonal responses, leads to a little more body fat accumulation, and for longer, than it should. And I’m talking here about people without any metabolic damage. Saturated and monounsaturated fats are healthy when eaten, but when they are stored as excess body fat, they become pro-inflammatory.
Body fat is like an organ, secreting many hormones into the bloodstream, several of which are pro-inflammatory. One of those pro-inflammatory hormones, which I believe is closely linked with many diseases of civilization, is tumor necrosis factor. (The acronym is now TNF. Apparently the “-alpha” after its name and acronym has been dropped recently.) Dietary fat, particularly saturated fat, seems to be anti-inflammatory. In other words, body fat accumulation is the problem. You only need 30 g/d of excess body fat accumulation to gain around 24 lbs of fat per year. Over three years, that will add up to over 70 lbs of body fat.
In my view, ultimately it is excess inflammation (which is, in essence, a vascular response) that is at the source of most of the diseases of civilization.
That is where the nonlinearity comes in. Insulin is healthy up to a point. Beyond that, it starts causing health problems, over time. And one of the main mechanisms by which it does so is via excessive body fat accumulation, with different damage threshold levels for different people. Insulin may decrease appetite as it goes up, but it increases it if goes down too much. If it goes up abnormally, typically it will go down too much. As it reaches a trough it induces hypoglycemia, even if mildly.
Take a look at the graph below, from this post showing the glucose variations in normoglycemic individuals. There is a lot of variation among different individuals, but it is clear that the magnitude of the hypoglycemic dips is inversely correlated with the magnitude of the glucose spikes. That inverse correlation is due primarily to the effect of insulin. Under normal circumstances, a decrease in circulating insulin would promote an increase in free fatty acids in circulation, which would normally have a suppressing effect on hunger in the hours after a meal. But industrial carbohydrate-rich foods lead to increases and decreases in glucose and insulin that are too steep, causing the opposite effect.
You may ask: why do you keep talking about industrial carbohydrate-rich foods? Why not talk about industrial protein- or fat-rich foods as well? The reason is that the food industry has not been very successful at producing industrial protein- or fat-rich foods that are palatable without adding a lot of carbohydrate to them.
More often than not they need enough carbohydrate added in the form of sugar to become truly addictive.
Dietary protein does not become body fat if you are on a low carbohydrate diet
By definition LC is about dietary carbohydrate restriction. If you are reducing carbohydrates, your proportional intake of protein or fat, or both, will go up. While I don’t think there is anything wrong with a high fat diet, it seems to me that the true advantage of LC may be in how protein is allocated, which seems to contribute to a better body composition.
LC with more animal protein and less fat makes particularly good sense to me. Eating a variety of unprocessed animal foods, as opposed to only muscle meat from grain-fed cattle, will get you that. In simple terms, LC with more protein, achieved in a natural way with unprocessed foods, means more of the following in one's diet: lean meats, seafood and vegetables. Possibly with lean meats and seafood making up more than half of one’s protein intake. Generally speaking, large predatory fish species (e.g., various shark species, including dogfish) are better avoided to reduce exposure to toxic metals.
Organ meats such as beef liver are also high in protein and low in fat, but should be consumed in moderation due to the risk of hypervitaminosis; particularly hypervitaminosis A. Our ancestors ate the animal whole, and organ mass makes up about 10-20 percent of total mass in ruminants. Eating organ meats once a week places you approximately within that range.
In LC liver glycogen is regularly depleted, so the amino acids resulting from the digestion of protein will be primarily used to replenish liver glycogen, to replenish the albumin pool, for oxidation, and various other processes (e.g., tissue repair, hormone production). If you do some moderate weight training, some of those amino acids will be used for muscle growth.
In this sense, the true “metabolic advantage” of LC, so to speak, comes from protein and not fat. “Calories in” still counts, but you get better allocation of nutrients. Moreover, in LC, the calorie value of protein goes down a bit, because your body is using it as a “jack of all trades”, and thus in a less efficient way. This renders protein the least calorie-dense macronutrient, yielding fewer calories per gram than carbohydrates; and significantly fewer calories per gram when compared with dietary fat and alcohol.
