The response to Part 1 of this series has been quite positive, so I want to thank all of you who have provided feedback, whether positive or negative. I like to consider myself an open-minded learner, so I always welcome constructive criticism. However, I’m not open to those who want to chastise my writing simply because it doesn’t mesh with their preconceived bias. I’ve come to realize that people read what they want to read, hear what they want to hear, regardless of what is actually written or said.
Some immediately assumed my previous post was promoting a one-size-fits-all approach in which everyone should eat a high carb diet, and some even came to the conclusion that I just was trying to ‘stir the pot’; neither of which are justified. I do not feel like I should have to step back and defend my writing from nonsensical rebuttals, so I encourage you to read the entire post with an open mind (and open eyes). I never said everyone should eat a high carb diet, I never said everyone should eat gluten, and I never said anyone needs to eat ‘junk’ food.
What I did say is that demonizing one macronutrient is not productive, and that calories are the main determinant in weight gain and weight loss. If anyone has controlled evidence to the contrary, please drop it in the comment section.
With that out of the way, let’s get to the second post in this series, in which I will do my best to debunk three more common, damaging myths about dietary carbohydrates.
Myth #4: Carbohydrates Make You Hungry
Everyone is different. Everyone is satiated by different foods, and everyone is satisfied with different eating habits. For that reason, it is silly to make the blanket statement that “carbohydrates make you hungry”, which I hear time and time again.
The argument, in most cases, goes something like this: you eat carbohydrates (typically those of the high GI variety), your blood sugar rises rapidly, then falls rapidly, and BAM, you’re hit with ravenous hunger and cravings; which subsequently leads to weight gain due to overeating. While this may occur in individuals who have diabetes or severe insulin resistance, it doesn’t seem to be too common otherwise.
Hypoglycemia certainly causes hunger, but again, hunger-inducing hypoglycemia does not seem to occur frequently in non-diabetics. So while it does make sense that rapidly rising and falling blood glucose levels would cause hunger even in metabolically healthy individuals, there just doesn’t seem to be conclusive evidence to support this claim. There does, however, seem to be evidence that sugar intake has appetite regulatory effects (3, 4) which is contrary to the common belief that sugar stimulates hunger.
Another common argument is that the lower the GI, the more satiating and less likely to promote fat gain in comparison to high GI. However, this doesn’t seem to be supported by evidence either (6, 7, 8, 9, 10).
For a practical example, let’s look at the white potato. The white potato has a very high glycemic index, but it is one of the most satiating foods one can consume, based on “a satiety index of common foods” (1). You would think that the rapid rise and fall of blood glucose caused by eating a potato would cause ravenous hunger, but what seems logical doesn’t always play out in the research.
While we’re on the topic of blood glucose, it would make sense to discuss insulin spikes and their effects on hunger. It seems to be common knowledge that large insulin spikes cause hunger, but as with the glycemic index of foods, this does not play out in the research either. Quite the opposite, actually. A study done on women in 2012 showed that “postprandially administered intranasal insulin enhances the satiating effect of meals and reduces palatable snack intake, suggesting that insulin acts as a relevant signal in the short-term regulation of satiety in humans” (2). Whether the intranasal administration is relevant to a normal physiological insulin response post-meal remains to be seen, but it is definitely interesting.
A review paper in the British Journal of Nutrition (2007) concluded that insulin “may be an important satiety signal, and that central nervous system insulin resistance in overweight might explain the blunted effect on appetite” (5). And, as James Krieger discusses in his excellent series on insulin, large insulin spikes seem to be associated with appetite suppression, not appetite stimulation. So insulin in and of itself doesn’t seem to be an appetite stimulant, but resistance to the effects of insulin (which is common among overweight and obese individuals) does.
So as you can see, the evidence that carbohydrates (and insulin) are inherently able to stimulate appetite is shaky at best.
Context undoubtedly plays a huge role here. If 80% of the diet is made up of refined carbohydrates, you would probably end up hungrier than someone with a more balanced approach. Is that because of the large consumption of carbohydrates, or is it because of the lack of fiber, vitamins and minerals, dietary fat, and protein? I lean towards the latter. If the diet consists of adequate protein, adequate fat, adequate calories, adequate fiber, and adequate micronutrient composition, processed carbohydrates in moderation are probably not going to induce hunger to any noticeable degree.
