Eat Fat, Get Thin: Why the Fat We Eat Is the Key to Sustained Weight Loss and Vibrant Health

Overall score

Scientific accuracy

Reference accuracy

Healthfulness

How hard would it be to apply the book's advice? Fairly difficult

Book published in 2016

Published by Little, Brown and Company

First Edition, Hardcover

Review posted March 23, 2021

Primary reviewer: Travis Masterson

Peer reviewer: Maggie Burhans

Table of contents

1. Introduction
2. Scientific accuracy
3. Reference accuracy
4. Healthfulness
5. Most unusual claim
6. Other
7. Conclusion
8. Updates

Claim 1

Eating a high percentage of calories from fat is better for weight loss.

Supporting quote(s) and page number(s)

Page 4: ”It turns out that eating less fat results in more obesity”

Page 55: “Eating Fat Does Not Make You Fat!”

Page 56: “More and more scientists are confirming that calories coming from fat are better for weight loss…”

Criterion 1.1. How well is the claim supported by current evidence?

1 out of 4

This claim received a score of 1, indicating that evidence for the claim is neutral, or nonexistent. One of the first studies mentioned by Eat Fat, Get Thin to support its claim that eating more fat is better for weight loss is a metabolic ward study. The book does not provide a reference the study but does provide this description on page 56, “Kevin Hall from the National Institutes of Health, has found that in a metabolic ward where every ounce of food and every movement and every calorie burned are carefully measured, those who ate more fat calories (compared to an identical number of calories from carbs) burned more than 100 addtional calories a day. Over a year that amounts to a ten-pound weight loss.” The passage is likely referring to this paper. The interpretation of the study made by Eat Fat, Get Thin is problematic for several important reasons. First, the study found that in the first week of consuming a very-low-carbohydrate diet participants’ resting energy expenditure did indeed increase by about 100 kcal/d. However, the increased energy expenditure returned to near baseline after about a week. Eat Fat, Get Thin specifically suggests that this increased energy expenditure would continue to last over a year long period, which is not supported by this study. Additionally, the authors of the study highlighted that there is a need to adhere to a very-low-carb diet, not just a high fat diet, in order for this short term effect to be observed. In contrast it has been previously shown that diets higher in fat but not extremely low in carbohydrate can actually lead to lower energy expenditures. In the scientific literature there is still some uncertainty about whether low carbohydrate diets lead to higher energy expenditures, with some meta-analyses showing no effect and others showing an effect. Therefore, there is some evidence for the claim made by the book. The second problematic part of the argument made by Eat Fat, Get Thin is the suggestion that a 100 kcal difference per day would lead to a 10 pound weight loss over a year. Previous work suggests that if a 100kcal difference was maintained long term would lead to approximately a 10 lb weight loss over 3 years. This is because as an individual’s weight changes so does the body’s requirements for energy which is why weight gains and losses do not continue in a linear fashion over time. It is also interesting that Eat Fat, Get Thin would make this argument as on the previous page Eat Fat, Get Thin specifically says, “If… you ate an additional 100 calories a day…you would gain ten pounds. After a decade you would gain one hundred pounds. This just doesn’t happen.” It appears that Eat Fat, Get Thin reverses their position to promote the effects of very-low-carbohydrate intake. Overall, this information appears to be overstated and misinterpreted to the reader.

There are several other studies cited by Eat Fat, Get Thin that we found to be misrepresented or overstated. For example, Eat Fat, Get Thin references the DIRECT trial and claims that this trial shows that a low-carb, high-fat diet showed greater weight loss than a low-fat diet. However, the group that was given the “low-fat” label by the researchers were not actually following a low-fat diet, as has been previously noted by others. Additionally, the carbohydrate levels were not very different between the two groups with the low-fat group consuming ~50% of their calories from carbohydrate whereas the low-carb group consumed ~40% of calories from carbohydrate. Instead the participants in the “low-fat” diet group were instructed to consume their typical diets and did not make any significant changes to their daily diets. There was, however, another group in the study that was not mentioned by Eat Fat, Get Thin. That group was following a version of the Mediterranean diet which instructed participants to keep their fat intake to under 35% of their daily calories. This level of fat intake was similar to the “low-fat” group, with only a 3% difference in calories from fat between groups. Of note, 35% fat intake is within the suggested fat intake range found in the Dietary Guidelines for Americans. When comparing this lower-fat Mediterranean diet to the prescribed low-carb diet there was no difference in weight outcomes. This study’s findings ultimately undermine the weight loss claims made by Eat Fat, Get Thin.

Eat Fat, Get Thin also tends to withhold study nuances from the reader. An example of this is a study by Kennedy et al. In this study mice were placed onto 1 of 4 diets: a ketogenic diet (78.9% fat, 9.5% protein, and 0.76% carbohydrate), a typical chow diet (6.5% fat, 23.5% protein, and 56% carbohydrate), a high-fat, high-sugar “obesogenic diet” (24% fat, 24% protein, and 41% carbohydrate), and a calorie restricted diet (66% calorie restricted). The obesogenic diet group gained weight, the low-fat diet group appeared to maintain their weight, and the ketogenic and calorie restricted diet groups both lost about equivalent amounts of weight. Eat Fat, Get Thin decided to compare the keto group to the control group (which has a higher carb content than the keto group) as they specifically state that “weight loss was greater than in rats fed a high-carb diet, even though they ate exactly the same number of calories”. While the results of the study do support the weight loss claim we do note that the mice on the low-carb diet lost their weight from the nonfat component of their weight. So, although there was a difference in weight between the control diet and the keto diet mice there was no difference in body fatness. The significant change in weight is mentioned but the non significant change in fat is withheld from the reader.

