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Carbs & Fiber
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In one pass Carbohydrate is not one thing, so asking whether it is good or bad in general gets you little.
Educational content, not medical advice — consult a clinician.
Rest · GLUT4 sequestered In a resting muscle cell, GLUT4 sits almost entirely in cytoplasmic vesicles, with little on the membrane, so a fasting muscle that is not contracting takes up little glucose.
Fermentable fiber reaches the colon The stomach and small intestine have no enzymes that can cleave fermentable fibre, so it reaches the colon intact, where bacteria break it down.
reactive hypoglycemia Fast-digesting high-glycemic-index food pushes glucose up and insulin runs high, and in some people glucose drops below its pre-meal level around 2 hours later, bringing sleepiness.
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Chapter 1
Not one thing
Carbohydrate is not one thing, so asking whether it is good or bad in general gets you little. It comes in at least three layers:
Sugars: glucose, fructose, sucrose, which are absorbed fastStarches: long chains of glucose, found in rice, potatoes, noodles, and legumesFiber: human digestive enzymes cannot cut it apart, but gut bacteria can use some of it
The problem is usually not carbohydrate itself but the package it comes in. Foods that combine refined sugar, refined flour, little fiber, and a lot of fat and salt are a completely different kind of thing from legumes, whole grains, tubers, and fruit.
Sugars: glucose, fructose, sucrose, which are absorbed fastStarches: long chains of glucose, found in rice, potatoes, noodles, and legumesFiber: human digestive enzymes cannot cut it apart, but gut bacteria can use some of it
The problem is usually not carbohydrate itself but the package it comes in. Foods that combine refined sugar, refined flour, little fiber, and a lot of fat and salt are a completely different kind of thing from legumes, whole grains, tubers, and fruit.
Numbers · What GI and GL each measure
The glycemic index () is measured like this: eat a portion of a food containing 50 g of available carbohydrate, record the blood-glucose curve over the next two hours, and compare the area under that curve with the area after 50 g of pure glucose, which is set at 100. It measures how much blood glucose rises and for how long, not how fast it rises.But 50 g of carbohydrate from watermelon means eating six or seven hundred grams of flesh, and nobody eats that in one go. So you also need the glycemic load (): the GI multiplied by the grams of carbohydrate actually in a serving, divided by 100. That is the blood-glucose exposure a real serving brings:
Watermelon: GI 72 (high), but a serving is about 150 g, so the GL is about 5 (low)White rice: GI 73, and a 150 g serving has a GL of about 30 (high)Oatmeal: GI 55, and a serving has a GL of about 13 (medium)Lentils: GI 30, and a serving has a GL of about 8 (low)
So avoid high-GI foods is a crude rule. What matters more for a meal's effect on blood glucose is the GL, how foods are combined, and how processed they are. Since continuous glucose monitors (, small devices worn on the skin that measure glucose all day) became widespread, this layer of difference has become visible in everyday life.
Chapter 2
Glycogen: fuel stored for exercise
The liver and the muscles pack glucose into glycogen, a storage form made of glucose units joined together:
Liver glycogen (about 100 g) keeps blood glucose steady, especially overnight and between mealsMuscle glycogen (about 400 g) is for the muscle's own use, supplying energy () quickly during high-intensity exercise
The higher the intensity, the more you rely on glycogen. Long endurance sessions, interval running, ball sports, and high-volume phases of strength training all draw down muscle glycogen noticeably.
So in sports nutrition, carbohydrate is not a moral question. It is a question of whether you want the battery charged for high-intensity output.
Liver glycogen (about 100 g) keeps blood glucose steady, especially overnight and between mealsMuscle glycogen (about 400 g) is for the muscle's own use, supplying energy () quickly during high-intensity exercise
The higher the intensity, the more you rely on glycogen. Long endurance sessions, interval running, ball sports, and high-volume phases of strength training all draw down muscle glycogen noticeably.
So in sports nutrition, carbohydrate is not a moral question. It is a question of whether you want the battery charged for high-intensity output.
