Why are some people “carboholics”?

In a recent editorial in the New York Times titled “Are You a Carboholic? Why Cutting Carbs Is So Tough”, Gary Taubes describes a phenomenon that is familiar to many of us (1):

The holidays and family vacations are a particular problem. Desserts and sweets, it seems, will appear after every lunch and dinner, and I’m not particularly good at saying no when everyone else is partaking. The more sweets I eat, the more we eat as a family, the longer it takes upon returning home before that expectation of a daily treat fades away.

What I’ve realized is that eating a little of a tasty dessert or a little pasta or bread fails to satisfy me. Rather it ignites a fierce craving for more, to eat it all and then some. I find it easier to avoid sugar, grains and starches entirely, rather than to try to eat them in moderation.

Like Taubes, I have a hard time controlling my intake of certain foods when they’re in front of me, and occasionally, I may continue to think about them for days after I eat them (chocolate-covered ice cream bars, I’m looking at you).  Taubes goes on to provide his explanation: these foods elevate insulin levels, and that in turn increases cravings for carbohydrate-rich foods.  Par for the course, he provides no evidence for this model other than a few quotes from Drs. Robert Lustig and David Ludwig, which are nothing more than personal speculation.  I’m not aware of any research suggesting that high circulating insulin levels promote cravings for carbohydrate, sugar, or dessert foods, and I’m fairly certain those data don’t exist.

What Taubes may not be aware of is that there is no need to propose a speculative new explanation for why we crave desserts, because researchers have already provided an explanation that’s quite compelling.  And it doesn’t involve insulin.

It starts with drugs

To understand why we crave food, sex, gambling, winning, catching fish, driving fast cars, playing video games, and everything else we crave in our lives, it’s helpful to start with drugs of abuse.  This is because the way in which drugs create cravings is very simple, and we can consider it without burdening ourselves with all of our preconceived notions and feelings about food.

Habit-forming drugs, including drugs of abuse, are habit-forming because they stimulate the dopamine signaling pathway in the brain (2)*.  This pathway determines your gut level of motivation for things– what we often call a craving.  It evolved to motivate us to get food, water, sex, shelter, social status, and other things that were important for the reproductive success of our distant ancestors.  So when a drug increases the level of dopamine in key structures of your brain, you will become more motivated to take the drug– you will crave it.  This is called reinforcement.

Some drugs, like amphetamine and injected or smoked (crack) cocaine, are very good at increasing dopamine levels in the brain (3).  This means they are also very good at increasing your motivation to take them.  If you take the drug repeatedly and your level of motivation/craving crosses a certain threshold, your brain begins to implicitly prioritize drug-seeking behaviors over constructive behaviors like keeping a job and obeying the law.  We call that addiction.

When a person with an addiction doesn’t use a drug for a long time, his craving for it will slowly subside.  This is why a person who quits smoking will initially feel very strong cravings, but these will diminish to a low level over a period of months to years.  Yet when that person exposes himself to the drug again, or cues associated with it– for example, by taking a puff of a cigarette– it often re-awakens those latent brain pathways and triggers a relapse into addictive behavior (4).  This can leave a person struggling with strong cravings once again.  Note that this abstinence -> cue -> relapse cycle is precisely what Taubes describes in his article, only for sweets instead of cigarettes.

Drug reinforcement and relapse behavior, of course, are not mediated by insulin.  The drug goes straight to the brain and spikes dopamine– there is no pit stop in the pancreas.  High background levels of circulating insulin are not known to exacerbate addictive behavior.  I don’t think anyone believes that cravings and addictions to alcohol, gambling, sex, or video games are due to elevated insulin levels.  Is food reinforcement the one exception?

Nope

We actually have a pretty good idea of how food reinforcement works, thanks in large part to the research of Anthony Sclafani, which I describe in more detail in my book.  As with drugs, food reinforcement works by spiking dopamine in the brain, a fact that Taubes has come around to (5).  The question is, how does food increase dopamine levels in the brain?

Research by Sclafani and others shows that food reinforcement primarily occurs when the upper small intestine detects carbohydrate, fat, and protein, causing a spike in brain dopamine levels (taste receptors in the mouth that detect sugars also contribute, to a lesser extent)** (6, 6b).  Researchers can also spike brain dopamine and cause reinforcement by injecting glucose into the liver’s portal vein, but this finding has not been consistently replicated (7, 8).  After performing multiple experiments and reviewing the evidence on the role of insulin in reinforcement, Sclafani’s group concluded that “these data do not suggest a primary role for insulin in glucose-based [reinforcement]” (9).  Part of the reason why they came to this conclusion is evidence suggesting that “insulin may act in the brain to reduce sweet taste signaling and sugar activation of brain reward systems” (emphasis mine)(10, 11).

Furthermore, if insulin is responsible for spiking dopamine and ultimately food reinforcement, then dietary fat shouldn’t have the same effect because it causes less insulin release.  Yet fat is highly reinforcing– a key fact that Taubes neglects to share with readers (12, 13, 14).

Essentially, the brain is wired to be motivated by the food properties that kept our distant ancestors alive and fertile***.  When you eat food, the brain analyzes its composition via receptors in your mouth, upper small intestine, and perhaps liver that measure the amount of fat, sugar, starch, protein, and salt it contains.  This all happens on a nonconscious level.  If the brain “likes” what you just ate, it will release dopamine.  The more fat, sugar, starch, protein, and salt your food contains (up to the “bliss point”), the more dopamine your brain releases.  The more dopamine your brain releases, the more your cravings increase.  This is why we crave cookies and bacon but not lentils and plain celery.

Foods that are skillful combinations of fat, sugar, starch, salt, and delightful flavors likely cause your brain to release high levels of dopamine, sometimes provoking addiction in susceptible people.  And when a person excludes a problem food for a long time, then suddenly has it in front of them at the dinner table, those latent craving pathways are reactivated– just as they are for drugs.  No insulin required.

I’m not aware of any evidence that insulin is involved in this process, or that chronically high insulin levels accentuate it, and available evidence suggests that insulin is probably not involved.  Why propose this unsupported mechanism when we already have an evidence-based mechanism that makes far more sense?

What about fatoholics?

Taubes’s story breaks down further when we consider that many of the most common food cravings aren’t for sweet foods.  Rob Markus and colleagues recently published a paper in which they identified the food types that are most commonly associated with addiction-like behavior (15).  Here’s what they found:

The majority of respondents experienced these problems for combined high-fat savoury (30%) and high-fat sweet (25%) foods, whereas only a minority experienced such problems for low-fat/savoury (2%) and mainly sugar-containing foods (5%). Overweight correlated only with addictive-like problems for high-fat savoury and high-fat sweet foods (P < 0.0001), while this was not found for foods mainly containing sugar.