When considering review papers, Eat Fat, Get Thin also misrepresents the data. For example, Eat Fat, Get Thin cites a review paper of clinical trials comparing low-carb and low-fat diets. This review reported that 4 out of 8 randomized control trials showed better weight outcomes for low-carb diets when compared to low-fat diets at 6 months. However, the rapid initial weight loss for low-carbohydrate diets is well known and may involve changes in body water compared to low-fat diets. Importantly, this initial benefit in overall weight loss does not typically last over time. When we look at differences in weight loss at one year rather than just the first 6 months, we see that the difference is small and not statistically significant. This data is available in the same paper cited by Eat Fat, Get Thin. The book cites one other review paper worth discussing which is presented as the “final nail in the coffin for proving that high-fat diets did much better than low-fat diets for weight loss”. The main conclusion of the review, however, is that low-fat diets and high-fat diets show similar amounts of weight loss. There was a small but statistically significant difference observed between very rigorously delivered versions of very-low-carb diets when compared to low-fat diets. But even the difference in weight between these two groups was only about 2 pounds, which is clinically insignificant. Additionally, there was no difference in weight loss between low-carb and low-fat diets when comparing the less restrictive low-carb diets, which is the diet pattern prescribed by Eat Fat, Get Thin. Again, this data ultimately undermines the claim made by the book.

More recently, Ge et al. meta-analyzed 121 dietary randomized control trials which allowed for high-quality comparisons between 17 specific dietary patterns. This included low-carb and low-fat diets. The authors found that overall, low-fat and low-carb diets had similar weight outcomes at both 6 and 12 months. It would appear, based on the bulk of the scientific literature, that there is no meaningful long-term difference in weight loss between low-fat and low-carb diets. In conclusion, there is little to no evidence to support the claim that low-carb, high-fat diets are superior to low-fat diets for weight loss either in the broader literature or in the studies presented by Eat Fat, Get Thin. In fact, much of the research cited by the book undermines their claim and shows that there is little, if any, long-term difference between the effectiveness of these diets for weight loss. Additionally, Eat Fat, Get Thin often misinterprets and overstates the conclusions of studies discussed and withholds critical nuances of the studies presented to the reader.

Criterion 1.2. Are the references cited in the book to support the claim convincing?

0 out of 4

The book’s references received a score of 0, indicating that they generally undermine the book’s claim.  As noted above many of the references provided by Eat Fat, Get Thin show no differences between low-fat and low-carb diets on weight loss.

Criterion 1.3. How well does the strength of the claim line up with the strength of the evidence?

1 out of 4

This claim received a score of 1, indicating that the evidence is neutral or nonexistent for the claim. While low-carb diets may be a beneficial tool for some individuals attempting to lose weight, the current evidence, including that cited by Eat Fat, Get Thin, appears to show that in the long run, low-carb diets are no more or less effective than other dietary options on average.

Overall (average) score for claim 1

0.7 out of 4

Claim 2

Saturated fat does not cause heart disease.

Supporting quote(s) and page number(s)

Page 17: “Dietary fat, and saturated fat specifically, does not cause heart disease.”

Page 36: “Eating saturated fat does not cause heart disease.”

Page 40: “…could not find any association between saturated fat and heart disease.”

Page 92: “…there was no link between total fat or saturated fat and heart disease.”

Page 94: “saturated fat was not shown to be associated with increased risk of heart attack.”

Criterion 1.1. How well is the claim supported by current evidence?

1 out of 4

This claim received a score of 1, indicating that evidence for this claim is neutral or nonexistent. The primary study that Eat Fat, Get Thin uses to make the argument for saturated fat is by Chowdhury et al., which is a systematic review and meta-analysis of primarily epidemiological studies  examining the relationship between saturated fats and heart disease. Studies that included self-report measures of diet and studies that obtained circulating blood measurements of a variety of fatty acids were included in the meta-analysis. The self-report data showed that fat intake did not generally show a relationship to heart disease. The exception to this was that long chain omega-3 fatty acids intake appeared to be protective against heart disease. When looking at the studies that took blood draws and measured circulating blood fatty acids, there was 1 saturated fat (17:0, Margaric) that showed to be protective against heart disease. Eat Fat, Get Thin uses this finding to suggest that the intake of butter, which contains small amounts of margaric acid, will be beneficial. However, butter is higher in other saturated fatty acids, including stearic and palmitic acid. This should serve as a reminder that humans don’t typically eat individual saturated fatty acids in isolation and so the entirety of the food product should be considered. Confusingly, the book actually states that these two specific saturated fats may have a negative effect on cardiovascular disease, although the study actually showed no relationship. While Eat Fat, Get Thin does not mention this point to the reader, it appears to make this claim in an attempt to vilify carbohydrates, as these fatty acids are major products of de novo lipogenesis, or fat synthesis by the body. However, they provide no references for the claim that carbohydrate intake is responsible for circulating levels of these fats (stearic and palmitic acid).