Mechanism · How muscle takes in glucose
The gate that lets glucose into a muscle cell is a glucose transporter called . Most of the time it hides inside the cell in small vesicles rather than sitting on the membrane, which is why resting muscle barely responds to blood glucose.Two independent routes can push GLUT4 up to the cell surface:
1. The insulin route: insulin switches on a chain of signaling enzymes inside the cell (PI3K, Akt), and the vesicles carrying GLUT4 then fuse with the cell membrane
2. The exercise (muscle contraction) route: driven by the cell's energy sensor , by the calcium released during contraction, and by mechanical tension, with no insulin needed
In the 30–60 minutes right after exercise, the GLUT4 that the contraction route pushed to the membrane has not all been pulled back yet, and for several hours afterward the insulin route also works better than usual. Carbohydrate eaten then goes preferentially to the muscles to restock glycogen.
This mechanism explains several things:
In type 2 diabetes the insulin route is blunted, but the exercise route is independent, so exercise still helps control blood glucoseEating carbohydrate after training matters for endurance athletes' recoverySitting for long periods leaves the exercise route idle for long stretches, which is one of the risk factors for insulin resistance
Chapter 3
When carbs stop coming
When carbohydrate stops coming in, the sugar the brain needs cannot be conjured out of fat's long chains. Fatty acids are clipped into acetyl-CoA, which enters the citric acid cycle (the loop in which cells burn fuel), and the carbon ends up breathed out as carbon dioxide, never to return. The liver's route for making new glucose is called gluconeogenesis, and its raw materials are mainly amino acids from muscle, a little glycerol, and lactate. So a person with plenty of body fat who goes without food for a few days is still taking apart their own muscle.
Ketones are a second fuel that lets the body take apart less muscle, but they cannot cover all of it. So carbohydrate being non-essential does not mean this bill is free.
Ketones are a second fuel that lets the body take apart less muscle, but they cannot cover all of it. So carbohydrate being non-essential does not mean this bill is free.
Mechanism · Why fat cannot become glucose
When carbohydrate stops coming in, your body does not turn to fat to make the glucose your brain is asking for. It turns to your muscle first.Everything so far has been about carbohydrate arriving; this is about what happens when it does not.
The brain needs glucose all the time, and blood glucose cannot pause. So the liver (joined by the kidneys during prolonged starvation) opens a production line that makes glucose from other raw materials. That line is called gluconeogenesis.
The catch is that only three raw materials can get onto it:
The carbon skeletons of glucogenic amino acids, taken off your own muscle proteinGlycerol, the three-carbon head of a fat molecule, which falls off when fat is broken down; it is only a small part of the fatLactate, left over from muscle, which cycles back to the liver
The bulk of fat, those long fatty-acid chains, cannot get on at all.
Why not? Inside the cell, fatty acids are clipped into two-carbon pieces of acetyl-CoA, and acetyl-CoA has exactly one destination: it joins oxaloacetate to form citrate and enters the citric acid cycle. To replace the oxaloacetate it used up, the cycle has to go all the way around, and the price of that lap is breathing those two carbons out as carbon dioxide. Once the carbon is breathed out, it does not come back.
So a person with plenty of body fat, a few days into going without food, is still taking apart their own muscle. The warehouse is piled with more fuel than they could ever burn, yet there is no road from it to the molecule the brain needs.
Ketones are the second fuel the body evolved so that it would take apart less muscle. The liver packages the acetyl-CoA it cannot burn into ketones and sends them to the brain. Once the brain switches to burning ketones, less glucose has to be made from scratch, and less muscle has to be taken apart. This is what Cahill spent most of his career on: ketones are the reason people can survive prolonged starvation.
This one chain ties together three things that are usually covered separately:
Why a fat-loss phase costs muscle (Protein During a Deficit): this gluconeogenesis line is one of the reasonsWhy ketones can cover only about two-thirds of the brain's energy, with the rest still needing glucose: the part of nervous on the brain's backup fuel covers thisWhy the kidneys take on roughly 40% of gluconeogenesis in prolonged starvation: see renal
The chain also forces a counterintuitive conclusion: carbohydrate is the only one of the three macronutrients that is not essential.
There is no such thing as an essential carbohydrate: no sugar exists that would give you a deficiency disease if you went without it, because the line above shows that the body can make its own glucose. By contrast, there are 9 essential amino acids and 2 essential fatty acids (linoleic acid and alpha-linolenic acid). Those 11 the body genuinely cannot make, and going short of them causes real problems.
The same ruler can measure alcohol (see Alcohol Metabolism): ethanol supplies energy, but it is not essential, so it has no recommended intake. Measured with this ruler, carbohydrate and ethanol land in one box, and protein and fat in the other.