Making blanket statements while ignoring context gets us nowhere.
Myth #5: Carbohydrates are Addictive
Fear-mongering is an all too common marketing ploy in today’s nutrition industry.
You hear things like “sugar is toxic” and “gluten is this generation’s tobacco”. Utter nonsense, but a lot of people believe it because the authors of such ridiculous assertions invoke emotion with descriptive words like ‘toxic’ and relating a food item to a chemical such as ‘tobacco’.
Another common claim is that carbohydrates are addictive, and in order to lose weight, we must break this insidious addiction.
Typically, when someone says carbohydrates are addictive, they’re referring to refined carbohydrates; so that’s precisely what I will focus on here (as a side note, anyone who says you should stop eating potatoes or fruit because they are ‘addictive’ should be disregarded completely, in my
Now let’s make this clear: ‘addictive’ is a serious description, and as of late, many have made associations between drugs and refined carbohydrates. Being clear about what food addiction actually entails is crucial, and I think Stephan Guyenet does a great job explaining the phenomenon below:
“In common parlance, if we really like a food, we’re motivated to get it, or we tend to eat more of it than we think we should, we often say we’re “addicted” to it. This is not quite accurate, but it does point toward an important truth. Clinical food addiction is a serious phenomenon, akin to drug or gambling addiction, that only affects a few percent of the population. Food is something we have to consume to survive, which makes it qualitatively different from drugs of abuse, although of course we don’t have to consume Slurpees.”
As a personal example, I love to eat ice cream. I will make adjustments to my diet and leave room for carbs and fat, just so I can have a bowl of ice cream every night. I will not, however, go bankrupt for ice cream. I will not alienate myself from friends and family for ice cream. I will not commit crimes or become violent for ice cream. That seems to be the difference between foods we like eating and highly-addictive drugs. Enjoying a food and being motivated to eat more of it is not an addiction, it’s a natural human desire.
Palatability seems to be the issue, more so than refined carbohydrates in isolation. You would be hard-pressed to find someone who can eat pounds of plain white potatoes, but slap some butter on them, and most people can plow their way through and still desire more afterwards. Does this mean potatoes and butter are bad in isolation? No. Does this mean potatoes and butter are bad when combined? No. But when they are combined, they are easy to overeat due to increased palatability. It is easiest to take a look at this issue from a common sense perspective: when the food tastes better (has a better mouth-feel, fits individual preference) it is more likely to be overeaten (you might be thinking: duh).
So placing the blame on refined carbohydrates as being addictive in isolation is misleading. Most of the time, the foods that are highly palatable are treats donuts, pastries, cupcakes, Twinkies, etc.; all of which are high in both sugar and fat, and lacking in fiber, water, and micronutrients. Placing the blame on one component or the other is misleading.
On the issue of sugar addiction: much of the research on sugar addiction is done on rats. While rat studies are great for forming tentative hypotheses, they are not enough to draw meaningful conclusions that are applicable to humans. The studies base their research on sugar activating the same ‘reward centers’ as drugs. This is quite interesting, however, it would make sense from an evolutionary perspective that humans are designed to seek out sweetness as breast milk is sweet, and glucose is the brain’s main fuel source. Sure, sugar may be highly rewarding. But so is sex. And so is bacon.
Even as someone who has suffered from a degree of binge eating disorder in the past, I can eat refined sugars in moderation. I used to restrict ice cream and other treats, only to go on a massive binge a week or two later, leaving my progress in the ruins. Now, with a more moderate approach, I don’t feel restricted so I never binge. You may be different. You may need a more cut and dry approach, and that’s fine as well, as long as it works for you and you’re not miserable. Rigid dietary commandments seem to be tough to sustain over the long term, but if you’re one who does well with extremes, more power to you.
The sensationalism surrounding the supposed addictive qualities of refined carbohydrates is unsubstantiated at this point in time (11). Sure, refined carbohydrates have certainly played a role in the obesity epidemic. But so have poor lifestyle habits (not enough sleep), excess stress, lack of exercise, the increased consumption of artificial oils, as well as, of course, the increase in overall calorie intake.
