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Nutrition Past and Future

The Drivers of the Herd, Part 13

The NuSI Guys, Part 3, Fattening Fats, in Animals as in Man

Slide 3                   Considering the fact that it’s called Why We Get Fat, this book suffers from a rather glaring omission. It never presents any evidence at all of how people who are not fat become fat. This book can’t answer that question.


Slide 4                   p.89. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Sure, you get lots of low carb dogma on the subject, which Taubes tries to pass off as accepted science with the phrase, “Laws of Adiposity.” But he never shows us what we know about fattening. You can see he writes about fat rats in addition to fat people. So then would the book be more appropriately called How Lab Rats Get Fat? Not really. He doesn’t answer that question, either. Why not? He says we can learn a lot from rats. I agree, so I’ll do for you what he did not. I’ll show you how to make thin rats into fat rats. You’ll see that not only does this body of research argue against the claims of the NuSI guys, it actually shows us why the NuSI enterprise itself is based on false premises.


Slide 5                   p.102. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Instead of writing about how thin rats can be made into fat rats, he writes about inbred genetic freaks that are prone to obesity. Are you a genetic freak who’s been specially bred for obesity? If you’re not into that he also writes about rats that have had their ovaries removed. Is that closer to your situation? What about his anecdotes about rats who had their hypothalamuses surgically damaged? Does any of this seem especially pertinent to your life?


Slide 6                   p.67.Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

He’ll also shows us provocative pictures of cows bred to have different characteristics. It’s all about their genes, he says. But again, it’s not clear how this applies to us.



Slide 7                   p.105. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.


So where is he going with all these observations of animals? Taubes says all these examples of purposeful breeding and ghoulish surgical alterations tell us that people who run are naturally thin just the same way that greyhounds are naturally more energetic than basset hounds. And I’m not joking.


Slide 8         

This reminds me of a recent post on a blog called Dog Behavior Science. The next two slides were inspired by this post.


Slide 9                   p.181. Mason, Walter E. Panama-Pacific International Exposition: Breeds of All Nations. 1915. Accessed at

Scott Feldstein.

These are greyhounds separated by about a century. They look as if they’ve been engineered from the ground up for maximum speed. From these pictures, it looks like the breed has changed a bit in 100 years.


Slide 10                 p.45. Mason, Walter E. Panama-Pacific International Exposition: Breeds of All Nations. 1915. Accessed at

Here are basset hounds. Here especially, it looks like the breed has undergone some changes. The basset doesn’t look built for speed. Judging from these two, bassets are looking quite a bit slower than 100 years ago. The basset and the greyhound are both descendants of the same ancestor, yet they’ve been bred to be this different. Do you think a typical distance runner was bred like a greyhound? Were you bred like a basset?


Slide 11                 p.102. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Mayer, Jean. Overweight: Causes, cost, and control. Englewood Cliffs, NJ: Prentice-Hall, 1968. Print.


Taubes also refers to an obese strain of mice. Notice that he is talking about their genes. The bottom part of the slide is his reference. The author says that in a way, these mice were obese since birth. Does this really apply to any of us? If it does, why bother telling us to eat low-carb diets? If we’re born obese like these rats, how could our diets make any difference? What’s the point of all this?


Slide 12                 p.80. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Do you remember how Taubes said that the very idea of energy balance has done incalculable harm? Somehow he thinks it’s scarred the psyches of the obese.


Slide 13                 p.103. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Do you think it’s less damaging to have his readers think this passage applies to them? He tells us that the fat of a Zucker rat will cling to it even as it starves to death, as if the rat were possessed by some fat demon that parasitizes it until the end. Not even in death can the rat escape the fat demon. That might strike you as a slightly more harmful idea than calories in/calories out, especially since it isn’t true.


Slide 14                 Zucker, Lois M., and Theodore F. Zucker. "Fatty, a new mutation in the rat."Journal of Heredity 52.6 (1961): 275-278.