But non-essential is a long way from should not be eaten; do not blur the two:
Very low carbohydrate intake is survivable; that follows directly from the chain aboveThe cost depends on the situation. In prolonged starvation, muscle breakdown slows once ketones take over, but it does not stop. On a low-carbohydrate diet with enough calories and protein, the amino acids for gluconeogenesis come mostly from the protein you eat, so muscle does not have to fill the gapSo this neither recommends nor opposes a ketogenic diet. It answers one question only: when carbohydrate stops coming in, who pays the bill?
Numbers · Non-essential, yet it has an RDA
In 2005 the US Institute of Medicine (IOM) set a Recommended Dietary Allowance () for carbohydrate: 130 g a day. Why would a non-essential nutrient have an RDA at all?The answer is in the basis the IOM itself printed in the Function column of that Dietary Reference Intakes () table: the RDA rests on carbohydrate's role as the primary energy source for the brain.
In other words, 130 g is not the amount below which you get sick. It is the amount that covers the brain, so gluconeogenesis does not have to take protein apart. It is a voucher that spares your muscle, not a certificate of essentiality.
Put two other rows of the same table beside it, and the ruler becomes fully visible:
Linoleic acid (n-6) and alpha-linolenic acid (n-3): the IOM gives them an Adequate Intake (), and the Function column reads "essential component of structural membrane lipids" and "required for normal skin function". That is what essential looks like in printSaturated fat, trans fat, and cholesterol: the IOM writes that no required role other than as an energy source was identified, and that the body can make what it needs. So they get neither an RDA nor an AICarbohydrate: it has an RDA, but the basis is the brain's use, not a deficiency disease
Read the three rows together and it becomes clear what the essentiality ruler measures: whether there is a deficiency disease, not whether the body has a use for the nutrient.
The body certainly has a use for carbohydrate, and a big one. But has a use for and essential are two different things. This is the pair most often confused in nutrition, and it is the same trap that makes the term essential amino acid misleading.
Mechanism · Does no fat carbon get in at all?
The claim above, that not one fatty-acid chain gets into gluconeogenesis, is the textbook line; the biochemistry textbooks by Lehninger, Stryer, and Voet all print it. To be honest, that sentence has two frayed edges.Edge one: odd-chain fatty acids. Clipping two carbons at a time, an odd-numbered chain leaves a final three-carbon piece, propionyl-CoA, and that piece really can enter gluconeogenesis. But almost all the fat people eat is even-chain, so this gap is narrow.
Edge two: in 2011, Kaleta and colleagues reworked this old question on a genome-scale model of metabolism and argued that pathways bypassing the glyoxylate cycle may exist in humans, making fatty-acid-to-glucose conversion theoretically possible. This is a computer-model prediction, not something measured in people, and they themselves stated plainly in the paper that the efficiency is low.
Neither edge changes the conclusion. When you are going without food, your brain cannot wait on a low-efficiency theoretical bypass, and the muscle gets taken apart anyway. Saying fat cannot become glucose is slightly rough chemically, and correct metabolically.
This is also a move worth practicing when you read about nutrition: the same sentence often has one answer at the is it possible level and another at the is it fast enough level. For gluconeogenesis, the one that decides whether you lose muscle is the second.
kaleta-2011-fat-to-glucose
Chapter 4
Fiber feeds gut bacteria
Sorting fiber into soluble and insoluble cannot answer what you actually want to know. What a fiber does is set by two independent axes. Viscosity acts in the small intestine: it thickens the food mass, so sugar and bile acids spread more slowly. Fermentability acts in the colon: bacteria eat the fiber and make short-chain fatty acids, along with gas. The two axes vary separately, so there are four combinations.
Oats blunt a blood-glucose spike and inulin does not; psyllium relieves constipation without bloating precisely because bacteria cannot eat it. Constipation calls for high viscosity and low fermentability; feeding your gut bacteria calls for high fermentability; if fiber bloats you, steer clear of the highly fermentable kinds. When you see high fiber, ask first: which axis?
Oats blunt a blood-glucose spike and inulin does not; psyllium relieves constipation without bloating precisely because bacteria cannot eat it. Constipation calls for high viscosity and low fermentability; feeding your gut bacteria calls for high fermentability; if fiber bloats you, steer clear of the highly fermentable kinds. When you see high fiber, ask first: which axis?