Dietary fat is easily stored as body fat after digestion. In LC, it is difficult for the body to store amino acids as body fat. The only path would be conversion to glucose and uptake by body fat cells, but in LC the liver will typically be starving and want all the extra glucose for itself, so that it can feed its ultimate master – the brain. The liver glycogen depletion induced by LC creates a hormonal mix that places the body in fat release mode, making it difficult for fat cells to take up glucose via the GLUT4 transporter protein.
Excess amino acids are oxidized for energy. This may be why many people feel a slight surge of energy after a high-protein meal. (A related effect is associated with alcohol consumption, which is often masked by the relaxing effect also associated with alcohol consumption.) Amino acid oxidation is not associated with cancer. Neither is fat oxidation. But glucose oxidation is; this is known as the Warburg effect.
A high-protein LC approach will not work very well for athletes who deplete major amounts of muscle glycogen as part of their daily training regimens. These folks will invariably need more carbohydrates to keep their performance levels up. Ultimately this is a numbers game. The protein-to-glucose conversion rate is about 2-to-1. If an athlete depletes 300 g of muscle glycogen per day, he or she will need about 600 g of protein to replenish that based only on protein. This is too high an intake of protein by any standard.
A recreational exerciser who depletes 60 g of glycogen 3 times per week can easily replenish that muscle glycogen with dietary protein. Someone who exercises with weights for 40 minutes 3 times per week will deplete about that much glycogen each time. Contrary to popular belief, muscle glycogen is only minimally replenished postprandially (i.e., after meals) based on dietary sources. Liver glycogen replenishment is prioritized postprandially. Muscle glycogen is replenished over several days, primarily based on liver glycogen. It is one fast-filling tank replenishing another slow-filling one.
Recreational exercisers who are normoglycemic and who do LC intermittently tend to increase the size of their liver glycogen tank over time, via compensatory adaptation, and also use more fat (and ketones, which are byproducts of fat metabolism) as sources of energy. Somewhat paradoxically, these folks benefit from regular high carbohydrate intake days (e.g., once a week, or on exercise days), since their liver glycogen tanks will typically store more glycogen. If they keep their liver and muscle glycogen tanks half empty all the time, compensatory adaptation suggests that both their liver and muscle glycogen tanks will over time become smaller, and that their muscles will store more fat.
One way or another, with the exception of those with major liver insulin resistance, dietary protein does not become body fat if you are on a LC diet.
LC with more animal protein and less fat makes particularly good sense to me. Eating a variety of unprocessed animal foods, as opposed to only muscle meat from grain-fed cattle, will get you that. In simple terms, LC with more protein, achieved in a natural way with unprocessed foods, means more of the following in one's diet: lean meats, seafood and vegetables. Possibly with lean meats and seafood making up more than half of one’s protein intake. Generally speaking, large predatory fish species (e.g., various shark species, including dogfish) are better avoided to reduce exposure to toxic metals.
Organ meats such as beef liver are also high in protein and low in fat, but should be consumed in moderation due to the risk of hypervitaminosis; particularly hypervitaminosis A. Our ancestors ate the animal whole, and organ mass makes up about 10-20 percent of total mass in ruminants. Eating organ meats once a week places you approximately within that range.
In LC liver glycogen is regularly depleted, so the amino acids resulting from the digestion of protein will be primarily used to replenish liver glycogen, to replenish the albumin pool, for oxidation, and various other processes (e.g., tissue repair, hormone production). If you do some moderate weight training, some of those amino acids will be used for muscle growth.
In this sense, the true “metabolic advantage” of LC, so to speak, comes from protein and not fat. “Calories in” still counts, but you get better allocation of nutrients. Moreover, in LC, the calorie value of protein goes down a bit, because your body is using it as a “jack of all trades”, and thus in a less efficient way. This renders protein the least calorie-dense macronutrient, yielding fewer calories per gram than carbohydrates; and significantly fewer calories per gram when compared with dietary fat and alcohol.