Zucker rats are genetic freaks. They were discovered in 1961 and continuously inbred since then because they fatten so easily.


Slide 15                 p.75. Greenwood, M. R. C., et al. "Adipose tissue metabolism and genetic obesity: The LPL hypothesis." Recent Advances in Obesity Research (III). London: John Libbey (1981): 75-80.

The only possible reference Taubes lists in this chapter that might support his claim that obese Zucker rats will preserve their fat mass all the way until they are starved to death is this one, and it does not support this claim. First, from the title you can clearly see that the authors were concerned with genetic obesity. Secondly, the caloric restriction of the rats took place at the beginnings of their lives. I don’t think he has a reference that supports his demon fat idea.


Slide 16                 Cherel, Yves, et al. "Relationships between lipid availability and protein utilization during prolonged fasting." Journal of Comparative Physiology B 162.4 (1992): 305-313.


In my own research on this I could not verify his claim. As far as I can tell, rodents exhaust their fat stores completely during starvation before succumbing to protein wasting and death. It is true, however, that we humans can starve to death before exhausting our fat stores. Even if this story from Taubes were true, it wouldn’t tell us anything.


Slide 17                 p.25. Lieberman, Michael, Allan D. Marks, and Alisa Peet. Marks' Basic Medical Biochemistry: A Clinical Approach. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013. Google Books.

This is because we have tissues and cells that depend upon glucose for fuel. Once all the body’s protein is wasted from starvation, the glucose runs out and the lights go off.


Slide 18                 Zucker, Lois M. "Some effects of caloric restriction and deprivation on the obese hyperlipemic rat." The Journal of Nutrition 91.2 (1967): 247-254.

But let’s stay focused on his story. He was clearly writing about what happens to obese Zucker rats during starvation. Here is an article by Zucker himself. What did he say about this? “When totally starved, young fatties survived until all visible fat stores were exhausted.” There was no demon fat in Zucker rats according to Zucker himself and that does not agree with what Taubes wrote. It looks like he’s telling tall tales again, just to make you think you might have demon fat, too. How silly!


Slide 19                 Christakis, Nicholas A., and James H. Fowler. "The spread of obesity in a large social network over 32 years." New England journal of medicine 357.4 (2007): 370-379.

There is no reason that Taubes should be encouraging his readers to find lessons from these genetic freaks that apply to themselves. Genetics can’t be the explanation for our obesity problems. Our genes haven’t changed in the last hundred years like those dogs. If genetics were so important in obesity, why is it that obesity spreads through social networks, as was demonstrated by this very important study? It showed, for example, that if one spouse becomes obese, then the other is much more likely to become obese, too. Genes aren’t making that happen.


Slide 20                 With all this talk about genetic freaks you may be wondering if I’ll ever get around to answering my original question: How do you take thin rats and make them fat? How does diet quality affect weight gain in rats, whether they are genetic freaks or not?


Slide 21                 Hariri, Niloofar, and Louise Thibault. "High-fat diet-induced obesity in animal models." Nutrition research reviews 23.2 (2010): 270.

There is a reason why Taubes doesn’t get into this in his book. You can easily search studies of obesity in rodents to find what the typical diet composition looks like. They are usually very high-fat diets with added sugars. They are hardly ever high-carbohydrate diets. That’s because, as was stated in this review of the literature, “the use of high-carbohydrate-low-fat diets has not been found as efficient as high-fat-low-carbohydrate diets in inducing obesity.” That about sums it up. Bear in mind, as I’ve said in another video, experimental diets using very high proportions of sugars are sometimes used to create metabolic distress in animal studies. But no responsible nutrition expert says you should consume liberal quantities of refined sugars. However, high-fat diets used in experiments are typically around 60% fat, and that is actually less than the amount of fat recommended by low-carbers like Taubes.