I was lucky enough to read Joy Victoria’s article published yesterday titled “Your Problem With Sugar is THE Problem With Sugar“. Essentially, she points out that sugars (and carbohydrates) are not the lone bad guys, and they should not shoulder most of the blame. Give it a read with an open mind. It’s certainly easier to place the blame on one factor, but it’s certainly not right.
Myth #6: Carbohydrates Cause Insulin Resistance
Carbohydrates -> blood glucose spike -> insulin secretion -> chronic hyperinsulinemia -> insulin resistance.
Damn, I wish it was that simple. The reality is that insulin resistance, like all diseased states, is multi-factorial and extremely complex.
First, let’s look at what insulin resistance actually is. For that, I will defer to Stephan Guyenet yet again (yes, I quote his work ad nauseum, he does a great job interpreting the evidence). Stephan believes that insulin resistance is a result of “cellular energy excess”. Read his explanation below:
“…it appears to be a ‘deliberate’ process– cells activate specific signaling pathways that down-regulate insulin responsiveness. The rationale for this becomes clear when one considers what insulin does: it drives energy into cells. Insulin resistance is how the cell says “stop sending me more energy– I have too much already!” It is a deliberate response to mitigate the negative effects of cellular energy excess.”
So insulin resistance is an attempt to reject energy, as excess energy is toxic to the cell.
There seems to be evidence that greater energy intake (and consequently higher body fat levels) plays a causal role in the development of insulin resistance (15) . More specifically, visceral body fat accumulation seems to be a major contributing factor.
Also, another major cause of insulin resistance is chronically high levels of free fatty acids in the blood (12, 13). High FFA’s inhibit insulin-stimulated glucose oxidation, and lowering FFA’s restores glucose tolerance and insulin sensitivity (14). The state of chronically elevated FFA’s seems to be synonymous with stress as well, as the catecholamines and cortisol (stress hormones) play a large role in mobilizing body fat (therefore elevating FFA’s in the bloodstream) and raising blood glucose via gluconeogenesis respectively.
So, it seems that the best preventative measure is to avoid gaining excess body fat, specifically visceral body fat. Imposing a caloric deficit and losing body fat seems to be more important than the overall composition of the diet. As long as body fat is lost, insulin sensitivity is improved (16).
Could carbs play a role in developing pathological insulin resistance? Sure, if they contribute to a chronic excess of energy. But again, looking at carbohydrates in isolation ignores the big picture. Ensuring proper lifestyle habits (adequate sleep, minimal “stress”), eating to meet energy requirements, exercising (which improves insulin sensitivity), and consuming an overall balanced diet would seem to be the most logical way to avoid developing insulin resistance.
I’ll reiterate: insulin resistance is an extremely complex issue, so it’s difficult to fathom how someone could come up with one cause. As I mentioned above, there are a variety of factors that play an enormous role, and even that is an extremely shortened list.
There are several examples of cultures that thrive on a high carbohydrate diet without suffering from rampant insulin resistance, obesity, and diabetes. Of course, they aren’t exposed to silly amounts of refined oils, inhuman amounts of soft drinks, and the chronic stress associated with “living the American dream”. Maybe we should start living the Kitavan dream, and just chill the ‘F’ out.
One-size-fits-all avoidance of one macronutrient is not conducive to health and weight improvement on a macro level. Specific, individualize approaches to weight and metabolic management should be taken to ensure that dietary practices jive with the individual’s needs and preferences. Yes, some will be able to handle carbohydrate more effectively than others. But the reality is that if you cannot ‘handle’ carbohydrates, there is an underlying metabolic issue that needs to be addressed.
Understand that I’m not recommending that everyone eat a high carb diet containing as much sugar as they please. I’m simply asking that attention be paid to the objective evidence, and recommendations be made based on individual differences.
If you have any questions, comments, concerns, or feedback, feel free to drop a comment below. I accept all comments, no matter the viewpoint, as long as they are relatively civil of course. So please voice your opinion on this issue. I’m open for debate, and I’m open to hear both sides of the argument as that’s where the most learning takes place.
Have an awesome day.
