Metabolical: The Lure and the Lies of Processed Food, Nutrition, and Modern Medicine

Overall score

Scientific accuracy

Reference accuracy

Healthfulness

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

Book published in 2021

Published by Yellow Kite

First Edition, Paperback

Review posted January 19, 2024

Primary reviewer: Samuel Dicken

Peer reviewer: Seth Yoder

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

The primary cause of weight gain is a rise in insulin from consuming refined carbohydrates/sugar.

Supporting quote(s) and page number(s)

 

Page 110: “That doesn’t make glucose “good” – it raises insulin and drives obesity”

Page 152: “The glucose in the dietary sugar drives the insulin release, which drives the weight gain”

Page 176: “And so weight isn’t driven by dietary fat, which doesn’t raise insulin, but rather by dietary refined carbohydrate and sugar, which do.”

Page 185: “All of this adds up to a more rapid and higher insulin response with sugar, which drives weight gain.”

Page 186: “While rapid glucose spikes after refined starch lead to glycation and oxidative stress, it’s the insulin fluctuation that induces the other six subcellular pathologies (see Chapter 7), drives excess energy intake, and promotes obesity.”

Page 201: “In order for low-carb diets to be effective, you have to bring the insulin level way down so that the adipocytes can release their stored fat, or in the case of the keto diet, turn off insulin almost completely.”

Page 202; “The only diet that doesn’t work, never worked, and never will work is the processed food version of the low-fat diet. Remember Snack-Well’s low-fat cookies? No one lost weight because they were laden with sugar.”

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

2 out of 4

This claim received a score of 2 out of 4, meaning that it is weakly supported by current evidence. Metabolical argues that weight gain and obesity are driven by refined carbohydrate/sugar intake. This increases insulin, which drives energy intake and body fat storage. The book contends that dietary fat intake doesn’t drive weight gain. The book therefore claims that removing sugar is key to treating chronic disease.

Although refined carbohydrates probably do contribute to weight gain, a number of lines of evidence suggest that the impact of refined carbohydrates on insulin secretion is probably not the main determinant of body fatness. Key arguments are summarized in this review paper, and we highlight a few of them below.

1. Genetic studies find that the biology underlying obesity involves genes in the brain, not blood glucose or insulin.
2. Similarly, the effective new class of weight-loss drugs (GLP-1 receptor agonists) target satiety centers in the brain, while actually increasing insulin secretion around meals (discussed in more detail below).
3. Tightly controlled studies in mice report that dietary fat is more fattening than dietary carbohydrate, including sugar. Given that mice and humans have similar carbohydrate metabolism and insulin biology, it’s unclear why the supposed uniquely fattening effects of carbohydrate wouldn’t apply to mice.
4. Diet trials in humans report that low-fat/high-carbohydrate and low-carbohydrate diets both cause weight loss.

Metabolical suggests that the glycemic index of carbohydrates (how fast they are absorbed) is an important determinant of body weight: “The reduction in the rate of absorption also reduces the glycemic excursion in the blood, keeping the insulin response down, and reducing energy deposition into fat tissue.” (p.182), “But Real Food is glucose plus protein plus fat plus fiber. Those other macronutrients, or lack thereof, influence the glucose’s absorption in the intestine, the insulin response that follows, and risk for weight gain.” (p. 185). However, this is weakly supported. Diet trials tend to suggest that glycemic index/load itself has little or no impact on weight loss.

The book then suggests that by taking carbohydrates out of the diet, people will eat less and lose weight: “if none of these are true, but your weight is still a problem,… you might try a very low-carb diet to suppress insulin release.” (p.147-8), and “Conversely, if you take the carbs out and just eat the fat (as in low-carb and ketogenic diets), people eat less.” (p.281). While cutting out carbs does cause weight loss, the problem with the argument in Metabolical is that cutting out dietary fat does too. Diets varying in macronutrient composition (being low fat or low carb) tend to have similar weight loss outcomes over 12 months.

The book also suggests that meal replacement diets are ineffective for weight loss, because these diets don’t drive down insulin: “the no-food diet – partial meal replacement programs like Slim Fast, Medifast, and, most recently, Soylent. Some of these use a corn syrup base and virtually all of them drive up insulin. Despite the testimonials you see on TV, the controlled trials say they don’t work. In fact, a meta-analysis demonstrated a mean weight loss at one year of about sixteen pounds, only five pounds better than a very-low-calorie diet. These substitutions don’t get the insulin down – even when these formula diets contain slow-digesting starch instead of rapidly absorbed sugar.” (p.203). Despite the book claiming that such diets ‘don’t work’ as they drive up insulin, the cited review from 2003 still showed they produced more weight loss than a standard low-calorie diet.