Slide 22                 Ghibaudi, Lorraine, et al. "Fat Intake Affects Adiposity, Comorbidity Factors, and Energy Metabolism of Sprague‐Dawley Rats." Obesity research 10.9 (2002): 956-963.

The review on the previous slide referenced this study. It’s an interesting example to show you why high-fat diets fatten rodents so well. It found that a litany of metabolic defects were progressively made worse on a high-fat diet. The fat being used in this high-fat diet was 88% lard. No high-carb advocate will tell you high-fructose corn syrup is a good thing to consume, but high-fat advocates are huge fans of lard.


Slide 23                 p.189. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Taubes actually wrote, “As hard as this may be to believe, if you replace the carbohydrates in your diet with an equal quantity of lard, it will actually reduce your risk of having a heart attack. It will actually make you healthier.”

The reason that may be hard to believe is because it’s totally crazy-pants. This sums up Taubes so well. There is no evidence at all that supports this statement. It’s just double standards like we saw in video 11. Notice he also says “an equal quantity.” An equal quantity of lard would have around double the calories of the junkiest carbohydrates. This statement should be seen as obviously false by any thinking human.


Slide 24       

But there are people out there who read this rubbish and are inspired to part with $40 million. Don’t ever mistake the super rich for the super smart. How embarrassing!


Slide 25                 Ghibaudi, Lorraine, et al. "Fat Intake Affects Adiposity, Comorbidity Factors, and Energy Metabolism of Sprague‐Dawley Rats." Obesity research 10.9 (2002): 956-963.

Sure, lard will make you healthier. That is if you define “healthier” as fatter and more insulin resistant. These rats were turned into metabolic wrecks by lard. This is the evidence from lab animals that you should know about, not some tall tale about hibernating ground squirrels.


Slide 26                 Vander Tuig, Jerry G., Dale R. Romsos, and Gilbert A. Leveille. "Maintenance energy requirements and energy retention of young obese (ob/ob) and lean mice housed at 33 and fed a high-carbohydrate or a high-fat diet." The Journal of Nutrition 110.1 (1980): 35-41.

If you’re obese and you’re interested in what happens in studies of obese mice, then you might find it interesting that in this experiment, obese mice eating as much as they wanted of a high-fat diet became especially fat. Again, I encourage you to do your own research on this. You might find studies in which high-carb and high-fat diets produced similar weight gain, but I don’t think you’ll find studies showing animals getting fatter on high-carb, high-fiber diets. If you ever see such a study, please send it to me.


Slide 27                 p.103. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Of course, we should care about other things beside weight gain. Taubes claims that obesity is not just about eating too much. It is fundamentally a problem of fat tissue dysregulation. He says this is the clear message of eighty years of research on animals. The problem here is that he isn’t telling you the rest of that message.


Slide 28                 Hill, James O., et al. "Development of dietary obesity in rats: influence of amount and composition of dietary fat." International journal of obesity 16.5 (1992): 321-333.


This study provides an excellent example. Rats were made obese through two different types of high-fat diets. That’s nothing special. What’s interesting here is that the high-fat-fed rats were then switched to low-fat diets. The result? “Rats previously fed the HF (high-fat) diet required less food to maintain their body weight.” In other words, the high-fat diets caused the rats to retain their body mass on less food. Now that is an interesting message from animal research, and it’s a message Taubes won’t tell you.


Slide 29                 In this body of research it is usually observed that rodents fed high-fat diets simply consume more calories. That’s because high-fat foods taste good to them and it’s because high-fat foods pack a lot of calories. But the authors couldn’t explain what they saw this way. They said, “A period of dietary obesity may leave the rat permanently unable to maintain ‘normal’ body weight and body composition on similar energy intake.” A high-fat diet left the mice with a damaged metabolism that may not ever recover.