Mechanism · Viscosity and fermentability are two axes
Soluble vs insoluble cannot answer the question you actually have. Oats and inulin are both soluble, so why do oats blunt a blood-glucose spike while inulin does not? Why does inulin bloat you while psyllium does not?Because what a fiber does is set by two independent axes, and they act in two different organs:
Viscosity, in the small intestine: some fibers soak up water and thicken the food mass, so sugar and bile acids reach the gut wall more slowly. This is how oats blunt a glucose spike and lower low-density lipoprotein cholesterol ()Fermentability, in the colon: some fibers are eaten by bacteria, which make short-chain fatty acids and, as a by-product, gas. This is the mechanism for feeding your microbes, and also the mechanism for bloating
The two axes vary independently, so there are four combinations (McRorie 2017):
Psyllium: high viscosity, low fermentability. The gel reaches the rectum intact and works as a lubricant (Marlett 2000). It works precisely because bacteria cannot eat it, so it relieves constipation and lowers LDL without causing gasInulin: low viscosity, high fermentability. It feeds microbes hard and makes a lot of gas, but it does nothing for a glucose spikeWheat bran: low viscosity, low fermentability. Pure physical bulk, which keeps the gut moving by volumeOat beta-glucan: high viscosity, moderate fermentability. A bit of both
So when you see the words high fiber, ask first: which axis? Constipation calls for high viscosity and low fermentability; feeding your microbes calls for high fermentability; if fiber bloats you, avoid the highly fermentable kinds.
Fiber is not something to max out in a single day. Add it a little at a time, week by week, and drink enough water.
Mechanism · What each short-chain fatty acid does
Bacteria in the colon ferment fiber into short-chain fatty acids (). The three main ones go to different places and do quite different jobs:Acetate (about 60%): enters the general circulation and reaches the liver, where it takes part in making cholesterol and fat. The idea that it reaches the brain and regulates fullness comes mainly from animal studiesPropionate (about 20%): almost all of it is taken up by the liver. The findings that it holds back glucose production in the liver and lowers fasting blood glucose and cholesterol synthesis come mostly from animal and cell studies; human evidence is limitedButyrate (about 20%): the preferred fuel of the cells lining the colon (about 70% of their energy), and mostly used up right there, with little reaching the general bloodstream. It acts as a signal that maintains the barrier of the colon lining and has anti-inflammatory effects. People who eat more fiber and make more butyrate have a lower risk of colon cancer; this is an observed association
One point worth remembering: butyrate taken by mouth is mostly absorbed before it ever reaches the colon. To get butyrate to the colon, you have to feed fiber and let the gut bacteria make it themselves. The big butyrate producers include *Faecalibacterium prausnitzii* (often treated as one marker of a healthy gut microbiome), *Roseburia*, and *Eubacterium rectale*, and they like resistant starch (the part of starch that escapes digestion in the small intestine), beta-glucan, and inulin.
So gut health means taking probiotics is only half right. Most swallowed probiotic strains are just passing through and do not settle in the gut; feeding fiber to the bacteria already living there, which is what prebiotics do, is another route.
Chapter 5
Glucose curve
The same 50 g of carbohydrate can produce completely different blood-glucose curves after a meal.
The factors that shape it include particle size, how processed the food is, fiber, protein, fat, acidity, the resistant starch that forms when cooked food cools, and whether you have just exercised.
In practice, carbohydrate paired with protein, plus vegetables, legumes, or whole grains, usually gives a steadier curve than a sweet drink or white bread on its own. After exercise, muscle cells have more of the glucose transporter , the gate that lets glucose in, on their membranes, so the same carbohydrate goes more readily into restocking glycogen.
The factors that shape it include particle size, how processed the food is, fiber, protein, fat, acidity, the resistant starch that forms when cooked food cools, and whether you have just exercised.
In practice, carbohydrate paired with protein, plus vegetables, legumes, or whole grains, usually gives a steadier curve than a sweet drink or white bread on its own. After exercise, muscle cells have more of the glucose transporter , the gate that lets glucose in, on their membranes, so the same carbohydrate goes more readily into restocking glycogen.