Wait, what?  The primary foods that trigger addiction-like behaviors are “high-fat savory” foods that aren’t even sweet?  And only one person out of twenty reported addiction-like behavior for “mainly sugar-containing” foods?  It appears that fatoholics are more common than carboholics.

This lines up with my personal experience, and I suspect, the experience of most readers.  I don’t know about you, but to me, hard candy just isn’t that appealing.  I have no desire to eat fat-free frozen yogurt.  Candy corn and Tootsie Rolls are barely better than starvation.  Throw some fat into the mix, as in chocolate, ice cream, or brownies, and now you’re talking!  Savory foods like potato chips, bacon, pizza, and ribs are also high on my list.  Taubes doesn’t mention that the “desserts and sweets” that provoke his addiction-like behavior are probably also high in fat, tacitly assuming that only the sugar is relevant.

One thing that’s clear from reading Markus’s study is that different people find different foods “addictive”.  Most people have a hard time controlling their eating behavior around certain high-fat savory and/or high-fat sweet foods.  Yet a small minority have a hard time with low-fat savory foods like pasta or low-fat sweet foods like hard candy.

We’re all built differently, and we each have our own problem foods that drive us to overeat.  It’s entirely possible that Taubes is wired to have an unusually strong reinforcement response to foods like bread, pasta, and fatty sweet desserts that are typical on American dinner tables, but not to high-fat savory foods.  To him, the common denominator may seem like it’s carbohydrate, which is why the insulin explanation is so irresistible that even a total lack of evidence cannot restrain him from it.

So why are some people carboholics and fatoholics?

The reason is simple.  The human brain is hard-wired to be motivated by calorie-dense foods rich in fat, sugar, starch, protein, and salt, because these things kept our distant ancestors alive and fertile in a difficult world.  In the modern world, the food industry and home cooks are better at pushing our brain’s reinforcement buttons than ever before in history.  Our distant ancestors didn’t have ice cream or pizza, and the brains we inherited from them may not be designed to constructively handle that kind of powerful reinforcement stimulus.  We’re so good at pushing our own buttons that some of our modern foods probably provoke very high levels of dopamine release in the brain.  Like drugs of abuse, those high levels of dopamine make us crave in ways that don’t always support our health– and sometimes lead to addiction.  That’s why we crave dessert.

Due to individual differences in how we’re wired, some of us become “carboholics”, others become “fatoholics”, others become both, and still others become neither.  We have much work to do before understanding these individual differences.  Yet regardless of whether or not we have addiction-like eating behaviors, nearly all of us eat too much when we encounter foods that are highly reinforcing.

Postscript

I’m not surprised Taubes wrote this article, but I am surprised the New York Times published it.  It might seem like fun and games to publish provocative speculation written by people who seem incapable of doing a Google Scholar search, but pieces like this can harm the public understanding of health science, with potentially serious consequences.  How hard is it to run a piece like this by a few experts– people who are truly knowledgeable about the subject?  Here are names: Anthony Sclafani, Karen Ackroff, Leann Birch, Roy Wise, Paul Kenny, Nora Volkow, Hisham Ziauddeen, Leonard Epstein, Jennifer Temple, Ashley Gearhardt, Stephen Benoit, Dianne Figlewicz, and Kent Berridge.  As a reader and a scientist, can I please see some quality control?

 

* Typically by increasing dopamine levels, but also sometimes by acting on the same downstream pathway dopamine activates.  For example, caffeine blocks the adenosine receptor, which increases dopamine’s action on downstream reward pathways.

** We don’t know what mechanism gets the signal from the intestine to the brain yet.  Sclafani and Gary Schwartz found that cutting the nerves connecting to the small intestine doesn’t block reinforcement, suggesting that the signal may not be carried directly by nerves to the brain.  Instead, it may be a factor released by the intestine into the bloodstream, but that remains to be demonstrated.  This is a very important mechanism to understand because it’s so relevant to obesity.  I suspect it won’t be too long before we get a toehold on it.

*** Sugar was obviously not the only nutrient that kept our distant ancestors alive, and from an engineering standpoint it would make no sense to design a system that is only motivated by sugar.  That’s why our brains are strongly motivated by all concentrated sources of calories– including sugar.

67 Responses to Why are some people “carboholics”?

  1. Interesting how anything Gary Taubes writes can also stimulate the dopamine-signaling pathways in some who are addicted to either refuting or praising him. As an RSS subscriber to your blog posts, I’m even beginning to think that I’m in danger of getting caught up in this thing.

    • Haha, good point. I do focus on his writing a lot. But there’s a reason for it. 1) He writes about things I know about. 2) He’s good at convincing people of things that are wrong. 3) He gets a massive platform from the popular press so his writing influences many people.

      I’m one of the few people who has the ability to stand up to him effectively, and a number of my scientific colleagues have asked me to do so.

  2. Great article. I read the your book but still nice review. No need to post this comment. Just wanted to point out typo…

    ** signal may not be carried, is missing “be”

  3. Thank you for writing Stephan. You have a wonderful ability to communicate complex ideas in a simplified manner that retain the integrity of the research you discuss. You are a true expert on these topics and the world is better for you sharing your knowledge.

    In health,

    Someone who hopes to be as influential as you one day.

  4. This is a great article… I’d like to send it to my friend, who is a low-carb fanatic. He wouldn’t read it though. It is hard to get through to someone when theory has become ideology. Confirmation bias is strong.

    Our group of friends went to have ice cream and mr low carb wouldn’t have any. So he was in a pretty bad mood, just sitting there like a lemon, while we were having a nice time. After a while he burst out, “I can’t hang out with you guys when you are all hopped up on sugar like this. I guess you really can’t see it yourselves but you are totally high and annoying, why you would do this to yourselves is beyond me”. Then he stormed off, huffing. It was a little bit funny, but also pretty sad.

  5. Stephan, opiate addiction is probably due to oxidative stress. See this paper
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3871421/

    “Importantly, inactivation of NOS by inhibitors or inhibition of nitration and inactivation of MnSOD prevented the development of morphine-induced antinociceptive tolerance [65, 66]. Consistently, morphine was not able to induce antinociceptive tolerance in NOS-deficient mice [67].”

    High fat diets and refined carbs cause oxidative stress, and the hypothalamic satiety system is very sensitive to oxidative stress because it uses ROS to signal satiety.

    So this is not just a question of fat and carbs causing dopamine release, it’s also a question of brain damage, which is increasingly considered to be the cause of obesity.

    So you are right about Taubes and insulin, obviously, but you don’t have the whole story.