Slide 30                 Omagari, Katsuhisa, et al. "Effects of a long-term high-fat diet and switching from a high-fat to low-fat, standard diet on hepatic fat accumulation in Sprague-Dawley rats." Digestive diseases and sciences 53.12 (2008): 3206-3212.

In this one, rats were fed fatty diets for 23 weeks. They became obese and their livers became fatty, inflamed, and, in some cases, scarred. Then they were switched to a low fat diet for 20 weeks. Their health improved, but their livers never fully recovered. Most of the fat that did this damage was lard.


Slide 31                 Ravussin, Eric, et al. "Determinants of 24-hour energy expenditure in man. Methods and results using a respiratory chamber." Journal of Clinical Investigation 78.6 (1986): 1568.

This study on mice showed that saturated fats are especially likely to cause weight gain as well as fatty liver. The researchers identified changes in their gut flora that they thought were part of the explanation why. The high saturated fat diet produced a ratio between Firmicutes and Bacteroidetes bacteria well-known to associate with obesity. Maybe that accounts for the results of the previous study, in which the high-fat-fed mice needed less energy to maintain their weight.


Slide 32                 The weight gain in the mice fed the saturated fat took place despite their consuming less food and absorbing less energy.



Slide 33                 Omar, B. A., et al. "Enhanced beta cell function and anti-inflammatory effect after chronic treatment with the dipeptidyl peptidase-4 inhibitor vildagliptin in an advanced-aged diet-induced obesity mouse model." Diabetologia (2013): 1-9.

Here’s another very interesting study that was recently published. These researchers waited until their mice were a bit older and then they gave them a high-fat diet. The result was pancreatic inflammation and early-stage diabetes.


Slide 34       

One researcher from this study thought this might provide a warning to those considering low-carb diets.


Slide 35                 If you look up this paper, be sure to check out Figure 1, which shows the dramatic weight gain their high-fat diet caused.


Slide 36       

Taubes is critical of studies on animals that use whole foods because they introduce “an unholy host of variables.” They aren’t nice, clean experiments that look at a single question of interest because whole foods aren’t convenient for reductionist analysis.


Slide 37                 Taubes, Gary. "Which One Will Make You Fat?." Scientific American Magazine309.3 (2013): 60-65.

Taubes says the experiments done by NuSI won’t be like that. They’ll create unambiguous evidence because they’ll be so highly focused and well-designed.


Slide 38                 But the experiment he made up uses real food, introducing an unholy host of variables. He’ll end up with a result that could be explained in multiple ways. Sure, macronutrient ratios might be different between the experimental and control diets, but was that what really mattered? Notice, for example, how he calls the foods being used “real food sources.” Since when is vegetable oil a real food source? Do you know why it’s in there? I’ll think it’s because these characters know that polyunsaturated fats tend to lower cholesterol, and they have decided that their trial can’t show that cholesterol skyrockets on a high-animal-fat diet. Did their favorite low carb hero Viljalmur Stefansson use vegetable oil when he was with the Eskimos? Of course not. This diet has never occurred under natural conditions in all of human history and he is selling this as “real.” This is why study design matters. I’ve done many videos at this point about how these trials supporting low carb were designed to achieve the desired outcome of their funders. They take advantage of that “unholy host of variables” in their efforts to fool you. One of the first things you learn in science is isolate the independent variables. Now where have I heard that line before?


Slide 39       

Taubes: “One of the first things you learn in science is isolate the independent variable.”

Oh, right. That’s the guy who’s going to save nutrition science.



Slide 40       

The researchers who design studies of diet composition for animal experiments understand the need to use purified diets if they have any hope of coming up with unambiguous findings. Diets based on real foods are a poor choice for scientific research on macronutrient ratios. Of course, the artificiality of these diets is a problem as well, but they definitely have their utility answering the sort of questions NuSI says they want to answer. NuSI’s promises are even more flawed than that, though.