Evidence · Same food, different glucose responses
A 2015 study from the Weizmann Institute of Science in Israel (Zeevi and colleagues, Cell) had 800 people wear continuous glucose monitors for a week and recorded the blood-glucose responses to more than forty thousand meals. The result: people's responses to the same meal differed widely, and those differences were larger than the differences between foods. For the same food, some people's glucose rose sharply while others' barely moved.The researchers built a machine-learning model that combined blood tests, eating habits, body measurements, physical activity, and gut bacteria to predict each person's glucose after meals, and they checked it in a separate group of people. The model predicted fairly well, but it did not break the variation down into how much each factor contributes, so the commonly mentioned factors below are in no particular order:
The makeup of the gut microbiome (one type of information Zeevi's model used)Baseline insulin sensitivity, and (HbA1c, a marker of average blood glucose over the past two to three months)When you eat (the same food may produce a different response in the morning than at night)What you ate at the previous meal, known as the second-meal effectWhether you slept enough
So besides looking up a food's , you can also look at how your own body responds to it. People with prediabetes or metabolic syndrome have started using continuous glucose monitors for exactly this.
But be careful of one thing: as continuous glucose monitors have spread, they have also bred an anxious belief that any rise in blood glucose is bad. In healthy people, the ordinary rise and fall of glucose after a meal (mostly staying below 7.8 mmol/L) is normal physiology and no cause for panic.
Chapter 6
Why you get sleepy after meals
Feeling sleepy after a meal is common, but there is no single cause. Several explanations have been proposed, and their evidence differs in strength. After a big high-carbohydrate meal, blood glucose shoots up and then falls, and in some people it drops below where it was before the meal. Insulin pushes branched-chain amino acids into muscle, which makes it relatively easier for tryptophan to get into the brain; this is clear with pure-carbohydrate meals and much weaker with mixed meals. In slices of animal brain tissue, glucose can quiet the neurons in the hypothalamus that keep you awake, but this has not been measured in people. And the extra blood that flows to the gut after a meal takes a share too.
So the fix is not a blanket cut in carbohydrate. What human trials support is changing how and in what order you eat a meal, and taking a walk afterward.
So the fix is not a blanket cut in carbohydrate. What human trials support is changing how and in what order you eat a meal, and taking a walk afterward.
Mechanism · Four proposed explanations
Feeling sleepy, unfocused, and ready for a nap 30–90 minutes after eating, especially after a big high-carbohydrate meal, is something almost everyone has experienced. It probably has more than one cause, and four explanations have been proposed:1. Blood glucose shoots up, then falls: after a high-glycemic-index meal, a lot of insulin is released, and in some people blood glucose 90–120 minutes later drops below its pre-meal level (reactive hypoglycemia). The brain reads an energy shortfall, and you feel tired and unfocused
2. Tryptophan gets into the brain: insulin pushes the branched-chain amino acids (leucine, isoleucine, valine) into muscle, so tryptophan becomes relatively more plentiful in the blood. Tryptophan competes with them for the same transporter into the brain, so more tryptophan gets in, and the brain makes more serotonin and melatonin
3. The wake-keeping neurons are muted: in slices of animal brain tissue, glucose can directly inhibit the orexin (also called hypocretin) neurons of the lateral hypothalamus, which keep you awake
4. Blood flow is redirected: after a meal, much more blood flows to the gut and the body's blood is redistributed; on its own, this has only a small effect
The strength of the evidence for these four differs widely, and the page that goes through them one by one keeps them apart. What they have in common: sleepiness after meals is normal physiology that certain ways of eating amplify, not simply not enough sleep or getting old. Once you see that, the fix is not a blanket eat fewer carbs, but changing how a meal is built, taking a light 10-minute walk after it, and putting the heavy carbohydrate at breakfast and lunch.