Dietary fat is easily stored as body fat after digestion. In LC, it is difficult for the body to store amino acids as body fat. The only path would be conversion to glucose and uptake by body fat cells, but in LC the liver will typically be starving and want all the extra glucose for itself, so that it can feed its ultimate master – the brain. The liver glycogen depletion induced by LC creates a hormonal mix that places the body in fat release mode, making it difficult for fat cells to take up glucose via the GLUT4 transporter protein.
Excess amino acids are oxidized for energy. This may be why many people feel a slight surge of energy after a high-protein meal. (A related effect is associated with alcohol consumption, which is often masked by the relaxing effect also associated with alcohol consumption.) Amino acid oxidation is not associated with cancer. Neither is fat oxidation. But glucose oxidation is; this is known as the Warburg effect.
A recreational exerciser who depletes 60 g of glycogen 3 times per week can easily replenish that muscle glycogen with dietary protein. Someone who exercises with weights for 40 minutes 3 times per week will deplete about that much glycogen each time. Contrary to popular belief, muscle glycogen is only minimally replenished postprandially (i.e., after meals) based on dietary sources. Liver glycogen replenishment is prioritized postprandially. Muscle glycogen is replenished over several days, primarily based on liver glycogen. It is one fast-filling tank replenishing another slow-filling one.
Recreational exercisers who are normoglycemic and who do LC intermittently tend to increase the size of their liver glycogen tank over time, via compensatory adaptation, and also use more fat (and ketones, which are byproducts of fat metabolism) as sources of energy. Somewhat paradoxically, these folks benefit from regular high carbohydrate intake days (e.g., once a week, or on exercise days), since their liver glycogen tanks will typically store more glycogen. If they keep their liver and muscle glycogen tanks half empty all the time, compensatory adaptation suggests that both their liver and muscle glycogen tanks will over time become smaller, and that their muscles will store more fat.
One way or another, with the exception of those with major liver insulin resistance, dietary protein does not become body fat if you are on a LC diet.
What is a good low carbohydrate diet? It is a low calorie one
My interview with Jimmy Moore should be up on the day that this post becomes available. (I usually write my posts on weekends and schedule them for release at the beginning of the following weeks.) So the time is opportune for me to try to aswer this question: What is a good low carbohydrate diet?
For me, and many people I know, the answer is: a low calorie one. What this means, in simple terms, is that a good low carbohydrate diet is one with plenty of seafood and organ meats in it, and also plenty of veggies. These are low carbohydrate foods that are also naturally low in calories. Conversely, a low carbohydrate diet of mostly beef and eggs would be a high calorie one.
Seafood and organ meats provide essential fatty acids and are typically packed with nutrients. Because of that, they tend to be satiating. In fact, certain organ meats, such as beef liver, are so packed with nutrients that it is a good idea to limit their consumption. I suggest eating beef liver once or twice a week only. As for seafood, it seems like a good idea to me to get half of one’s protein from them.
Does this mean that the calories-in-calories-out idea is correct? No, and there is no need to resort to complicated and somewhat questionable feedback-loop arguments to prove that calories-in-calories-out is wrong. Just consider this hypothetical scenario; a thought experiment. Take two men, one 25 years of age and the other 65, both with the same weight. Put them on the same exact diet, on the same exact weight training regime, and keep everything else the same.
What will happen? Typically the 65-year-old will put on more body fat than the 25-year-old, and the latter will put on more lean body mass. This will happen in spite of the same exact calories-in-calories-out profile. Why? Because their hormonal mixes are different. The 65-year-old will typically have lower levels of circulating growth hormone and testosterone, both of which significantly affect body composition.
As you can see, it is not all about insulin, as has been argued many times before. In fact, average and/or fasting insulin may be the same for the 65- and 25-year-old men. And, still, the 65-year-old will have trouble keeping his body fat low and gaining muscle. There are other hormones involved, such as leptin and adiponectin, and probably several that we don’t know about yet.