Slide 41       

Peter Attia says his “dream” study would have the control diet be something resembling the standard American diet, with all of its refined carbs worthy of an experiment on rats. They would tilt the real food versus synthetic food balance in favor of the low-carb diet. The unholy host of variables will stack the deck in their favor. I’ve talked about this practice among low-carb researchers extensively in past videos. It’s what I call the “strawman diet.” The control diet is a diet no one would call healthy.


Slide 42                 You can see that this is the sort of biased research they are conducting already, with a control diet that is 15% sugar. I expect most of the rest of the carbs they get will be refined junk, too. Really, why would this be worthy of anyone’s charitable donations?



Slide 43                 p.174. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

Animal studies are an especially useful way to reality test the precepts of “Adiposity 101”. Here you see Taubes makes the categorical statement that protein and fat have no effect on fat accumulation. Only carbs are fattening. This is just nonsense. Fortunately, there is plenty of research on animals that can show you that.


Slide 44                 Matsuo, Tatsuhiro, et al. "Body fat accumulation is greater in rats fed a beef tallow diet than in rats fed a safflower or soybean oil diet." Asia Pacific journal of clinical nutrition 11.4 (2002): 302-308.

Here rats were fed diets with equal caloric content but differing in the type of fat used – safflower oil, soybean oil, or beef tallow. The beef tallow fed rats became the fattest. Omega-6 fats performed better than saturated fats when it came to limiting fat accumulation. We saw studies with similar findings in humans in the last of my videos about that Catalyst show.


Slide 45                 Borghjid, Saihan, and Richard David Feinman. "Response of C57Bl/6 mice to a carbohydrate-free diet." Nutrition & metabolism 9.1 (2012): 1-6.

Here was a very interesting study coauthored by a very well-known low-carb promoter. These researchers conducted a feeding experiment using the most commonly used strain of mice in lab experiments. They fed them no carbohydrate at all. If we believe Gary Taubes, then it should have been impossible for these mice to get fatter since only carbs are fattening. But that’s not how this turned out. Despite similar caloric intake, the low-carb mice became considerably fatter than the mice fed standard chow. Their livers and hearts became full of fat.

Other researchers did a similar experiment but got different results. These guys said the problem with the other experiment was that they deprived their rats of adequate protein.


Slide 46                 The fats being used here were lard and butter, which are low-carber favorites.


Slide 47                 p.174. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.

This experiment exposes Taubes’ dogmas for the dangerous fictions that they are.



Slide 48       

As I said, one of the authors of this paper is a prominent low carber and the journal that published it has a distinct low-carb bias. The article is full of qualifiers meant to minimize the damage their findings do to the low-carb belief system but they did include the data we need. I applaud them for publishing findings they surely found uncomfortable to face.


Slide 49                 Jornayvaz, François R., et al. "A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain." American Journal of Physiology-Endocrinology And Metabolism 299.5 (2010): E808-E815.

As you saw, it’s not just weight gain that we see in experiments using high-fat diets. Here mice were put on the sort of extreme high-fat ketogenic diet that the NuSI leaders think is so great. The mice did lose weight, but they became severely insulin resistant.


Slide 50                 Savard, Christopher, et al. "Synergistic interaction of dietary cholesterol and dietary fat in inducing experimental steatohepatitis." Hepatology 57.1 (2013): 81-92.

The researchers who ran this study had a novel idea. They wanted to see how adding fat and dietary cholesterol to the diets of mice might affect their tendency to develop fatty livers. The control diet was low-fat. The test diets were either low-fat high-cholesterol, high-fat no cholesterol, or high-fat high-cholesterol. All of the test diets caused fatty livers not seen in the low-fat controls. But the mice who were subjected to both higher fat intake and dietary cholesterol developed a seriously deranged metabolism, featuring obesity, high cholesterol, profound fatty liver, and substantial inflammation.