    Taubes thinks insulin inhibits satiety neurons, or at least his friend Lustig does. It has now been shown that insulin does not inhibit them, it activates them as expected, and the confusion arose because insulin preparations are contaminated with zinc, which inhibits them.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4183666/

    • Hi Jane,

      Opiates are addictive because they stimulate the dopamine pathway. We know this because blocking dopamine signaling blocks the reinforcing actions of heroin, for example.
      http://www.sciencedirect.com/science/article/pii/0024320581905191
      http://www.jneurosci.org/content/12/2/483.short

      Thanks for the insulin/zinc paper, I hadn’t seen it and it is interesting. I wonder if that accounts for the spotty reproducibility of the effect of icv insulin on food intake and body weight?

      • Hi Stephan

        Yes opiates are addictive because they stimulate the dopamine pathway. I’m talking about what happens downstream of the receptor, and oxidative stress is one of the things that happens. Pleae read the paper I linked, I think you will find it interesting in light of the oxidative stress and/or damage caused by the ‘addictive’ foods and high fat diets.

        Glad you liked the insulin/zinc paper. I did too. Yes I do wonder what else it might explain.

        • Here’s an abstract about what sugar does to mu-opioid receptors, which are the ones that cause oxidative stress, potentially in dopamine neurons.

          https://www.ncbi.nlm.nih.gov/pubmed/11733709
          “Palatable food stimulates neural systems implicated in drug dependence; thus sugar might have effects like a drug of abuse. Rats were given 25% glucose solution with chow for 12 h followed by 12 h of food deprivation each day. They doubled their glucose intake in 10 days and developed a pattern of excessive intake in the first hour of daily access. After 30 days, receptor binding was compared to chow-fed controls. Dopamine D-1 receptor binding increased significantly in the accumbens core and shell. In contrast, D-2 binding decreased in the dorsal striatum. Binding to dopamine transporter increased in the midbrain. Opioid mu-1 receptor binding increased significantly in the cingulate cortex, hippocampus, locus coeruleus and accumbens shell. Thus, intermittent, excessive sugar intake sensitized D-1 and mu-1 receptors much like some drugs of abuse.”

          What this suggests, to me anyway, is that the reason sugar can appear addictive is because white sugar doesn’t have the manganese it should have, to keep MnSOD active. Mu-opioid receptors cause oxidative stress (and addiction, apparently) by inactivating MnSOD, according to the paper I quoted earlier. The dopamine system is very dependent on manganese, as demonstrated by this paper showing that it can prevent experimental Parkinsonism.
          https://www.ncbi.nlm.nih.gov/pubmed/9681949

          • I have never heard of any evidence that specific foods must be accompanied by their own essential nutrients (minerals or vitamins) at the time of consumption (which is what you seemed to be describing). Mn can be found in a variety of ordinary foods to maintain the range of bodily levels adequate to meet physiologic needs for the mineral.

          • @David Stone

            Thank you for your comment.

            The average manganese intake in the US is 2 mg/day. Surprisingly, the RDA is also 2 mg/day. According to the Linus Pauling Institute, it was decided on the basis of no evidence that the average intake was enough. It might be enough in a low-iron diet, but the western diet is very high in iron.

            Manganese deficiency is implicated in diabetes, and the Ma Pi diet which apparently cures diabetes has 16 mg/day of manganese. This is 8 times more than the RDA.
            https://www.ncbi.nlm.nih.gov/pubmed/22247543

            Iron overload is also implicated in diabetes, as it is in many other diseases, for example Alzheimer’s (see below) in which excess iron is found in damaged parts of the brain. The iron-manganese ratio in the Ma Pi diet is around 1, while the ratio in the averge American diet is 10. Yes, 10 times higher.

            Free iron causes oxidative stress, and manganese prevents it.

            Battles With Iron: Manganese in Oxidative Stress Protection (2012)
            https://www.ncbi.nlm.nih.gov/pubmed/22247543
            The redox-active metal manganese plays a key role in cellular adaptation to oxidative stress. As a cofactor for manganese superoxide dismutase or through formation of non-proteinaceous manganese antioxidants, this metal can combat oxidative damage without deleterious side effects of Fenton chemistry. In either case, the antioxidant properties of manganese are vulnerable to iron. …

            Alsheimer’s disease is a very interesting case because a key role has been found for an enzyme called PP2A, which regulates autophagy and breaks down the protein aggregates found in Alzheimer brain. PP2A is a manganese enzyme.

            PP2A Blockade Inhibits Autophagy and Causes Intraneuronal Accumulation of Ubiquitinated Proteins (2013)
            https://www.ncbi.nlm.nih.gov/pubmed/22892312
            Using cultured cortical neurons, we show that the blockade of protein phosphatase 2A (PP2A), either pharmacologically by okadaic acid or by short hairpin RNA (shRNA)-mediated silencing of PP2A catalytic subunit, inhibited basal autophagy and autophagy induced in several experimental settings … Conversely, PP2A upregulation by PP2A catalytic subunit overexpression stimulates neuronal autophagy. … These data are important to human neurodegenerative diseases, especially Alzheimer’s disease, because they provide links for the first time between the pathological features of Alzheimer’s disease: PP2A downregulation, autophagy disruption, and protein aggregation.

          • Correction: “The iron-manganese ratio in the Ma Pi diet is around 1, while the ratio in the averge American diet is 10. Yes, 10 times higher.”

            The iron-manganese ratio in the Ma Pi diet is 1.5, which means my last sentence should read ‘7 times higher’ not ’10 times higher’.

          • Interesting this stuff on manganese. But couldn´t other antioxidants such as those found in fruits, vegetables and legumes – including dark chocolate – play a similar role? Or zinc or copper?

            I am wondering why the rate of diabetes, pre diabetes and non alcholic fatty liver disease is as high in China as in the US, despite a per capita sugar intake of just 16 grams vs 126 grams in the US (according to a 2015 estimate), and a BMI below 25 vs almost 30 in the US.

            We also know that Sumo wrestlers despite being sometimes morbidly obese with BMI above 35, have much lower (maybe half) rate of diabetes as the average Chinese. Besides being more physically active, a major difference is that the Sumo wrestlers as a percentage of energy eat less fat but perhaps 50% more protein (on average). They also obtain more iron due to higher meat intake. Animal foods provides almost no manganese, but white rice can supply sometimes a lot, maybe 2-5 mg or more on the average Chinese diet (http://nutritiondata.self.com/facts/cereal-grains-and-pasta/10641/2).

            It has been suggested that high protein intake can effectively remove liver fat. So perhaps it is needed to «transport» an excess of calories to the right places, so it´s not stored in liver, around organs etc – presumably a cause of diabetes. But choline and betaine may also be helpful and help «spare» protein for this purpose (see for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806659/).