A low carbohydrate diet appears to be ideal for many people, whether that is due to a particular health condition (e.g., diabetes) or simply due to a genetic makeup that favors this type of diet. By adopting a low carbohydrate diet with plenty of seafood, organ meats, and veggies, you will make it a low calorie diet. If that leads to a calorie deficit that is too large, you can always add a bit more of fat to it. For example, by cooking fish with butter and adding bacon to beef liver.
One scenario where I don’t see the above working well is if you are a competitive athlete who depletes a significant amount of muscle glycogen on a daily basis – e.g., 250 g or more. In this case, it will be very difficult to replenish glycogen only with protein, so the person will need more carbohydrates. He or she would need a protein intake in excess of 500 g per day for replenishing 250 g of glycogen only with protein.
For me, and many people I know, the answer is: a low calorie one. What this means, in simple terms, is that a good low carbohydrate diet is one with plenty of seafood and organ meats in it, and also plenty of veggies. These are low carbohydrate foods that are also naturally low in calories. Conversely, a low carbohydrate diet of mostly beef and eggs would be a high calorie one.
Seafood and organ meats provide essential fatty acids and are typically packed with nutrients. Because of that, they tend to be satiating. In fact, certain organ meats, such as beef liver, are so packed with nutrients that it is a good idea to limit their consumption. I suggest eating beef liver once or twice a week only. As for seafood, it seems like a good idea to me to get half of one’s protein from them.
Does this mean that the calories-in-calories-out idea is correct? No, and there is no need to resort to complicated and somewhat questionable feedback-loop arguments to prove that calories-in-calories-out is wrong. Just consider this hypothetical scenario; a thought experiment. Take two men, one 25 years of age and the other 65, both with the same weight. Put them on the same exact diet, on the same exact weight training regime, and keep everything else the same.
What will happen? Typically the 65-year-old will put on more body fat than the 25-year-old, and the latter will put on more lean body mass. This will happen in spite of the same exact calories-in-calories-out profile. Why? Because their hormonal mixes are different. The 65-year-old will typically have lower levels of circulating growth hormone and testosterone, both of which significantly affect body composition.
As you can see, it is not all about insulin, as has been argued many times before. In fact, average and/or fasting insulin may be the same for the 65- and 25-year-old men. And, still, the 65-year-old will have trouble keeping his body fat low and gaining muscle. There are other hormones involved, such as leptin and adiponectin, and probably several that we don’t know about yet.
A low carbohydrate diet appears to be ideal for many people, whether that is due to a particular health condition (e.g., diabetes) or simply due to a genetic makeup that favors this type of diet. By adopting a low carbohydrate diet with plenty of seafood, organ meats, and veggies, you will make it a low calorie diet. If that leads to a calorie deficit that is too large, you can always add a bit more of fat to it. For example, by cooking fish with butter and adding bacon to beef liver.
One scenario where I don’t see the above working well is if you are a competitive athlete who depletes a significant amount of muscle glycogen on a daily basis – e.g., 250 g or more. In this case, it will be very difficult to replenish glycogen only with protein, so the person will need more carbohydrates. He or she would need a protein intake in excess of 500 g per day for replenishing 250 g of glycogen only with protein.
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The China Study II: Carbohydrates, fat, calories, insulin, and obesity
The “great blogosphere debate” rages on regarding the effects of carbohydrates and insulin on health. A lot of action has been happening recently on Peter’s blog, with knowledgeable folks chiming in, such as Peter himself, Dr. Harris, Dr. B.G. (my sista from anotha mista), John, Nigel, CarbSane, Gunther G., Ed, and many others.
I like to see open debate among people who hold different views consistently, are willing to back them up with at least some evidence, and keep on challenging each other’s views. It is very unlikely that any one person holds the whole truth regarding health matters. Unfortunately this type of debate also confuses a lot of people, particularly those blog lurkers who want to get all of their health information from one single source.