One other key study presented by Eat Fat, Get Thin, is a review paper by Dias et al. The book uses this study to make the argument that saturated fat intake is not problematic for health if there is an adequate intake of omega-3 fatty acids. However, most of the data reviewed by Dias et al. actually shows that higher levels of saturated fat intake contribute to poor cholesterol levels and heart disease risk. The paper does highlight that many previous studies have not accounted for the intake of omega-3 fatty acids in their analyses. As omega-3 fatty acids may have a protective effect against heart disease, the authors suggest that future studies need to consider this as a variable. However, at no point does the cited paper present evidence that directly supports the hypothesis that intake of omega-3 fatty acids will actually provide protection in the presence of high saturated fat intake.

Most of the data referenced by Eat Fat, Get Thin to support their claim that there is no link between heart disease and saturated fat are generated from epidemiological studies, which we consider to be relatively unconvincing evidence. Additionally, many of the studies cited primarily rely on self-reported dietary data, which is typically considered to be unreliable. Therefore, we chose to look at more well-controlled studies, such as randomized controlled trials, as they are likely to provide better insight into the isolated effect of saturated fat on heart disease risk. In a review of 395 metabolic ward experiments (most lasting around 1 month in duration), removing saturated fat from the diet, in a variety of ways, led to significant decreases in both total and LDL cholesterol. Cholesterol is an important biomarker for heart disease, with LDL being a particularly strong biomarker for the development of heart disease. Additionally, small and medium sized LDL particles have also been linked to heart disease and are more prevalent when consuming diets high in saturated fat. We can also turn to other reviews and meta-analyses of randomized controlled trials which have also concluded that there is consistent evidence in humans that replacing saturated fat, particularly with polyunsaturated fat, lowers the risk of developing heart disease.

We feel that it is important to note that Eat Fat, Get Thin was apparently aware of the strong experimental data connecting saturated fat intake to reductions to cholesterol and heart disease. In a later section of the book, the book references a 2014 review that also concluded that there was convincing evidence from both randomized control trials and prospective cohort studies that partial replacement of saturated fat with mono- and polyunsaturated fats is likely to lead to decreases in total and LDL cholesterol. The paper also concluded that there was convincing evidence that replacement of saturated fatty acids with polyunsaturated fat will decrease the risk of cardiovascular disease, particularly in men.

One of the reasons fat replacement studies are important is that when saturated fat is removed from the diet it must be replaced by something else in order for the individual to maintain a consistent level of calorie intake. The swapping of foods has implications to an individual’s overall dietary patterns. For example, it is well known that replacing saturated fat in the diet with refined carbohydrate will not lead to improvements in heart disease risk. This highlights the need to consider the replacements being made, particularly in terms of actual food. A recent meta-analysis was conducted by Ge et al. looking at 121 dietary randomized control trials. The meta-analysis allowed the authors to compare 17 different dietary patterns with each other. They found that 2 diets, low-fat diets and the Mediterranean diet, showed greater improvements in LDL cholesterol when compared to low-carb diets. Additionally, the Mediterranean diet showed sustained decreases in LDL over a one year period while no other diet did. Although the Mediterranean diet is typically characterized as having moderate fat intake (~40% of daily calories) it is typically low in saturated fat (less than 7% of fat calories). These dietary pattern comparisons suggest that diets low in saturated fat are likely to lead to improvements in both cholesterol profiles and heart disease risk, particularly when compared to low-carb diets.

In summary, the evidence overall does not support the position that saturated fat does not play a role in the development of heart disease. At best, it appears that sufficient intakes of “healthier fats”, such as omega-3 fatty acids, may negate some of the negative effects that higher intakes of saturated fats may have on cholesterol and heart disease risk, although, no strong evidence of this is presented by Eat Fat, Get Thin. In humans it appears that substituting unsaturated fats for saturated fat in the diet is likely to improve an individual’s cholesterol profile and reduce their risk for heart disease.

Criterion 1.2. Are the references cited in the book to support the claim convincing?

1 out of 4

Eat Fat, Get Thin’s references received a score of 1, indicating poor support for the book’s claims. The majority of the studies cited by the book do not support its claims. In some cases Eat Fat, Get Thin appears to mischaracterize, overstate, or withold elements of the studies that are cited.

Criterion 1.3. How well does the strength of the claim line up with the strength of the evidence?

1 out of 4

The claim received a score of 1, indicating that the claim is greatly overstated.  As noted previously, while there is epidemiological evidence to support the claim made by Eat Fat, Get Thin there is also much that disputes it. Stronger forms of evidence such as randomized controlled trials and metabolic ward studies are unsupportive of the claim made by the book. Additionally, dietary patterns low in saturated fat appear to be beneficial for both cholesterol and heart disease outcomes, particularly when compared to dietary patterns higher in saturated fat. Overall, the claim made by the book does not line up with the bulk of the scientific literature available.

Overall (average) score for claim 2

1.0 out of 4

Claim 3

There is not a significant relationship between fat intake and cancer.

Supporting quote(s) and page number(s)

Page 166: “Let’s take a look at whether we should be worried about fat and cancer. This probably won’t surprise you by this point, but there is conflicting evidence.”

Page 166: “In some studies it was found that people who had more saturated fat might be at higher risk for more cancer. But was it the saturated fat…? It may not be the saturated fat at all.”

Page 167: “Large reviews have trouble finding consistent links between fat and cancer.”

Criterion 1.1. How well is the claim supported by current evidence?