            In many of these countries (such as India or China) with high rate of diabetes yet BMI within the normal range, intake of betaine may be low, as rice is more or less deficient in this nutrient. Wheat and other gluten grains, for comparison, are decent sources. Quinoa seems to supply the most, a whopping 630 mg/100 gram dry weight, 5x more than the whole rye and 10x more than whole wheat according to http://nutritiondata.self.com/foods-000145000000000000000-w.html. Additionally quinoa has more protein (and of better quality), and more choline than wheat, while wheat has more protein than rice. Whole grains have more betaine then refined grains, and modern varieties likely less than those available 50 years ago. I read somewhere that spelt supplies 3x more betaine than regular wheat.

            Although I haven´t checked the data very much, it seems that in some of these countries like Bolivia and Peru who eat a fair amount of quinoa, the diabetes rate is lower than for example China despite a 5 fold higher sucrose intake and a vastly higher BMI. This was also indicated here: http://wholehealthsource.blogspot.com/2010/10/potatoes-and-human-health-part-iii.html ; Despite a relatively high BMI of 24.5, the rate of diabetes and pre-diabetes was surprisingly low among the Aymara people. I wonder if the quinoa played a role in this.

          • Hi Guiseppe

            Thanks for that betaine paper, I didn’t know betaine activates transcription of the PPARalpha gene and it’s very interesting indeed. I’ve been wondering about this for years. It looks like betaine inhibits PPARalpha gene methylation independently of its normal role in the methylation pathway. So now we have betaine -> PPARalpha -> FGF21 -> all kinds of goodies like fat oxidation and browning of white fat.

            I’m not sure about the Sumo wrestlers and protein. I looked it up and found that protein might under some circumstances make fatty liver worse.
            http://time.com/4758402/protein-fatty-liver-disease/

            So I’m wondering whether it might be the reduced fat. A recent study showed that a high fat diet causes iron overload in the liver.
            https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315491/

            Iron overload apparently causes fatty liver disease, and involves copper deficiency because copper is needed to get the iron out.
            https://www.ncbi.nlm.nih.gov/pubmed/18505688

            If iron overload causes fatty liver, perhaps it might also cause fatty pancreas? Very interesting what you say about quinoa, betaine and diabetes.

          • Hi Jane,

            Thanks for the comment!

            I am also a bit uncertain about the protein vs fatty liver after reading the Time article you mentioned (and to be honest, as a layman don´t understand so much of all of this).

            Was thinking about this article looking at old research suggesting that when protein intake was 20E% (casein), fatty liver didn´t develop, but did so in a massive way on 5% protein, however not if large quantities of choline was added. https://chrismasterjohnphd.com/2010/11/23/sweet-truth-about-liver-and-egg-yolks/

            I estimated the average protein intake among Sumo wrestlers was 20E%, but it seems to vary a lot. In the Chinese population it may be around 12-14E%.

            And studies like these:

            Fatty liver
            http://www.gastrojournal.org/article/S0016-5085(16)35229-5/abstract
            https://www.ncbi.nlm.nih.gov/pubmed/23414424

            Reversal of diabetes
            https://www.ncbi.nlm.nih.gov/pubmed/17583796
            https://www.ncbi.nlm.nih.gov/pubmed/6373464 (1200 kcal, and a whopping 52E% protein, mostly from meats meaning enormous quantities of iron)

            Also consider this study (from 2016):

            Higher Dietary Choline and Betaine Intakes Are Associated with Better Body Composition in the Adult Population of Newfoundland, Canada

            «Significantly inverse correlations were found between dietary choline and betaine intakes, with all obesity measurements: total percent body fat (%BF), percent trunk fat (%TF), percent android fat (%AF), percent gynoid fat (%GF) and anthropometrics: weight, body mass index, waist circumference, waist-to-hip ratio in both women and men (r range from -0.13 to -0.47 for choline and -0.09 to -0.26 for betaine, p<0.001 for all). Dietary choline intake had stronger association than betaine. Moreover, obese subjects had the lowest dietary choline and betaine intakes, with overweight subjects in the middle, and normal weight subjects consumed the highest dietary choline and betaine (p<0.001). Vice versa, when subjects were ranked according to dietary choline and betaine intakes, subjects with the highest intake of both had the lowest %TF, %AF, %GF, %BF and highest %LM among the groups in both sexes.»

            http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0155403

            In practice I think high choline intake typically reflects a high intake of eggs, meat and milk/yogurt (but not cheese).

          • Thanks Guiseppe, those papers were very helpful. The conclusion seems to be that high protein diets work because certain amino acids activate mitochondrial biogenesis. That makes perfect sense.

            On the other hand a recent study, discussed by Stephan here http://blog.dansplan.com/is-high-protein-actually-bad-during-weight-loss/
            showed that high protein diets can cause oxidative stress. So under different circumstances such diets could be good or bad for fatty liver.

          • In regards to the study you mentioned where one group obtained 54 grams of protein, and the other the same plus 27 grams from whey bars (total 81 grams of protein), I think it should be considered that whey has a lot of bio-active compounds which may make it work differently than other proteins, such as from meat. This could alter the results.

            In the study I linked, where one group ate a mediterranean type diet with 89 gram protein, and the other a «paleo diet» – in practice the mediterranean diet minus whole grains and dairy – with 90 grams of protein, the «paleo» group saw a 26% decline and normalization of blood glucose, compared to just 7% decline in the mediterranean groups. This was independently of weight loss and change in waist circumference.

            My thinking anyway, is that choline and/or betaine can act to «spare» protein (as can high potassium low phosphorus foods like fruits, vegetables, and potatoes/tubers). And so it is possible that under certain circumstances our protein requirement could be very low. It has been shown that feeding only potatoes for 6 months didn´t result in protein loss/deficiency for example, even when half the calories came from butter/lard, and many people lose weight effectively by eating only potatoes. Another example would be human milk which supplies just 6% protein, but also 500 mg choline per 2000 kcal (it also has a high potassium/phosphorus ratio). Human milk is notoriously low in nutrients, and supplies typically just 30-50% of the RDA for most vitamins and minerals. But it nevertheless supplies about 50% more choline than what´s found in the diet of the average person. And so it´s possible that most people are severely deficient in choline and that the RDA is set too low. Eating whole grains and especially breakfast cereals made with whole wheat bran, can probably compensate for this to some extent however, via the betaine, as can eating leafy greens like spinach which are high in both folate and betaine (leafy green consumption seems to lower risk of diabetes too).