Part of that “great blogosphere debate” debate hinges on the effect of low or high carbohydrate dieting on total calorie consumption. Well, let us see what the China Study II data can tell us about that, and about a few other things.
WarpPLS was used to do the analyses below. For other China Study analyses, many using WarpPLS as well as HealthCorrelator for Excel, click here. For the dataset used here, visit the HealthCorrelator for Excel site and check under the sample datasets area.
The two graphs below show the relationships between various foods, carbohydrates as a percentage of total calories, and total calorie consumption. A basic linear analysis was employed here. As carbohydrates as a percentage of total calories go up, the diet generally becomes a high carbohydrate diet. As it goes down, we see a move to the low carbohydrate end of the scale.
The left parts of the two graphs above are very similar. They tell us that wheat flour consumption is very strongly and negatively associated with rice consumption; i.e., wheat flour displaces rice. They tell us that fruit consumption is positively associated with rice consumption. They also tell us that high wheat flour consumption is strongly and positively associated with being on a high carbohydrate diet.
Neither rice nor fruit consumption has a statistically significant influence on whether the diet is high or low in carbohydrates, with rice having some effect and fruit practically none. But wheat flour consumption does. Increases in wheat flour consumption lead to a clear move toward the high carbohydrate diet end of the scale.
People may find the above results odd, but they should realize that white glutinous rice is only 20 percent carbohydrate, whereas wheat flour products are usually 50 percent carbohydrate or more. Someone consuming 400 g of white rice per day, and no other carbohydrates, will be consuming only 80 g of carbohydrates per day. Someone consuming 400 g of wheat flour products will be consuming 200 g of carbohydrates per day or more.
Fruits generally have much less carbohydrate than white rice, even very sweet fruits. For example, an apple is about 12 percent carbohydrate.
There is a measure that reflects the above differences somewhat. That measure is the glycemic load of a food; not to be confused with the glycemic index.
The right parts of the graphs above tell us something else. They tell us that the percentage of carbohydrates in one’s diet is strongly associated with total calorie consumption, and that this is not the case with percentage of fat in one’s diet.
Given the above, one may be interested in looking at the contribution of individual foods to total calorie consumption. The graph below focuses on that. The results take nonlinearity into consideration; they were generated using the Warp3 algorithm option of WarpPLS.
As you can see, wheat flour consumption is more strongly associated with total calories than rice; both associations being positive. Animal food consumption is negatively associated, somewhat weakly but statistically significantly, with total calories. Let me repeat for emphasis: negatively associated. This means that, as animal food consumption goes up, total calories consumed go down.
These results may seem paradoxical, but keep in mind that animal foods displace wheat flour in this dataset. Note that I am not saying that wheat flour consumption is a confounder; it is controlled for in the model above.
What does this all mean?
Increases in both wheat flour and rice consumption lead to increases in total caloric intake in this dataset. Wheat has a stronger effect. One plausible mechanism for this is abnormally high blood glucose elevations promoting abnormally high insulin responses. Refined carbohydrate-rich foods are particularly good at raising blood glucose fast and keeping it elevated, because they usually contain a lot of easily digestible carbohydrates. The amounts here are significantly higher than anything our body is “designed” to handle.
In normoglycemic folks, that could lead to a “lite” version of reactive hypoglycemia, leading to hunger again after a few hours following food consumption. Insulin drives calories, as fat, into adipocytes. It also keeps those calories there. If insulin is abnormally elevated for longer than it should be, one becomes hungry while storing fat; the fat that should have been released to meet the energy needs of the body. Over time, more calories are consumed; and they add up.
The above interpretation is consistent with the result that the percentage of fat in one’s diet has a statistically non-significant effect on total calorie consumption. That association, although non-significant, is negative. Again, this looks paradoxical, but in this sample animal fat displaces wheat flour.
Moreover, fat leads to no insulin response. If it comes from animals foods, fat is satiating not only because so much in our body is made of fat and/or requires fat to run properly; but also because animal fat contains micronutrients, and helps with the absorption of those micronutrients.