2 out of 4

This claim received a score of 2, indicating that it is weakly supported by current evidence. Most of the research presented by Eat Fat, Get Thin is in relation to breast cancer and prostate cancer. So let’s first take a look at some of the arguments and evidence provided by the book as it relates to breast cancer. Eat Fat, Get Thin states, “Many large population studies found, for example, that increased fat intake was linked to breast cancer, but then when large randomized controlled experiments were done to assess true cause and effect, no link between dietary fat and breast cancer could be found.” To support this statement they cite a meta-analysis conducted by Brennan et al. which evaluated 15 prospective cohort studies. This study actually concluded that there was a link between saturated fat intake and breast cancer. Eat Fat, Get Thin suggests that there are randomized controlled trials disputing this conclusion, however, they provide no evidence of this. We do note that in the Brennan et al. paper the authors discuss two randomized controlled trials that evaluated the link between fat intake and breast cancer. It is possible that this is what Eat Fat, Get Thin is referring to. However, one of these RCTs actually did demonstrate a link between saturated fat and breast cancer while the other did not. Limitations of both RCTs are discussed by the authors, primarily that in these two studies many dietary and lifestyle factors were adjusted as part of the study interventions and therefore it is hard to isolate the specific role that fat may or may not have played. The paper actually concludes that reducing both total and saturated fat is likely to be beneficial for cancer outcomes. A more recent review of dietary patterns found that diets low in saturated fat are associated with lower breast cancer risk. Additionally, a population level study found a correlation between per capita fat intake in 88 countries and breast cancer incidence. They found a strong positive correlation suggesting that the higher a country’s fat intake the higher the rate of breast cancer incidence, although we do not consider this to be particularly compelling evidence as there are many behaviors, environmental, and lifestyle factors that can differ between countries and it is impossible to account for all of these variations. These data taken together suggest a possible relationship between breast cancer and saturated fat intake.

Turning to prostate cancer, Eat Fat, Get Thin provides some weak epidemiological evidence derived from a single food frequency questionnaire that found that individuals who consume more dairy products are more likely to develop prostate cancer. The book also cites a review paper that summarizes the evidence for the relationship between dietary factors and prostate cancer. This paper reports a link between saturated fat and prostate cancer, although the association between total fat intake and prostate cancer risk is inconsistent. Eat Fat, Get Thin uses this paper to argue that intakes of omega-3 fatty acids have been shown to reduce the risk of prostate cancer, which the paper does state, but withholds that they also found that increased saturated fat intake was associated with a higher risk of prostate cancer. One other piece of evidence that Eat Fat, Get Thin provides for their argument is an opinion paper, which calls for restrained enthusiasm around the topic of fat intake and prostate cancer. The paper actually provides references to a large amount of preclinical and case-control data demonstrating a link between fat and prostate cancer while urging caution when looking at human data. Particularly it highlights conflicting data found in observational and prospective cohort data in humans. This paper is used to try to undermine the claims that fat is related to both prostate and breast cancer risk. However, this paper was published several years before the papers previously cited by Eat Fat, Get Thin. This means that this opinion piece was published prior to the publication of the human data showing stronger links between fat and prostate and breast cancer risk.

When we looked for more recent studies and meta-analyses related to prostate cancer we found conflicting evidence. For example, a 2015 meta-analysis found no link between total fat and prostate cancer. However, in a more recent population level study published in 2019, known as the SABOR study, a relationship was observed between both total fat intake and saturated fat and the risk of developing prostate cancer. Although we do note that this study was published after Eat Fat, Get Thin was released. Another recent paper reviewed the current state of the literature and also highlighted that there is some disagreement in the literature. They found that most preclinical trials show a relationship between fat and prostate cancer while only some human trials demonstrate this relationship. They do however note that dietary patterns that are low in saturated fat (specifically, the Mediterranean diet and the DASH diet) appear to have more reliable evidence for their efficacy in protecting against developing prostate cancer. Overall we found that for prostate cancer the connection with fat does appear to be conflicting as Eat Fat, Get Thin suggests.

While breast cancer and prostate cancer are the cancers discussed by Eat Fat, Get Thin there may be others worth considering. A review cited by the book found weak evidence for a link between ovarian cancer and saturated fat. We also conducted a search for recent papers examining the relationship between cancers and fat intake. We found evidence, primarily from meta-analyses of observational studies, for relationships between total fat intake and bladder cancer, ovarian cancer, lung cancer, and endometrial cancer. Overall, in most of these cases it appears that omega-3 fatty acids appear to be protective whereas saturated fat appears to be problematic. In fact, this was a common theme we found throughout all of the literature we reviewed. Even in cases where dietary fat was not definitively linked to cancer, such as within the prostate cancer literature, it was often still recommended by the authors to reduce saturated fat intake. This was suggested in order to reap the health benefits of lower saturated fat intake, such as reductions in heart disease risk, while also potentially improving cancer outcomes.

In conclusion, there does seem to be some initial evidence for a link between some specific cancers and fat intake while evidence for others are more tenuous. The strength of the relationship appeared to vary based on the type of cancer. We specifically found conflicting information when investigating the relationship between fat and prostate cancer. Regardless, the general advice provided by most of the studies reviewed was that individuals should seek to decrease their intake of saturated fat and increase the intake of omega-3 fatty acids. Diet patterns that encourage low saturated fat and high omega-3 fatty acid intake such as the DASH diet and the Mediterranean diet also appeared to be more beneficial for reducing cancer risk.