Mechanism · Each explanation, with its evidence
Explanation 1 · blood glucose shoots up, then falls (reactive postprandial hypoglycemia)After a high-glycemic-index meal (white rice with a sugary drink and white bread), blood glucose climbs fairly high over the first half hour to an hourThe pancreas releases a generous amount of insulin (healthy people do this too, and it tends to be more marked in people with insulin resistance)In some people, around 2 hours after eating, blood glucose falls below its pre-meal level. In people without diabetes, falling to true hypoglycemia is not common. As glucose comes down, people feel sleepy and irritable and want something sweet (the classic 3 p.m. craving for milk tea)On a , it shows up as a spike followed by a steep drop rather than a gentle waveType of evidence: it makes physiological sense and can be seen on a glucose monitor, but how much of after-meal sleepiness it explains has never been measured directly
Explanation 2 · competition between tryptophan and other large neutral amino acids (Wurtman's classic work)
Serotonin and melatonin are both made from tryptophan, a large neutral amino acidTryptophan enters the brain through a transporter in the blood-brain barrier called LAT1, competing with the branched-chain amino acids (leucine, isoleucine, valine) for the same channelA high-carbohydrate meal makes insulin push the branched-chain amino acids into muscle, their level in the blood drops for a while, tryptophan's relative share rises, and more tryptophan gets into the brainThis effect is clearest with carbohydrate meals that contain almost no protein. By the same mechanism, protein in a meal brings more branched-chain amino acids to compete, so in ordinary mixed meals the effect may be much weakerA side note: turkey makes you sleepy because of tryptophan is folklore. Turkey has no more tryptophan than chicken; what holiday meals really have more of is high-carbohydrate side dishes
Explanation 3 · the orexin wake system is inhibited (Burdakov 2006, Neuron)
The orexin neurons of the lateral hypothalamus are one of the brain's wake switches, sending connections to several wake-promoting centers in the brainstem and forebrainIn electrophysiology experiments on slices of mouse brain tissue, Burdakov 2006 found that glucose, acting through a class of potassium channels (tandem-pore potassium channels), makes these neurons hyperpolarize and fall quiet, and that this mechanism is sensitive enough to track the normal rise and fall of glucose between mealsLosing these neurons (most likely through an autoimmune process) is the core of type 1 narcolepsyWhether this effect occurs in healthy people, and how large it is, has not been measured directly
Explanation 4 · more blood flow to the gut after meals (postprandial mesenteric vasodilation)
Over the first half hour to an hour after a meal, blood flow to the gut, pancreas, and liver rises markedly to handle absorption and metabolismThe blood pumped by the heart is redistributed. In healthy people, blood flow to the brain barely changes (the brain's blood flow is protected by autoregulation), but older adults or people with autonomic neuropathy may see a mild drop in blood flow to the brainOn its own, this has only a small effect; it simply adds to the others
So sleepiness after meals probably has more than one cause. Interestingly, the most direct evidence among these explanations sits on the side of the fixes: changing how and in what order you eat a meal, and walking afterward, have both been tested in people, as the practical chapter describes.
In practice · Fix the meal, not the carb
A common misconception is that sleepiness after meals comes from eating carbs, so cutting carbs fixes it. Cutting carbohydrate across the board does not necessarily solve the problem: in the first few days of very low carbohydrate intake, many people feel more tired rather than less, and performance on training days may suffer.The approaches with support from human studies are these:
1. Change the order of the meal: vegetables and protein first, carbohydrate last
The order is vegetables, then protein and fat, and carbohydrate last. Shukla 2015 (Diabetes Care) was a pilot study: 11 people with type 2 diabetes treated with metformin ate the same meal (bread, orange juice, chicken breast, salad) on two days, once with the carbohydrate first and once with it last; the order was not randomized. On the day the carbohydrate came last, blood glucose 30 and 60 minutes after the meal was about 30–40% lower. Its limits: few participants, a single meal, and people who already had type 2 diabetes. The proposed mechanism is that vegetables, protein, and fat eaten first slow stomach emptying and bring forward the release of gut hormones such as ; this study did not measure those. You do not have to refuse carbohydrate; you only change the order, which is simple enough to do right away.
2. Walk lightly for 10–15 minutes after meals (DiPietro 2013, Diabetes Care)
10 inactive people aged 60 or older with raised fasting blood glucose each completed three protocols in random order inside a metabolic chamber: a 15-minute walk after each of three meals, or a single 45-minute walk in the morning or in the afternoon (at the same intensity). Each protocol was a 48-hour stay in the chamber, with the first day as a no-exercise control day, and everyone wore a throughout. Walking after each meal and the single morning walk lowered 24-hour blood glucose compared with the no-exercise day, while the afternoon walk had almost no effect, and walking after meals brought down blood glucose in the 3 hours after dinner more than either 45-minute walk did. Mechanistically, muscle contraction uses the route through the glucose transporter that does not depend on insulin (see the chapter on glycogen), so part of the sugar just eaten is taken straight up by muscle instead of piling up in the blood. A version you can keep up: take out the trash, pick up a delivery, or walk the dog after dinner, with no need to change clothes or shoes. The lower the bar, the easier it is to stick with.