*Special thanks go out to Stephan Guyenet for his interpretations and extensive research on these topics.
1. Holt SH, Brand-Miller JC, Petocz P, Farmakalidis E. A satiety index of common foods. Eur J Clin Nutr 1995;49:675–90.
2. Hallschmid M, Higgs S, Thienel M, Ott V, Lehnert H. Postprandial administration of intranasal insulin intensifies satiety and reduces intake of palatable snacks in women. Diabetes 2012;61:782–789
3. Anderson GH, Woodend D. Consumption of sugars and the regulation of short-term satiety and food intake. Am J Clin Nutr. 2003;78:S843–9.
4. Anderson GH. Sugars, sweetness and food intake. Am J Clin Nutr. 1995;62 Suppl:S195–201.
5. Flint, A., Gregersen, N. T., Gluud, L. L., Møller, B. K., Raben, A., Tetens, I., et al. (2007). Associations Between Postprandial Insulin And Blood Glucose Responses, Appetite Sensations And Energy Intake In Normal Weight And Overweight Individuals: A Meta-analysis Of Test Meal Studies. British Journal of Nutrition, 98(01), 17.
6. Aston, L. M., Stokes, C. S., & Jebb, S. A. (2007). No Effect Of A Diet With A Reduced Glycaemic Index On Satiety, Energy Intake And Body Weight In Overweight And Obese Women.International Journal of Obesity, 32(1), 160-165.
7. McMillan-Price, J. (2006). Comparison Of 4 Diets Of Varying Glycemic Load On Weight Loss And Cardiovascular Risk Reduction In Overweight And Obese Young Adults: A Randomized Controlled Trial. Archives of Internal Medicine,166(14), 1466-1475.
8. Sichieri R, Moura AS, Genelhu V, Hu F, Willett WC. An 18-mo randomized trial of a low-glycemic-index diet and weight change in Brazilian women. Am J Clin Nutr. 2007;86:707–13.
9. Wolever TM, Mehling C. Long-term effect of varying the source or amount of dietary carbohydrate on postprandial plasma glucose, insulin, triacylglycerol, and free fatty acid concentrations in subjects with impaired glucose tolerance. Am J Clin Nutr 2003;77:612–21.
10. Jebb, S. A., Lovegrove, J. A., Griffin, B. A., Frost, G. S., Moore, C. S., Chatfield, M. D., et al. (2010). Effect Of Changing The Amount And Type Of Fat And Carbohydrate On Insulin Sensitivity And Cardiovascular Risk: The RISCK (Reading, Imperial, Surrey, Cambridge, And Kings) Trial. American Journal of Clinical Nutrition, 92(4), 748-758.
11. Benton, D. (2010). The Plausibility Of Sugar Addiction And Its Role In Obesity And Eating Disorders. Clinical Nutrition,29(3), 288-303.
12. Ferrannini, E., Barrett, E. J., Bevilacqua, S., & DeFronzo, R. A. (1983). Effect Of Fatty Acids On Glucose Production And Utilization In Man.. Journal of Clinical Investigation, 72(5), 1737-1747.
13. Boden, G., Jadali, F., White, J., Liang, Y., Mozzoli, M., Chen, X., et al. (1991). Effects Of Fat On Insulin-stimulated Carbohydrate Metabolism In Normal Men.. Journal of Clinical Investigation,88(3), 960-966.
14. Santomauro ATMG, Boden G, Silva MER, Rocha DM, Santos RF, Ursich MJM, Strassman PG, Wajchenberg BL 1999 Overnight lowering of free fatty acids with acipimox improves insulin resistance and glucose tolerance in obese diabetic and non-diabetic subjects. Diabetes 48:1836–1841
15. Tam, C. S., Viardot, A., Clement, K., Tordjman, J., Tonks, K., Greenfield, J. R., et al. (2010). Short-Term Overfeeding May Induce Peripheral Insulin Resistance Without Altering Subcutaneous Adipose Tissue Macrophages In Humans.Diabetes, 59(9), 2164-2170.
16. Goodpaster BH, Kelley DE, Wing RR, Meier A, Thaete FL (1999) Effects of weight loss on regional fat distribution and insulin sensitivity in obesity. Diabetes 48:839–847