Criterion 1.2. Are the references cited in the book to support the claim convincing?

2 out of 4

The book’s references received a score of 2, indicating that they provide moderate support for the book’s claim.  Although the cited studies did examine the association between fat and cancer they are often mischaracterized or crucial pieces of information are withheld from the reader.

Criterion 1.3. How well does the strength of the claim line up with the strength of the evidence?

2 out of 4

The claim received a score of 2, indicating that the claim is moderately overstated. In some cases, such as with prostate cancer, there did appear to be conflicting evidence. However, for other types of cancer, such as breast cancer, the relationship with fat was more apparent.

Overall (average) score for claim 3

2 out of 4

Overall (average) score for scientific accuracy

1.2 out of 4

Reference 1

Reference

Chapter 8, reference 6. Bier DM. Crit Rev Food Sci Nutr. 2015 Mar 16:0. and Lawrence GD. Adv Nutr. 4:294-302. 2013.

Associated quote(s) and page number(s)

Page 144: “The truth is there is no good evidence proving [Butters’] link to heart disease.”

Criterion 2.1. Does the reference support the claim?

1 out of 4

This reference received a score of 1, indicating that it offers little support for the claim. The paper by Bier is a broad discussion of papers and studies focused on saturated fat. However, the article does not specifically mention butter at any time, although butter is primarily saturated fat. The article points out that replacing carbohydrates in the diet with mono- or poly-unsaturated fats will reduce LDL levels. It also points out that replacing carbohydrates with saturated fat increases LDL. LDL is typically considered “bad” cholesterol and high levels of LDL is linked to the development of arterial plaque and heart disease. Other literature supports the view that high saturated fat intake typically leads to poor health outcomes by raising both LDL and total cholesterol. One of the main points of the article is that saturated fat and refined carbohydrates may have similar effects on cardiovascular disease outcomes. The overall conclusion of the article is that people should place more emphasis on eating “whole” or “less processed” foods. Overall, it would seem that reducing saturated fat would be beneficial. The article does not specifically talk about butter or the relationship that butter has with heart disease.

Reference 2

Reference

Chapter 5, reference 29. Wang et al. Nutrition, Metabolism and Cardiovascular Diseases 13(5):256-66. 2013.

Associated quote(s) and page number(s)

Page 98: “Many studies confirm that blood levels of saturated fat (palmitic, stearic, and palmitoleic acid) are significantly correlated with the development of type 2 diabetes and heart disease.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2 indicating it offers weak support for the claim. The study demonstrates that stearic acid is linked to heart disease but not palmitic or palmitoleic acids. In the paper after adjustment for age, gender, and several relevant lifestyle factors, stearic acid only in the phospholipid fraction was significantly and positively associated with CHD. Type 2 diabetes is not mentioned but reference 29 was indicated to support the heart disease claim only. Additionally, we would like to clarify for the reader that palmitoleic acid is actually a monounsaturated fatty acid not a saturated fatty acid as suggested by Eat Fat, Get Thin. 

Reference 3

Reference

Chapter 2, reference 13.  Liu et al. Am J Clin Nutr. 71:1455-61. 2000. and Yang et al. JAMA Intern Med. 174(4):516-24. 2014.

Associated quote(s) and page number(s)

Page 39-40: “Despite the data that flooded in showing that cholesterol and dietary fat may not be the real drivers of heart disease — that sugar and refined carbs are the true drivers of heart disease…medical associations and the food industry pressed onward with the promotion of a low-fat diet for heart health”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers little support for the claim and even refutes the main argument made by Eat Fat, Get Thin. The two studies cited by the book are observational data showing that specific  carbohydrates have associations with heart disease. The paper by Liu et al. showed that specific carbohydrates that spike blood sugar (defined by their glycemic index and load) are associated with heart disease. However, they did not find a relationship between either total carbohydrate or when considering all refined carbohydrate intake and heart disease. Rather the authors highlight that it is more likely the glycemic load of some refined carbohydrates that may be problematic, but only in those who are not healthy weight. The paper by Yang et al. found that individuals with high added sugar intake, but not total carbohydrate intake, had significantly increased risk of cardiovascular disease death. The highest level of risk was found in individuals who had greater than 25% of their daily calories coming from added sugars, which is well above average intake in the US and other affluent countries. The authors of the study specifically note that all major health organizations recommend restricting added sugars below this level. This statement itself refutes the claim of Eat Fat, Get Thin makes, that medical associations continued to make recommendations in spite of this knowledge. Additionally, the Dietary Guidelines for Americans recommend limiting total intake of discretionary calories, which include both refined sugars and solid fats, to 5%-15% of daily caloric intake combined. This amount is far lower than the intake level for the high risk group in this study. Therefore, Eat Fat, Get Thin’s claims that heart disease is driven by refined carbohydrate intake and not saturated fat and that medical associations are unaware of the risks of high refined carbohydrate intake are not supported by these studies. The study by Liu et al. actually refutes the claim that refined carbohydrates in general are associated with heart disease. More importantly neither of these studies tested or reported on the effects of saturated fat or whether there was a relationship between the combination of saturated fat and refined carbohydrates and heart disease. These studies simply show the isolated effects of some types of carbohydrates under specific conditions at intake levels not supported by major health organizations.