3. Put heavy carbohydrate at breakfast and lunch, not dinner
For most people, the body handles glucose better in the morning than in the evening. In one randomized trial (Jakubowicz 2013), overweight women with metabolic syndrome ate about 1400 kcal a day for 12 weeks; one group ate the largest share at breakfast, the other at dinner. The breakfast group had lower glucose and insulin across the day and also lost more weight. Insulin, GLP-1, and the liver's glucose production all follow 24-hour rhythms. In practice, put rice, noodles, and potatoes at breakfast and lunch, and make dinner mainly protein and vegetables with a moderate amount of carbohydrate. For shift workers and people on night shifts, the rhythm itself has been disrupted, so this may not apply (see Shift Work).
4. Use a continuous glucose monitor to see your own response (Zeevi 2015)
The same food raises glucose very differently in different people, and the variation between people is larger than the variation between foods. People with prediabetes or type 2 diabetes, or who get sleepy after meals again and again, can wear a continuous glucose monitor for about 2 weeks to see which foods raise their glucose the most. It is not recommended for healthy people to wear one just for this, as it tends to breed the anxious belief that any rise in blood glucose is bad.
Watch out: if postprandial slump is severe enough to include orthostatic dizziness, palpitations, cold sweats, near-syncope (not just sleepiness), it may not be ordinary slump but reactive hypoglycemia (true low glucose), dumping syndrome (post-gastric-surgery), hypotension, arrhythmia, or autonomic dysfunction. See a doctor — don't self-treat.
Chapter 7
Three rules for everyday carbs
First, on days when you mostly sit, swap your carbohydrate for versions that come with structure: legumes, whole grains, tubers, fruit, and vegetables. The beta-glucan in oats (see Oats), the pectin in apples (see Apple), and the fiber in avocado (see Avocado) are all this kind of structure.
Second, on training days, do not fear carbohydrate. Before and after hard training, carbohydrate supports your output and recovery; it does not automatically turn into fat.
Third, add fiber gradually. Jump from 10 g to 35 g a day overnight and your gut will protest; adding one more serving of legumes or whole grains each week is more realistic.
Second, on training days, do not fear carbohydrate. Before and after hard training, carbohydrate supports your output and recovery; it does not automatically turn into fat.
Third, add fiber gradually. Jump from 10 g to 35 g a day overnight and your gut will protest; adding one more serving of legumes or whole grains each week is more realistic.
In practice · Building up fiber slowly
The US Institute of Medicine (IOM 2005) set the Adequate Intake () for fiber for adults under 50 at 25 g a day for women and 38 g for men. According to the US Dietary Guidelines, the great majority of American adults do not reach this amount, and the gap is large.Building up over 3 weeks means less bloating and fewer chances of setting off irritable bowel syndrome () symptoms:
1. Week 1: each day, replace 1 serving of white rice or white flour with 1 serving of whole grain (oats, brown rice, quinoa, whole-wheat noodles)
2. Week 2: each day, add 1 serving of legumes (red kidney beans, chickpeas, lentils, edamame) to a main meal, cooked any way you like
3. Week 3: each day, add 1 serving of fruit eaten with its skin, plus 30 g of raw nuts or seeds (almonds, walnuts, chia seeds)
At the same time, drink about 500 ml more water a day. Fiber needs water, and if the fiber goes up but the water does not, some people actually become more constipated.
Situations where fiber should not be ramped up: an acute flare of irritable bowel syndrome, active inflammatory bowel disease (), the early period after stomach surgery, and severe gastroparesis. In these situations high fiber can make symptoms worse, and changes should be made under a doctor's guidance.
References · 15
- Institute of Medicine. (2005). Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. National Academies Press. nap.nationalacademies.org/catalog/10490/dietary-reference-intakes-for-energy-carbohydrate-fiber-fat-fatty-acids-cholesterol-protein-and-amino-acids
- U.S. Department of Agriculture & U.S. Department of Health and Human Services. (2020). Dietary Guidelines for Americans, 2020-2025 (9th ed.). www.dietaryguidelines.gov/sites/default/files/2020-12/Dietary_Guidelines_for_Americans_2020-2025.pdf
- Hargreaves, M., & Spriet, L. L. (2020). Skeletal muscle energy metabolism during exercise. Nature Metabolism, 2(9), 817–828. 10.1038/s42255-020-0251-4
- Melkonian, E. A., Asuka, E., & Schury, M. P. (2023). Physiology, Gluconeogenesis. In StatPearls. StatPearls Publishing. www.ncbi.nlm.nih.gov/books/NBK541119
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