            As a side note, it´s possible that the reason folic acid has some beneficial effects for pregnant women is really related to their low choline intake, and that it like betaine can partially compensate for this. I think the average intake of folic acid is already approx 500 mcg, and yet they are often recommended to take 400 mcg on top of this. 2000 kcal human milk provides just 150 mcg folate. For comparison the average intake of choline among US women is just 250-300 mg. I noticed the recommendation for dogs is about 1350 mg choline and 200 mcg folic acid per kg feed, indicating that choline is the more important nutrient. It may be that our choline intake declined after the «cholesterol hypothesis» so that people started to eat less eggs and egg yolks. Additionally we eat much less organ meats such as brains and kidneys nowadays (which alone can supply 200-400 mg choline/100 gram). And in the past it was not uncommon to make ice cream with large quantities of egg yolks, see for example this recipe from 1901 http://www.vintagerecipes.net/books/century_cook_book/french_icecream_1.php, or add «bernaise sauce» composed mostly of egg yolks to the steak, or have the steak tartar with egg yolks on top etc. I think it´s possible that the low intake of choline has contributed not only to the fatty liver and obesity epidemic, but also organ dysfunction, as well as the mentioned birth defects.

          • Copper is interesting. I´ll look more into it when I get the time. Thanks again for your comments.

          • In regard to the interesting post by Guiseppe about betaine, I note that the top 4 foods (quinoa, spinach, lambquarters, beets) belong to the chenopodiaceae family. Alas, my favorite chenopodiacea and favorite potherb, chard, is the exception and has very little. Amaranth leaves and grain content is not reported on nutritiondata.

          • Thanks for your comments too, Guiseppe. Very helpful.

            Yes copper is interesting and it just got a whole lot more interesting. We now know that copper is needed for lipolysis in fat cells. This suggests it’s copper deficiency that prevents lipolysis, not insulin! Yet another nail in Taubes’ coffin.

            Copper is Key in Burning Fat
            https://www.sciencedaily.com/releases/2016/06/160606200439.htm
            For the first time copper’s role in fat metabolism has been established by research, further burnishing the metal’s reputation as an essential nutrient for human physiology. …
            “We find that copper is essential for breaking down fat cells so that they can be used for energy,” said Chang. “It acts as a regulator. The more copper there is, the more the fat is broken down. We think it would be worthwhile to study whether a deficiency in this nutrient could be linked to obesity and obesity-related diseases.” …

          • But copper has to be intaken within a certain ratio with zinc, right? Specifically about 10 parts of zinc per part of copper. so where are we going if we follow this rabbit hole? Lots of liver together with lots of oysters?

          • I think the optimal ratio is probably closer to 5 than 10. There is a lot of hype about zinc deficiency and I suspect it doesn’t really exist, at least in the west. Zinc deficiency causes anorexia and the problem today is not anorexia but obesity.

            I’m not sure about the need to eat liver or oysters. I don’t eat them but I don’t eat refined carbs either.

  6. “This lines up with my personal experience, and I suspect, the experience of most readers. I don’t know about you, but to me, hard candy just isn’t that appealing. I have no desire to eat fat-free frozen yogurt. Candy corn and Tootsie Rolls are barely better than starvation. Throw some fat into the mix, as in chocolate, ice cream, or brownies, and now you’re talking! Savory foods like potato chips, bacon, pizza, and ribs are also high on my list. Taubes doesn’t mention that the “desserts and sweets” that provoke his addiction-like behavior are probably also high in fat, tacitly assuming that only the sugar is relevant.”

    Your suspicion is safe with me.

    Lock me up with endless baby back ribs and Buffalo wings and after the life is ended, good chance I’ll call it a good one.

  7. “To him, the common denominator may seem like it’s carbohydrate, which is why the insulin explanation is so irresistible that even a total lack of evidence cannot restrain him from it.”

    Oh, I know you were grinning when you wrote that.

  8. Great article, Stephan. Thanks for dispelling some of the low-carb myths Gary Taubes is promoting. Your writings have gotten me off the CIHO bandwagon and my health has improved significantly because of it. I’ve lost over 50 lbs since January by finally letting go of the idea that carbs and sugar are inherently fattening in some way. We need people like you explaining the real science of obesity to laymen . Keep up the excellent work.

  9. It’s important to provide counter arguments in an intelligent way, with good solid logic. And this Mr. Guyenet accomplishes. So thank you for that.

    I was thinking about Taubes’ article, is it really only carbs and insulin? Well, the explanation here makes more sense. I deduce this from personal experience. While it’s true that white bread, pizza, candy etc can trigger overeating for me, beans, lentils, even whole grain sourdough bread, rice, doesn’t. It keeps me full and feeling good for many hours, despite maybe providing just 400-500 kcal.

    Also, if it was all about insulin, lean meat should do the same. It’s also high in the insulin index, higher than pasta even. But lean meat, protein in general, seem to prevent overeating, not cause people to binge.

    And third, who binges on pure carbs? Just the bread, no butter and cheese? Just potatoes, not deep fried in oil? Just pasta, no olive oil or creamy sauce?

  10. So why did you conveniently ignore this paragraph in Taube’s piece (was it just to shill your book?)

    “Sugar and sweets might be a particular problem because of several physiological responses that may be unique to sugar. Sugar cravings appear to be mediated through the brain reward center that is triggered by other addictive substances. Both sugar and addictive substances stimulate the release of a neurotransmitter called dopamine, producing an intensely pleasurable sensation that our brains crave to repeat. Whether this really is a significant player in sugar cravings is one of many areas of controversy in the field.”

    • Hi Nick,

      I’m not sure what you mean. I mentioned in my post that Taubes acknowledges the role of dopamine in food craving. What exactly are you suggesting I ignored?

      There are two mistakes in the paragraph you quote. First, his statement that this dopamine response is “unique to sugar” is clearly incorrect– we know it happens for fat as well. Also, dopamine release does not produce a “pleasurable sensation”.

      • Are you ignoring Lustig’s research that hyperinsulinemia causes leptin resistance?

        https://www.youtube.com/watch?v=SEFowqGmfAM

        http://jneurosci.org/content/30/7/247
        Another paper describing this.

        In slide #40 Lustig cites a paper which more directly shows that insulin directly inhibits leptin signalling; that is as long as insulin is elevated the functions of leptin are inhibited.