Reference 4

Reference

Chapter 8, reference 41. Elnagar et al. Planta Med. 2011 and Escrich et al. Curr Pharm Design. 17(8):813-30. 2011.

Associated quote(s) and page number(s)

Page 156: “As little as one to two tablespoons a day [of olive oil] lowers the risk of many cancers, including stomach, colon, breast, and lung cancer.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers some support for the claim. The study by Elnagar et al. evaluated the effects of a specific plant compound extracted from extra virgin olive oil on breast and prostate cancer cells in the lab. The purpose of the study was to try to find a possible reason why intake of extra virgin olive oil may provide protection from cancer on a cellular level. The paper by Escrich et al. is a review of studies related to olive oil and breast cancer and also discusses potential reasons why olive oil may be protective against the development of breast cancer, the paper largely focused on studies conducted in cell culture and animal models. However, neither of these papers suggest consuming “one to two tablespoons a day” as suggested by Eat Fat, Get Thin. Additionally, the effects of individual components of extra virgin olive oil and their effects on cells may not translate to humans due to a number of factors including diet complexity, bioavailability, etc. It is also important to note that these papers are primarily focused on breast cancer and do not talk about the other cancers listed by Eat Fat, Get Thin such as stomach, colon, or lung cancer and no other references are provided to support the claims for those types of cancer by the book. However, we would like to note that there is evidence that the Mediterranean diet, which uses plenty of olive oil, may be protective against a wide range of cancers. The high use of olive oil is often cited by researchers as a potential reason for the diet’s protective effects and was recently tested in a secondary analysis by the PREDIMED trial.

Reference 5

Reference

Chapter 12, reference 14. Udayappan et al. Clin Exp Immunol. 177(1):24-29. 2014

Associated quote(s) and page number(s)

Page 203: “We know that you can reverse diabetes by taking the fecal matter of a thin healthy person and putting it in a diabetic. I would say that eating potato starch is more appealing to most of us than getting a fecal transplant.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim.  The paper cited is a review paper discussing the possibilities and potential of modifying the gut microbiome to improve obesity and insulin sensitivity outcomes. Within this review, the authors specifically discuss a trial in humans where faecal matter was transplanted from lean participants to participants with metabolic syndrome. This transplant led to an alteration of the gut bacteria of some of the recipients but not all of them. Some of the transplants from lean individuals had no effect on those with metabolic syndrome. However, some of the donors were considered “super-faecal” donors because following their transplant individuals with metabolic syndrome showed great improvements in their insulin sensitivity. The authors of the paper thought that the reason some of the transplants were successful and others were not was because of the transfer of some specific bacteria that were found in a high amount in some of the lean donors but not others. Of note, there was no claim that any of the individuals who received a transplant “reversed” their diabetes, only that their sensitivity to insulin improved. Overall, what we can take from this study is that some bacteria may play a role in improving insulin sensitivity, although perhaps not reversing diabetes. It also suggests that not all lean individuals have a microbiome that would cause the reversal of diabetes, as suggested by Eat Fat, Get Thin. In fact, in the conclusion of the paper the authors remind the reader that there is no definitive proof that intestinal bacteria play a causal role in either obesity or insulin resistance.

Reference 6

Reference

Chapter 2, reference 24.  Suez et al. Nature. 514(7521):181-86. 2014.

Associated quote(s) and page number(s)

Page 43: “Even though we know that artificial sweeteners…alter gut flora or bacteria to promote obesity and type 2 diabetes,…they are still recommended by the ADA…”

Criterion 2.1. Does the reference support the claim?

3 out of 4

This reference received a score of 3, indicating that it provides only moderate support for the claim, primarily for the diabetes claim but only weakly for the obesity claim. The cited paper is a report of a series of experiments in both mice and humans. As studies in mice are preclinical and typically used to generate hypotheses for human studies we will focus on the human studies reported, however the mouse studies are fairly supportive of the diabetes claim made by Eat Fat, Get Thin. The authors report two analyses in humans. The first study describes an analysis of self-reported artificial sweetener intake in 381 individuals. The researchers found that individuals who self-reported higher intakes of artificial sweeteners also tended to have higher waist to hip ratios, fasting blood glucose levels, worse HbA1c levels, and performed worse on a glucose tolerance test compared to those with lower intakes. However, all 381 individuals in the analyses were non-diabetic and it is unclear if the observed differences between individuals were clinically meaningful. The analyses were all controlled for BMI in an attempt to isolate the effect of the sweetener intake from the impact of weight on health. However, as sweetener intake was significantly related to participants’ waist to hip ratio it is curious that the researchers did not perform sensitivity analyses with waist to hip ratio as a control variable rather than BMI. Waist to hip ratio is a stronger health indicator and of body fatness compared to BMI so controlling for waist to hip ratio would have allowed the research team to rule out the effects of body fatness rather than just height and weight. As the research team didn’t do this, we can’t rule out that the relationship between sweetener intake and the other health indicators was not just related to the individuals’ body fatness. The second experiment in the paper describes a feeding study conducted in 7 individuals. The researchers had the 7 individuals in the study consume the maximum amount of artificial sweeteners allowed by the FDA over 7 days, but did not forcibly change any other aspect of their diet or lifestyle. Of the 7 individuals, about half of them (4 individuals) had poorer glycemic response at the end of the 7 days while 3 showed no change. The four individuals who appeared to be negatively influenced by the sweeteners actually started the study with a very different gut bacteria profile than those who were unaffected. However, gut bacteria can be influenced by a variety of dietary and lifestyle factors. We cannot rule out that the observed changes in the four individuals were not induced by some other factors. No dietary or physical activity records were collected or reported by the researchers. Therefore, there is no way to rule out the potential influence of these lifestyle factors during the study. Overall, the study was conducted with an extremely small sample size, the effect of sweeteners was only apparent in half of the individuals tested, and there was no control over other factors that may have influenced response. At best, this data shows us that some individuals with a specific set of gut bacteria may be influenced to some extent by artificial sweeteners. Therefore, it is difficult to conclude that artificial sweeteners  “alter gut flora or bacteria to promote obesity and type 2 diabetes” as suggested by Eat Fat, Get Thin.