Fats from oils, even the healthy ones like coconut oil, just do not have the latter properties to the same extent as unprocessed fats from animal foods. Think slow-cooking meat with some water, making it release its fat, and then consuming all that fat as a sauce together with the meat.
In the absence of industrialized foods, typically we feel hungry for those foods that contain nutrients that our body needs at a particular point in time. This is a subconscious mechanism, which I believe relies in part on past experience; the reason why we have “acquired tastes”.
Incidentally, fructose leads to no insulin response either. Fructose is naturally found mostly in fruits, in relatively small amounts when compared with industrial foods rich in refined sugars.
And no, the pancreas does not get “tired” from secreting insulin.
The more refined a carbohydrate-rich food is, the more carbohydrates it tends to pack per unit of weight. Carbohydrates also contribute calories; about 4 calories per g. Thus more carbohydrates should translate into more calories.
If someone consumes 50 g of carbohydrates per day in excess of caloric needs, that will translate into about 22.2 g of body fat being stored. Over a month, that will be approximately 666.7 g. Over a year, that will be 8 kg, or 17.6 lbs. Over 5 years, that will be 40 kg, or 88 lbs. This is only from carbohydrates; it does not consider other macronutrients.
There is no need to resort to the “tired pancreas” theory of late-onset insulin resistance to explain obesity in this context. Insulin resistance is, more often than not, a direct result of obesity. Type 2 diabetes is by far the most common type of diabetes; and most type 2 diabetics become obese or overweight before they become diabetic. There is clearly a genetic effect here as well, which seems to moderate the relationship between body fat gain and liver as well as pancreas dysfunction.
It is not that hard to become obese consuming refined carbohydrate-rich foods. It seems to be much harder to become obese consuming animal foods, or fruits.
I like to see open debate among people who hold different views consistently, are willing to back them up with at least some evidence, and keep on challenging each other’s views. It is very unlikely that any one person holds the whole truth regarding health matters. Unfortunately this type of debate also confuses a lot of people, particularly those blog lurkers who want to get all of their health information from one single source.
Part of that “great blogosphere debate” debate hinges on the effect of low or high carbohydrate dieting on total calorie consumption. Well, let us see what the China Study II data can tell us about that, and about a few other things.
WarpPLS was used to do the analyses below. For other China Study analyses, many using WarpPLS as well as HealthCorrelator for Excel, click here. For the dataset used here, visit the HealthCorrelator for Excel site and check under the sample datasets area.
The two graphs below show the relationships between various foods, carbohydrates as a percentage of total calories, and total calorie consumption. A basic linear analysis was employed here. As carbohydrates as a percentage of total calories go up, the diet generally becomes a high carbohydrate diet. As it goes down, we see a move to the low carbohydrate end of the scale.
The left parts of the two graphs above are very similar. They tell us that wheat flour consumption is very strongly and negatively associated with rice consumption; i.e., wheat flour displaces rice. They tell us that fruit consumption is positively associated with rice consumption. They also tell us that high wheat flour consumption is strongly and positively associated with being on a high carbohydrate diet.
Neither rice nor fruit consumption has a statistically significant influence on whether the diet is high or low in carbohydrates, with rice having some effect and fruit practically none. But wheat flour consumption does. Increases in wheat flour consumption lead to a clear move toward the high carbohydrate diet end of the scale.
People may find the above results odd, but they should realize that white glutinous rice is only 20 percent carbohydrate, whereas wheat flour products are usually 50 percent carbohydrate or more. Someone consuming 400 g of white rice per day, and no other carbohydrates, will be consuming only 80 g of carbohydrates per day. Someone consuming 400 g of wheat flour products will be consuming 200 g of carbohydrates per day or more.
Fruits generally have much less carbohydrate than white rice, even very sweet fruits. For example, an apple is about 12 percent carbohydrate.
There is a measure that reflects the above differences somewhat. That measure is the glycemic load of a food; not to be confused with the glycemic index.