        The paper referenced can be found here:
        https://www.ncbi.nlm.nih.gov/pubmed/1

        Main Lustig Paper cites: http://www.nature.com/nrendo/journal/
        http://www.nature.com/nrendo/journal/

        And leptin is responsible for doapmine sensitivity working: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124796/
        Pharmacological studies have indicated that leptin also modulates behaviors associated with dopamine reward circuit. Leptin decreased lateral hypothalamic self-stimulation as well as sucrose self-administration and sucrose CPP (Figlewicz et al., 2001, 2004, 2006; Shalev et al., 2001). Moreover, leptin declined drug seeking behaviors caused by food deprivation (Shalev et al., 2001; Hao et al., 2004). In addition, direct leptin injection into the VTA reduced food intake (Homme et al., 2006; Morton et al., 2009; Bruijnzeel et al., 2011). These findings imply that leptin provides negative effects on DA reward neurons resulting in food intake reduction. Further evidence shows that leptin suppressed the mesolimbic DA signaling by decreasing the DA neuronal firing frequency and subsequently reducing DA levels in the NAc (Krügel et al., 2003; Homme et al., 2006). In addition, presynaptic leptin action can suppress excitatory synaptic transmission into DA neurons in VTA (Thompson and Borgland, 2013). Moreover, similar to the effects observed in insulin signaling, decreased DA concentrations by leptin could be attributed to increased DAT activity (Perry et al., 2010). However, investigations on the function of mesolimbic DA system in leptin-deficient animals showed opposite findings in that the DA signaling originating from the VTA was reduced. Ob/ob mice contained less tyrosine hydroxylase, the rate-limiting enzyme for DA synthesis, and showed decreased DA content in the VTA and NAc (Fulton et al., 2006; Roseberry et al., 2007). In addition, dopamine 2 (D2) receptor binding decreased in the VTA of these mice and this was reversed by leptin treatment (Pfaffly et al., 2010). It is difficult to explain the discrepancies observed in ob/ob mice but it is possible that chronic leptin deficiency stimulates other compensatory mechanisms, for example, chronic leptin deficiency might lead to changes in normal intracellular signaling pathways and activate a feedback regulatory loop that might be responsible for regulating DA content and function and ultimately decreasing the function of DA neurons (Opland et al., 2010, for review).?

        Lustig already summed it up in his book, fat chance:

        http://bit.ly/2h865fv

        https://oncohemakey.com/wp-content/uploads/2016/06/B9781455748587000317_f22-03-9781455748587.jpg

        • Hi Spraydom,

          Your links didn’t come through, except the YouTube link. I’m aware of Lustig’s claim that hyperinsulinemia causes leptin resistance. I have scoured his papers and his talks for references, and corresponded with him personally asking for anything else he may have. When you actually follow his references there is virtually no evidence supporting his claim.

          At the time I looked maybe two years ago, the only study he cited in his papers that was even remotely supportive was a cell culture study, and that is hardly convincing.

          The neuroscience of hormone action in the hypothalamus is a field I’ve actually done research in, unlike Lustig. Some of the papers he cites in the YouTube link you shared are by my mentor Mike Schwartz, who is a leader in the field. I can tell you that no one in the field, including Schwartz, believes Lustig’s hypothesis. If the cause of obesity were as obvious as Lustig claims, don’t you think people who study this for a living would be all over it?

          That doesn’t mean it’s false. There could be some truth to it, I don’t know. I can’t think of any reason off the top of my head why it couldn’t be true. But I haven’t seen evidence that is even remotely convincing. Until we have convincing evidence, I will continue to disapprove of the extreme confidence with which Lustig presents his hypothesis to the public.

          I also want to point out that Lustig’s hypothesis is not the same as Taubes’s. Lustig is a lot more advanced in that he acknowledges the role of the brain in body fat regulation. Taubes’s hypothesis is that it’s all about insulin acting directly on fat cells. Previously he argued that the brain is irrelevant, although he seems to be changing his mind lately as he has been advocating for the food reward concept (dopamine). I don’t know what he believes these days, but to date he has not written the word “leptin” in a single one of his books.

  11. in my own experience. I do suffer reactive hypoglycemia. Only if I eat excess refined carbs, particularly on their own, they push my blood glucose high. I get a consequent crash which is very unpleasant. Dizzy, irritable, and a low blood sugar reading. Back in the 95 I switched to Zone diet proportions of protein carbs and fats and swapped out refined grains for fruit and veg in meals. Satiety from the protein was fantastic and no more hypos. So I can see for some, at least like me that constantly eating only refined carbs can trigger hunger and overeating. So I’ve learned to eat in a way that stops the hypos, primarily ditching very high GI carbs and always eating protein with meals. However, even though this regulates my appetite really well, I can also gain weight now just be overeating the delicious stuff. Any deliciousness will trigger overeating for me, icecream, chocolate, fatty meat, lots of fat in general with meals, nuts, nut butters etc. By sticking to my slightly boring diet the majority of the time (animal protein and veg, including root veg) that I know works, and not being weird about treats like an icecream at the movies from time to time, I know that I maintain a healthy weight and dont get hungry. For what it’s worth I am homozygous for FTO, I don’t know if it affects me, but I am aware that those with this variant tend to eat more. So I always manage my portions so that I eat the right amount for maintaining my current weight / body fat. I sometimes feel that my brain is not good at regulating my intake.

  12. One reason why Taubes has been so successful at getting people to change their food habits (including me) is that he has approached the subject from a lot of
    different directions. What convinced me ten years ago was his argument that when native cultures begin to import sugar, flour, and vegetable oil people temd to gain weight and are much more prone to diabetes.

  13. I think we can learn some things from this old experiment where three newly weaned infants for 6-12 months selected their own foods, and ate as much as they wanted. They had free access to whole milk, whole sour milk, muscle meat, organ meats, seafoods, eggs, vegetables, potatoes, fruits, whole grains, bone marrow and bone jelly: http://www.medicine.mcgill.ca/epidemiology/hanley/Reprints/ClaraDavis1928.pdf

    It was concluded that «The immediate results appear to be equal at least to the best results obtained by commonly prescribed diets in growth, weight, bone development, musculature, general vigor and appearance of health and well-being.»

    While over time, the diet of the three was very balanced
    (and apparently perfect in terms of balance of minerals /acid and alkaline foods), in the short term it could be very unbalanced and extreme;

    «A tendency was observed in all the infants to eat certain foods in waves, i.e., after eating cereals, eggs, meats or fruits, in small or moderate amounts for a number of days, there would follow a period of a week or longer in which a particular food or class of foods was eaten in larger and larger quantities until astonishingly large amounts were taken ; after this, the quantities would decline to the previous level (…) In the diet kitchen such waves came to be known as “egg jags,” “meat jags,” “cereal jags,” etc. Symptoms of overeating did not accompany them, nor were the waves followed by a period of temporary disgust for and neglect of the particular food as is usual when appetite is surfeited.»

    There were differences in the food intake between the three children so that for example one obtained 25% of energy from bone marrow, while another just 5%; one obtained 40% of calories from fruits, and another just 10%. The amount of calories from sugars vs fats differed, while protein was somewhat more constant.