Reference 7

Reference

Chapter 10, reference 9.  Cortes-Giraldo et al. Food Chem Toxicol, 50(6):1951-54. 2012. 

Associated quote(s) and page number(s)

Page 176: “Some are concerned that beans contain lectins”.

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. The cited study reports on the extraction of polyphenols and lectins from a variety of beans, however, it does not report any data on the quantity of lectins that are contained within beans, how much remains after cooking, whether this quantity is concerning. Additionally, the paper is more heavily focused on the polyphenol content of the beans and the potential for polyphenols to agglutinate erythrocytes in cell cultures, but not in humans.

Reference 8

Reference

Chapter 8, reference 30.  Odia et al. World J Cardiol 7(3):144-49. 2015.

Associated quote(s) and page number(s)

Page 151: “In fact, [palm oil] has been shown to… reduce blood pressure and heart disease risk.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. The cited paper is a narrative review of palm oil and its relationship to heart disease. The authors of the study argue that palm oil contains equal parts saturated and unsaturated fatty acids along with high levels of antioxidants such as vitamin E. The main conclusion of the review is that palm oil can be consumed as part of a “healthy balanced” diet and that it is likely to have little effect on cardiovascular outcomes. The authors of the cited article do mention that replacing palm oil with mono- or polyunsaturated fats may provide some slight benefit to cardiovascular outcomes but the focus of the clinical trials discussed by the authors was largely on the effect of palm oil on the blood lipid profile. The authors of the article also conclude that there is a need to directly compare palm oil to other oils such as olive oil in order to understand the difference between these oils’ effects on heart disease and lipid profiles. Eat Fat, Get Thin claims that this reference supports the statement that palm oil has been shown to reduce blood pressure but this article never once mentions blood pressure. This study also does not make any statement that palm oil will reduce heart disease only that it appears to have similar heart outcomes as other cooking oils.

Reference 9

Reference

Chapter 1, reference 21. Accurso et al. Nutr Metab (Lond). 3:19. 2008.

Associated quote(s) and page number(s)

Page 17: “Diets very high in fat and low in carbs can reverse type 2 diabetes.”

Criterion 2.1. Does the reference support the claim?

3 out of 4

This reference received a score of 3, indicating that it offers moderate support for the claim. The article cited is a review of studies summarizing data around low-carbohydrate diets and diabetes. The paper reviews a variety of information around low-carb diets but highlights two studies around the idea that high-fat, low-carb diets can “reverse” diabetes. In the first study, 9 individuals participated in a low carb diet intervention for 2 weeks. Four of the participants were able to reduce their use of medication and 1 was able to discontinue use. However it is important to note that daily calorie intake was reduced by 1000 kcal on average. Additionally, no control diet was used as a comparison. Therefore, it is not clear whether the reduction and elimination of the medication can be attributed to the low-carb aspect of the diet or if it was the hypocaloric diet and reduction in weight that caused the change. It is also important to note that only one of the individuals was actually able to discontinue the use of their medication. In the second study, 28 individuals were placed onto a low-carbohydrate, ketogenic diet for 16 weeks. Nineteen of the individuals were taking medication at the start of the trial and 7 of them were able to discontinue their medication with 10 others being able to reduce their medication by the end of the study period. However, as with the previous study, there was no comparison group, so again it is not clear whether improvements were because of the diet or because of reductions in weight. Only about a third of the patients (7 of the 19) were able to discontinue use of their medications. This may actually highlight that ketogenic diets are not a universal cure for all individuals but may be a potentially useful therapy for some. Overall, the data shows that a very high-fat, low-carb diet is a viable diet option for controlling blood glucose and insulin sensitivity in some individuals. The data also show that a high-fat, low-carb diet shows some promise to “reverse” type 2 diabetes for some individuals.

Reference 10

Reference

Chapter 3, reference 14.  Kennedy et al. Am J Physiol Endocrinol Metab. 292(6):E1724-39. 2004.

Associated quote(s) and page number(s)

Page 60: “Another study on rats fed a ketogenic diet (very, very low-carb and very high fat) again found that weight loss was greater than in rats fed a high-carb diet, even though they ate exactly the same number of calories.”

Criterion 2.1. Does the reference support the claim?