The right parts of the graphs above tell us something else. They tell us that the percentage of carbohydrates in one’s diet is strongly associated with total calorie consumption, and that this is not the case with percentage of fat in one’s diet.
Given the above, one may be interested in looking at the contribution of individual foods to total calorie consumption. The graph below focuses on that. The results take nonlinearity into consideration; they were generated using the Warp3 algorithm option of WarpPLS.
As you can see, wheat flour consumption is more strongly associated with total calories than rice; both associations being positive. Animal food consumption is negatively associated, somewhat weakly but statistically significantly, with total calories. Let me repeat for emphasis: negatively associated. This means that, as animal food consumption goes up, total calories consumed go down.
These results may seem paradoxical, but keep in mind that animal foods displace wheat flour in this dataset. Note that I am not saying that wheat flour consumption is a confounder; it is controlled for in the model above.
What does this all mean?
Increases in both wheat flour and rice consumption lead to increases in total caloric intake in this dataset. Wheat has a stronger effect. One plausible mechanism for this is abnormally high blood glucose elevations promoting abnormally high insulin responses. Refined carbohydrate-rich foods are particularly good at raising blood glucose fast and keeping it elevated, because they usually contain a lot of easily digestible carbohydrates. The amounts here are significantly higher than anything our body is “designed” to handle.
In normoglycemic folks, that could lead to a “lite” version of reactive hypoglycemia, leading to hunger again after a few hours following food consumption. Insulin drives calories, as fat, into adipocytes. It also keeps those calories there. If insulin is abnormally elevated for longer than it should be, one becomes hungry while storing fat; the fat that should have been released to meet the energy needs of the body. Over time, more calories are consumed; and they add up.
The above interpretation is consistent with the result that the percentage of fat in one’s diet has a statistically non-significant effect on total calorie consumption. That association, although non-significant, is negative. Again, this looks paradoxical, but in this sample animal fat displaces wheat flour.
Moreover, fat leads to no insulin response. If it comes from animals foods, fat is satiating not only because so much in our body is made of fat and/or requires fat to run properly; but also because animal fat contains micronutrients, and helps with the absorption of those micronutrients.
Fats from oils, even the healthy ones like coconut oil, just do not have the latter properties to the same extent as unprocessed fats from animal foods. Think slow-cooking meat with some water, making it release its fat, and then consuming all that fat as a sauce together with the meat.
In the absence of industrialized foods, typically we feel hungry for those foods that contain nutrients that our body needs at a particular point in time. This is a subconscious mechanism, which I believe relies in part on past experience; the reason why we have “acquired tastes”.
Incidentally, fructose leads to no insulin response either. Fructose is naturally found mostly in fruits, in relatively small amounts when compared with industrial foods rich in refined sugars.
And no, the pancreas does not get “tired” from secreting insulin.
The more refined a carbohydrate-rich food is, the more carbohydrates it tends to pack per unit of weight. Carbohydrates also contribute calories; about 4 calories per g. Thus more carbohydrates should translate into more calories.
If someone consumes 50 g of carbohydrates per day in excess of caloric needs, that will translate into about 22.2 g of body fat being stored. Over a month, that will be approximately 666.7 g. Over a year, that will be 8 kg, or 17.6 lbs. Over 5 years, that will be 40 kg, or 88 lbs. This is only from carbohydrates; it does not consider other macronutrients.
There is no need to resort to the “tired pancreas” theory of late-onset insulin resistance to explain obesity in this context. Insulin resistance is, more often than not, a direct result of obesity. Type 2 diabetes is by far the most common type of diabetes; and most type 2 diabetics become obese or overweight before they become diabetic. There is clearly a genetic effect here as well, which seems to moderate the relationship between body fat gain and liver as well as pancreas dysfunction.
It is not that hard to become obese consuming refined carbohydrate-rich foods. It seems to be much harder to become obese consuming animal foods, or fruits.