    The average diet for the three over 6 months would probably be quite similar as Fred Kummerow´s (who lived to be 102) dietary recommendations (http://wphna.org/wp-content/uploads/2015/06/WN-2015-06-01-02-72-78-Idea-Fred-Kummerow-My-diet.pdf), with a macronutrient balance maybe of 15-20% protein, 40-45% carbs and 40% fat. Scaled up to 2500 kcal, it would be an average daily intake of something like 1 quart of milks, 4-5 fruits (mainly oranges, apples and bananas), 100 gram potatoes, 200 gram meat, 2-3 eggs, whole grains to supply 75-100 gram carbs, and bone marrow (monounsaturated fat) to supply 40 gram fat. They ate almost no vegetables.

  14. I have a hypothesis that LCHF diets work for some people because they are actually eating less fat. I think a key is “palate cleansers,” for want of a better word for it. Consider having a limitless supply of cookies that you eat with a glass of water. I could maybe eat two or three before something in my brain would start screaming “Too much sweetness!” and anything sweet would start to taste disgusting to me. But if I had milk or coffee with my cookies, I could easily eat 10, 11, 12 and wouldn’t want to stop until my stomach started to hurt. The milk or coffee cleanses the palate of sweetness and seems to trick the part of the brain that tells me I’ve had enough. I might have thought it was the fat in the milk, except that black coffee works even better than milk.

    Bread and potato are fantastic palate cleansers. If you eat some meat and cheese, you can’t get too far without feeling like you’ve had too much fat. Throw the meat and cheese on pizza dough and you could eat a huge portion. The pizza dough seems to soften the fatty taste so that you don’t feel like you’ve had too much fat. Mix a huge lump of butter directly into flour or mashed potato and you can have an enormous amount of fat without it tasting all that fatty.

    So that’s what I think is going on. Fat and sugar are what makes us fat, but grains and potato cleanse the palate of these tastes so that our brains don’t recognize when we have had too much. And the effect is even worse if the grains or potatoes are ground up or mashed up so that lots of fat can be mixed in with it.

    I’m sure you’re aware of this, Dr Guyenet, because you instruct us not to mix up food, but I haven’t seen you specifically mention it. Maybe I missed it?

  15. “I don’t think anyone believes that cravings and addictions to alcohol, gambling, sex, or video games are due to elevated insulin levels.”
    Which of these are merely cravings and which of these are proven/speculated to be addictions? (Thanks for the debunking the role of insulin in these.)

  16. Is there any reason to believe that the carbohydrates Taubes writes about are from refined grains and may be processed by his body (mouth, stomach, small intestine) more as a sugar than a complex carbohydrate? Or that they are loaded with fats? Eg, butter on bread, oil and cheese on pasta…. Might just be a sugarholic or fatholic confused by the “carbohydrate” transport media

  17. I think it gets back to the old studies of serotonin – the levels go up with carbohydrates (see Wurtman etc..)

    The early research led to the development of SSRI drugs. Comfort foods – comfort via serotonin.

    But I think most of over eating is driven by inappropriate insulin sensitivity caused by PUFA consumption. Thus causes over-storage of lipids and locks up energy – thus people carrying an extra 100Lbs are still so hungry they can’t resist.

    Seed oil sources of PUFA (Linoleic Acid in particular ) are likely the smoking gun of the obesity pandemic.

    The 2-year half life separates cause and effect – very hard to have human trials..

  18. There’s a lot that’s right in both of your articles, but the bottom line for me is this: When I used to “diet”, then inevitably go ‘off’ the diet, I would turn to breads, pasta, potatoes and desserts. Yes, there is fat involved in some of the carbs I would crave, but I don’t gain weight if I pig-out on fatty ribs and bacon, I gain weight when I turn to the carbs. So whether the glucose and insulin response is playing a part, or my brain is lighting up in the reward centre from the “food” as you insist on saying, it’s the carbs which cause my particular weight gain–massively.

  19. Really interesting post. Have you heard of the work of Gabor Mate? He works in the field of addiction and has a book called ‘When the body says No.’ He talks about our addictions stemming from psychological stress, usually related but not always, to a situation involving our parents and then we go on to develop coping mechanisms. For some people it’s drugs, some food, some shopping – but all with similar underlying causes. It’s fascinating and the book is a great read, especially if you have developed a disease or illness that seems to of come from nowhere.

  20. I think there is something to the combination of fat and carbs – presumably this most stimulates the dopaminergic pathways. Fatty foods like bacon, ribs, and ribeye can be crave-worthy and rewarding, but in their natural low-carb form are pretty self-limiting. I find it easy to push the plate away after I’ve had my fill; eating an unreasonable amount starts to get painful. But back when I hate high carb high fat foods like chips and pizza this mechanism didn’t come into play – I could eat and eat until all the food was gone!

    • Cookies are another example I just thought of. The low-fat ‘healthy’ ones were absolutely appaling, but standard higher fat cookies (and other pastries like donuts) I could literally eat whole trays of…

  21. Thanks for writing this, Stephan.

    Taubes commands a powerful position with the media, and can easily make himself to be heard/read. It’s a shame he doesn’t use this power to address this stuff from a more open-minded position.

    It’s most frustrating when he’s ‘almost right’ and misses a prime opportunity to teach a new audience something that could really help them.

    To the average person, it doesn’t matter whether cravings, overeating, and binges are caused by the insulin itself or by the carbs, fats, and the crispiness of their foods. They want to know how to handle their issues, plain and simple.

    It seems that Taubes might be one of the few who DOES get a dopamine response from insulin. But it’s from talking about it, not the insulin itself.

  22. Hey Stephan,

    Great response to a poor article. I completely agree large platforms like the New York Times need to be far more responsible with what they publish. As a gym owner and Personal Trainer I often feel i’m trying to clean up the mess explaining to members the real causes of weight-gain. Many come in after reading junk articles like Taubes and point at me as the bad guy for never telling them this stuff.

    I then have to try and explain why it’s wrong without making them feel frustrated and defensive. A simple vetting process could make my life a lot easier and everyone else a lot better informed.

    • Hi Robert,

      Thanks. All dietary carbohydrate reduces fat oxidation because the body switches to burning the fuel source it just ingested. If you eat fat, it burns fat, and if you eat carbs, it burns carbs.

      The DIT finding is interesting. I’d have to look through the lit to see if there’s other evidence supporting the idea that sugar suppresses DIT. It’s counterintuitive because in general carbohydrate (modestly) increases DIT and insulin release is supposed to be part of the mechanism (although I don’t know how strong the evidence is for that).

      • Not only that – when one eats a dose of carbs – insulin goes up – The oft repeated bit that “insulin controls Blood glucose” is wrong in it leaves out most of insulin’s effects. That insulin effects BG is only a small part of the story.