3 out of 4

This reference received a score of 3, indicating that it offers moderate support for the claim. In this study mice were placed onto 1 of 4 diets: a ketogenic diet (78.9% fat, 9.5% protein, and 0.76% carbohydrate), a typical chow diet (6.5% fat, 23.5% protein, and 56% carbohydrate), a high-fat, high-sugar “obesogenic diet” (24% fat, 24% protein, and 41% carbohydrate), and a calorie restricted diet (66% calorie restricted). The obesogenic diet group gained weight, the low-fat diet group appeared to maintain their weight, and the ketogenic and calorie restricted diet groups both lost about equivalent amounts of weight even though the keto group consumed more calories. It is clear that Eat Fat, Get Thin is trying to compare the keto group to the control group (which has a higher carb content than the keto group) as the quote from Eat Fat, Get Thin states “weight loss was greater than in rats fed a high-carb diet, even though they ate exactly the same number of calories”. While the results of the study do support the weight loss claim we do note that the mice on the low-carb diet lost their weight from the nonfat component of their weight, likely water weight. So, although there was a difference in weight between the control diet and the keto diet mice there was no difference in body fatness. Therefore, this study actually raises some questions as to how beneficial the reduction in weight from nonfat tissue is for health. We would also like to clarify that the cited paper reports on an experiment in mice, not rats as claimed by Eat Fat, Get Thin.

Overall (average) score for reference accuracy

2.2 out of 4

Summary of the health-related intervention promoted in the book

Eat Fat, Get Thin recommends a two-part diet. The first part of the diet is pitched as a “21-day detox” diet. For this part of the diet, individuals are required to avoid a variety of foods and food constituents, including most fruits. They are encouraged to have fat at each meal. The diet recommends a moderate level of carbohydrate at each meal, mostly from non-starchy vegetables. Eat Fat, Get Thin also recommends taking a long list of daily supplements. These products are for purchase on the book’s website, and a monthly supply of supplements will cost well over $200. Daily physical activity is also recommended.

Following the “21-day detox” participants can transfer to the first stage of a “pegan” diet. The “pegan” diet still has a high level of food restriction but allows for more fruit, legumes, and grains. The “pegan” diet also maintains a high fat intake. Continued supplement use is also recommended. In the second stage of the “pegan” diet individuals are moved to a less restrictive eating pattern. This less restrictive diet allows for the reintroduction of most foods. It is still recommended to consume the prescribed dietary supplements.

Condition targeted by the book, if applicable

Eat Fat, Get Thin is primarily focused on weight loss/obesity, but also addresses a variety of chronic diseases.

Apparent target audience of the book

Eat Fat, Get Thin appears to be written for a general audience, particularly those who are concerned about their weight.

Criterion 3.1. Is the intervention likely to improve the target condition?

2 out of 4

The intervention received a score of 2, indicating that it is likely to have some effect on the main target condition, which is weight loss. However, much of the success of this weight loss is left to the individual’s discretion. For weight loss, the diet is likely to cause a caloric deficit due to the shift away from refined carbohydrates and processed food products, as demonstrated by numerous low-carbohydrate diet trials. However, this shift in intake may be more or less successful for some individuals as it is possible to get the same amount of daily calories from other food sources promoted by Eat Fat, Get Thin. When looking at heart disease and cancer, there is some concern regarding the promotion of saturated fat in the diet. A large portion of the food sources promoted by the book are high in saturated fat and so some caution is warranted. As noted previously, increased intakes of saturated fat is linked to both increased LDL cholesterol, risk for heart disease, and possibly increases the risk for some cancers. Furthermore, most of the data provided by Eat Fat, Get Thin to make their arguments is taken from epidemiological studies, a weaker form of evidence, whereas randomized controlled trials, which provide stronger evidence that often contradicts the claims made by the book, are largely ignored.

Criterion 3.2. Is the intervention likely to improve general health in the target audience?

2 out of 4

The intervention received a score of 2, indicating that it is likely to slightly improve the general health of the target population. However, the success of the diet likely hinges on a variety of choices made within the broad guidelines suggested by Eat Fat, Get Thin. As the major focus of the diet proposed by the book is decreasing or eliminating the intake of refined carbohydrates, soda, alcohol, and processed foods, most people are likely to improve their overall dietary patterns leading to modest weight loss in most individuals. The reduction in weight and body fat are also likely to lead to improvements in a variety of health outcomes. However, we do note that the elimination of refined carbohydrates and processed products from the diet are typical recommendations made by many diets, as well as the Dietary Guidelines for Americans. The main concern with the diet proposed by Eat Fat, Get Thin is the suggestion to increase the intake of saturated fat. As noted in the previous sections, high intakes of saturated fat can potentially increase risk for heart disease and possibly cancer. The supplements suggested by the book are costly and we find it unlikely that they will contribute to the overall health of the individual. Additionally, the book provides no evidence for the effectiveness of the supplements it recommends.

Criterion 3.3. Does the diet portion of the intervention promote an adequate nutrient intake for general health in the target audience?

3 out of 4

The diet received a score of 3, indicating that it is likely nutritionally adequate. The diet’s main focus is in reducing refined carbohydrate intake but it still allows for some small amount of fruit and starchy vegetables. It also allows and encourages the intake of unlimited amounts of non-starchy vegetables. Additionally, dairy, meat, nuts, legumes, grains and a variety of animal products are allowed in varying amounts throughout the diet phases. If the right foods are selected the diet should be nutritionally adequate, however this is more or less left up to the individual to figure out. This does leave room for nutrient inadequacies to possibly develop. Eat Fat, Get Thin also promotes the intake of a long list of expensive supplements, for sale on its website, which are costly and probably unnecessary.

Overall (average) score for healthfulness

2.3 out of 4