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How much dietary protein can you store in muscle? About 15 g/d if you are a gifted bodybuilder
Let us say you are one of the gifted few who are able to put on 1 lb of pure muscle per month, or 12 lbs per year, by combining strength training with a reasonable protein intake. Let us go even further and assume that the 1 lb of muscle that we are talking about is due to muscle protein gain, not glycogen or water. This is very uncommon; one has to really be genetically gifted to achieve that.
And you do that by eating a measly 80 g of protein per day. That is little more than 0.5 g of protein per lb of body weight if you weigh 155 lbs; or 0.4 per lb if you weigh 200 lbs. At the end of the year you are much more muscular. People even think that you’ve been taking steroids; but that just came naturally. The figure below shows what happened with the 80 g of protein you consumed every day. About 15 g became muscle (that is 1 lb divided by 30) … and 65 g “disappeared”!
Is that an amazing feat? Yes, it is an amazing feat of waste, if you think that the primary role of protein is to build muscle. More than 80 percent of the protein consumed was used for something else, notably to keep your metabolic engine running.
A significant proportion of dietary protein also goes into the synthesis of albumin, to which free fatty acids bind in the blood. (Albumin is necessary for the proper use of fat as fuel.) Dietary protein is also used in the synthesis of various body tissues and hormones.
Dietary protein does not normally become body fat, but can be used in place of fat as fuel and thus allow more dietary fat to be stored. It leads to an insulin response, which causes less body fat to be released. In this sense, dietary protein has a fat-sparing effect, preventing it from being used to supply the energy needs of the body.
Nevertheless, the fat-sparing effect of protein is lower than that of another "macronutrient" – alcohol. That is, alcohol takes precedence over carbohydrates for use as fuel. However, protein takes precedence over carbohydrates. Neither alcohol nor protein typically becomes body fat. Carbohydrates can become body fat, but only when glycogen stores are full.
What does this mean?
As it turns out, a reasonably high protein intake seems to be quite healthy, and there is nothing wrong with the body using protein to feed its metabolism.
Having said that, one does not need enormous amounts of protein to keep or even build muscle if one is getting enough calories from other sources.
In my next post I’ll talk a little bit more about that.
And you do that by eating a measly 80 g of protein per day. That is little more than 0.5 g of protein per lb of body weight if you weigh 155 lbs; or 0.4 per lb if you weigh 200 lbs. At the end of the year you are much more muscular. People even think that you’ve been taking steroids; but that just came naturally. The figure below shows what happened with the 80 g of protein you consumed every day. About 15 g became muscle (that is 1 lb divided by 30) … and 65 g “disappeared”!
Is that an amazing feat? Yes, it is an amazing feat of waste, if you think that the primary role of protein is to build muscle. More than 80 percent of the protein consumed was used for something else, notably to keep your metabolic engine running.
A significant proportion of dietary protein also goes into the synthesis of albumin, to which free fatty acids bind in the blood. (Albumin is necessary for the proper use of fat as fuel.) Dietary protein is also used in the synthesis of various body tissues and hormones.
Dietary protein does not normally become body fat, but can be used in place of fat as fuel and thus allow more dietary fat to be stored. It leads to an insulin response, which causes less body fat to be released. In this sense, dietary protein has a fat-sparing effect, preventing it from being used to supply the energy needs of the body.
Nevertheless, the fat-sparing effect of protein is lower than that of another "macronutrient" – alcohol. That is, alcohol takes precedence over carbohydrates for use as fuel. However, protein takes precedence over carbohydrates. Neither alcohol nor protein typically becomes body fat. Carbohydrates can become body fat, but only when glycogen stores are full.
What does this mean?
As it turns out, a reasonably high protein intake seems to be quite healthy, and there is nothing wrong with the body using protein to feed its metabolism.
Having said that, one does not need enormous amounts of protein to keep or even build muscle if one is getting enough calories from other sources.
In my next post I’ll talk a little bit more about that.
Labels:
albumin,
alcohol,
carbohydrates,
free fatty acid,
glycogen depletion,
protein
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