Slide 51                 Once again, I decided to hold back a great graph from a recent study so you’ll seek it out yourself. I did include their description of it, though: “Mice on the high-fat, high-cholesterol diet consumed fewer calories, but gained more weight than mice on the isocaloric high-fat diet.” It was the cholesterol that really made the difference. You should have a look at the original paper if you can. Take note, they used cocoa butter as their added fat. Cocoa butter is a mostly saturated fat.


Slide 52                 Muller, Alexandre Pastoris, et al. "High saturated fat and low carbohydrate diet decreases lifespan independent of body weight in mice." Longevity & Healthspan 2.1 (2013): 10.

Here’s an especially important study. Mice were fed either a high-fat diet or a low-fat diet for the length of their lives. After they reached 15 months old, the mice eating high fat started dying at a greater rate. The death rates continued to diverge until 35% more high-fat mice were dead. You can’t do a study like this in humans, NuSI or not. But from studying mice you can see that trying to stick with a high-fat diet all your life is likely to shorten your life.


Slide 53                 Warwick, Zoe S., and Susan S. Schiffman. "Role of dietary fat in calorie intake and weight gain." Neuroscience & Biobehavioral Reviews 16.4 (1992): 585-596.

These researchers surveyed the animal studies literature on obesity and macronutrient ratios and found that 33 of 40 demonstrated greater weight gain when animals were fed high-fat diets. I looked at the table they provided and by my count, of the 11 experiments that used either tallow or lard, 9 resulted in weight gain. I wouldn’t take those odds if I were you. They stated that their findings were in accord with observations of how fat consumption affects humans.


Slide 54                 Horton, Tracy J., et al. "Fat and carbohydrate overfeeding in humans: different effects on energy storage." The American journal of clinical nutrition 62.1 (1995): 19-29.

You can find parallels to these studies from animals in studies involving humans. In this overfeeding study, people were overfed with either excess carbohydrate or excess fat. Contrary to the expectations of “Adiposity 101” the people consuming excess fat were the ones who became fatter. Of course, fat can be fattening. It’s just fantasy to pretend otherwise.


Slide 55                 Labayen I, et al., “High fat diets are associated with higher abdominal adiposity regardless of physical activity in adolescents; the HELENA study.” Clinical Nutrition (2013),

In this survey of adolescents in Zaragoza, Spain, it was found that the percentage of calories consumed as fat was “strongly and linearly associated with total, truncal and abdominal adiposity.”


Slide 56                 Elhuyar Fundazioa. "Lower fat content for adolescents' diets." ScienceDaily, 8 Jan. 2014. Web. 8 Jan. 2014.


The lead researcher for that one pointed out in a press release that dietary fat associated with abdominal obesity irrespective of how physically active the kids were.



Slide 57                 Lindström, Jaana, et al. "High-fibre, low-fat diet predicts long-term weight loss and decreased type 2 diabetes risk: the Finnish Diabetes Prevention Study."Diabetologia 49.5 (2006): 912-920.

Don’t tell yourself that those studies in rodents don’t mean anything for humans. Saturated fat associates with negative health outcomes and high-fiber, low-fat diets associate with positive outcomes just as these studies on animals would lead us to expect.


Slide 58       

We’ll be looking at a presentation used by Gary Taubes and Peter Attia later in this playlist. This presentation of theirs is now hosted by Dairy Australia.


Slide 59       

One frame asks an important question: “Why animals but not man?” Why not, indeed! We see what the research on animals tells us. Let’s not ignore it all like some people.



Slide 60       


Taubes: “What you do in bad science is you ignore any evidence that's contrary to your beliefs, your hypothesis, and you only focus on the evidence that supports it.”


That’s Gary Taubes telling you exactly how he plays this game of his.


My regular channel viewers first got to know me from my efforts to show people what a sham the Paleo fad diet is. Gary Taubes couldn’t resist the temptation to utilize a popular new form of pseudoscience so he tried to tie his ideas to Paleo in his book. I’ll show you how that turned out in my next video.