        Some of us remember that:
        LPL move fat in to fat cells. HSL moves fat out of fat cells.
        insulin is known to activate LPL in adipocytes
        HSL is inhibited by insulin.

        One must be somewhat insulin resistant in adipose tissue in order to lose weight.

        – Liver becomes insulin resistant first, muscles second, adipocyres last.

        – Insulin levels in the obese remain about 10 times those of a normal person even under complete starvation.

        The effect of dietary PUFA on adipose insulin sensitivity is not some ungrounded narrative. It causes inappropriate insulin sensitivity in adipose tissue causing weight lose to be very difficult.

        The medical community and public is ignorant of these effects..

        And once obese – elevated insulin is likely causative of heart disease and more:

        Insulin also has MANY other effects::

        controlling storage of fat – Decreased lipolysis
        as a growth factor.
        glycogen synthesis
        Increased cellular potassium uptake
        decreases production of glucose from noncarbohydrate substrates
        Increased lipid synthesis
        Increased production of trygly from fatty acids
        decreased breakdown of proteins
        Decreased autophagy – decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.
        forces cells to absorb circulating amino acids
        forces arterial wall muscle to relax
        Increase in the secretion of hydrochloric acid in the stomach
        Decreased renal sodium excretion
        enhances learning and memory
        increased fertility

        • Hi xtronics,

          I have addressed these points extensively in previous writing. The statement that “One must be somewhat insulin resistant in adipose tissue in order to lose weight” has been clearly disproven. All you need is an energy deficit to lose weight, regardless of what insulin is doing.

          The insulin-centric view of body fatness ignores the fact that many factors besides insulin determine fatty acid flux in/out of fat cells. One of these is simply the concentration gradient of fat outside vs. inside cells. If you eat more fat than your body burns, the excess ends up in your fat cells regardless of what insulin is doing. There is literally nowhere else for it to go.

          • Is it possible that some people just waste excess food? I’ve tried eating a huge amount of excess calories to gain muscle back when I lifted a couple times a week (5k+/day) and all I ended up doing was using the bathroom more (I’ve never been able to get over 185 lbs at 6’2″).

            Is it something to do with more passive/unconscious energy use? I never tracked my fidgeting and restlessness when I ate that much. Perhaps I just fidgeted more or “chose” to do more walking or other activities and actually burned the extra calories.

          • Hi Paul,

            Yes, some people do waste excess calories, while others don’t, even given the exact same diet and calorie excess. I discuss this is more detail in my book.

    • Hi John,

      Thanks for sharing that. Yes, I’m aware of that study. It’s part of a broader line of investigation suggesting that both insulin and leptin act in the brain to suppress food reward. I don’t know how important the effect is in normal physiology, but it can certainly be observed when you put high levels of insulin in the brain, as in the study you linked to.

      I alluded to this in my post where I said “Part of the reason why they came to this conclusion is evidence suggesting that “insulin may act in the brain to reduce sweet taste signaling and sugar activation of brain reward systems” (emphasis mine)”. The evidence originally came from rodents (work of Figlewicz and Benoit) but has expanded to humans with the intranasal administration procedure in the study you linked.

  23. A couple of thoughts.

    1) How would you explain excessive soda consumption? This is perhaps the single most damaging “food” for the obese/typeII population but has zero fat. It is the most obvious thing to eliminate but somehow people continue to consume in the face of serious detriment. Are they not addicted to sugar?

    2)I don’t think there are “fatoholics” addicted to just fat, are there? Obese butter eaters?
    The savory foods that are problematic are combinations of carbs and fat, e.g., potato chips.
    Low carb fat eaters have a hard time getting fat so the “addiction” doesn’t really matter if it exists at all.

    So maybe insulin is not causing “addiction” but it certainly seems like it might be a necessary condition.

    • Hi Tom,

      Soda consumption is clearly a reward-driven behavior. As I explained in my post, sugar is a strong reward factor; it’s just that sugar-only foods are not the most common foods that trigger addiction-like behavior. Just because you consume a food every day doesn’t mean you’re addicted to it, although I wouldn’t be surprised if some people were actually addicted to soda.

      You mentioned that few (if any) people have addiction-like behavior toward plain fat like butter. I’m sure that’s true, but when’s the last time you saw someone eating a bowl of plain white sugar? The most rewarding foods occur when we mix reward factors. Soda is mostly sugar but don’t forget that there is also 1) often caffeine, which is a habit-forming drug, 2) flavors like aromas and acid, and 3) carbonation which gives a nice sensation on the tongue. If it were just about the sugar then people would like plain sugar water an much as they like Coke, but they don’t.

      The last point I’ll make is that even if we assume for the sake of argument that carbohydrate is required for addiction-like behavior to occur, that still doesn’t automatically implicate insulin. Physiology is complex and although insulin is clearly a central aspect of the body’s physiological response to carbohydrate and protein, there is a lot going on besides insulin.

    • Hi G,

      Taubes has an undergrad degree from Harvard, a masters in aerospace engineering from Stanford, and a master’s in journalism from Columbia. He is obviously an intelligent person, although he is not an academic as you suggested. Which of those degrees makes him an expert on obesity and eating behavior? Answer: none of them.

      The truth is that he has no training or experience whatsoever in biomedical science of any kind. Not even an undergraduate degree. He has never performed a single experiment in the areas he writes about.

      So let me ask you this. When you need someone to fix your roof, do you go looking for them at a bakery? Does being a brain surgeon qualify a person to fly the space shuttle? Thanks for trying.

  24. I’ve been working on this since the ’70’s, and what I’ve found is that there are two types of men – and you can tell just by looking – thin skinned men, and thick skinned men (I’m sure it’s a continuum). Thin skinned men have naturally bulging veins in their forearms, even when they have a pot belly, and thick skinned men have no bulging veins, even when they’re in great shape. Thick skinned men gain weight all over, but do not develop pot bellies. That’s me.

    I do curls with forty pound dumbbells and there are no veins to be seen in my forearms. I can also eat two meals a day while averaging 750 reps per day and be fat. The only thing that keeps the fat at bay for me is LSD aerobics (Long, Slow, Duration). And, it’s not the pace or duration, per se, but the total number of calories burned. You have to burn about 150 calories before your body directly metabolizes fat for energy. It doesn’t matter if you do that in fifteen minutes or twenty, that’s the warmup. You need to burn over 300 calories to get the fat to begin to come off. Over 500 to be trim, over 600 to be cut. Every day.

    I discovered this when I began to run in high school. I’m 6’2″ and went from 200 to 165 just by running forty-five minutes every day. No diet. Now I do it on a Bowflex MAX aerobic trainer. Forget intervals! That’s just another BS fad. So are all diets.

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