Another reference Metabolical uses to support the idea that meal replacement doesn’t work is from 1983. Metabolical was published nearly 40 years after this study, and numerous others have since been done. These studies show greater weight loss with increasing use of meal replacements, regardless of sugar content. In fact, some of the strongest evidence for weight loss comes from randomized controlled trials of complete meal replacement diets, with over 50% of calories coming from carbohydrates. It’s notable that these meal replacement studies tend to report greater 12-month weight loss than the low-carb diet advised by Metabolical.

Regarding the role of insulin for weight change, Metabolical also argues that drugs do not result in weight loss as they also do not get insulin down: “especially when you consider the fact that none of them actually cause weight loss because they don’t get the insulin down either” (p.203). This quote refers to liraglutide, a weight loss drug which has been shown to produce ~5kg weight loss despite increasing meal-related insulin release. Newer drugs that also stimulate insulin release show even greater weight loss. Therefore, wider evidence also doesn’t support that insulin secretion is the primary driver of weight gain.

Despite this, added sugars in the diet can cause weight gain (such as sugar-sweetened beverages). But this is probably because they increase calorie intake, leading to fat storage, rather than sugar per se increasing insulin levels.

In summary, the evidence to date weakly supports the idea that the primary cause of weight gain is eating refined carbohydrates/sugar, via their effect on insulin release. Refined carbohydrate, refined sugar, and the processed foods that contain them probably do contribute to weight gain, but they probably aren’t as central as claimed in the book, and they probably don’t act primarily via insulin. And, low-carbohydrate and high-carbohydrate diets both cause weight loss.

Overall (average) score for claim 1

2.0 out of 4

Claim 2

Refined carbohydrate/sugar is the primary cause of insulin resistance and type 2 diabetes, independent of calorie intake.

Supporting quote(s) and page number(s)

Page 39: “In fact, the largest study of heart attacks in the US revealed that 66 percent of the victims had metabolic syndrome. And the primary driver? Insulin resistance. And its primary driver? Our out-of-control sugar consumption.”

Page 59: “Econometric analysis is more conducive to nutritional research, and is how we proved that sugar is causative for type 2 diabetes.”

Page 62-3: “It’s clear that sugar and processed food drive obesity, heart disease, stroke, diabetes, and fatty liver disease”

Page 151: “we’ve learned that sugar, the main component of processed food, is the primary driver of four chronic diseases.” [diabetes, heart disease, NAFLD, tooth decay]

Page 152: “In particular, dietary sugar, even more than starch, drives the metabolic reactions that lead to type 2 diabetes”

Page 157: “Sugar is a specific driver of insulin resistance”

Page 179: “Rather, the data show that sugar is a direct cause of metabolic syndrome”

Page 227: “That’s why, when consumed chronically and in high doses, fructose is similarly toxic and abused, unrelated to its calories or effects on weight. That’s why our children now get the diseases of alcohol (type 2 diabetes, fatty liver disease), without ever taking a drink.”

Page 325-6: “Sugar uniquely drives metabolic disease apart from its calories”

Page 354: “Every country consuming the Western diet has increased its prevalence of NCDs, and sugar is the driver.”

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

2 out of 4

This claim received a score of 2 out of 4, meaning that it’s weakly supported by current evidence. Metabolical argues that refined carbohydrate/sugar consumption is the main cause of insulin resistance and type 2 diabetes, and that this is independent of calorie intake or body weight. The book then claims that removing sugar is key to improving insulin resistance and treating diabetes.

Currently, the leading understanding of how insulin resistance and type 2 diabetes develop is that they are primarily due to overconsumption of calories and body fat gain, together with low physical activity, rather than caused by a specific nutrient. Excess calorie intake and fat gain lead to excess fat storage in visceral or ectopic fat (such as in muscle, liver and the pancreas). Insulin resistance happens before type 2 diabetes.

This concept is supported by strong evidence. Several large, rigorous studies (randomized controlled trials) have shown that weight loss greatly reduces the risk of developing type 2 diabetes among people with pre-diabetes, even when it’s done with a higher-carbohydrate, low-fat diet. In fact, if the weight loss is large enough, it can even put established type 2 diabetes into remission.

However, whether insulin resistance and metabolic disease develop depends on where the excess energy is stored. The energy surplus can also be stored in fat under the skin (subcutaneous fat), which tends to not have harmful effects. Energy storage can vary greatly, based on factors such as genetics, age, ethnicity or physical activity levels. As a result, not all people with obesity are insulin resistant or diabetic. Conversely, people with normal weight or overweight might still face these issues if they have a lot of fat stored in their liver and pancreas.

Metabolical however, argues that the primary driver of insulin resistance and type 2 diabetes is sugar consumption per se, independent of calorie intake. The book repeatedly refers to sugar as being toxic and states that fat is not toxic, except for trans-fats: “Conversely, we now know that dietary fat is not toxic (aside from trans-fat), and some fats can be therapeutic.” (p.11). This is weakly supported overall. The impact of sugar on insulin resistance actually varies depending on what it is replaced with in the diet. In general, randomized controlled feeding trials show that replacing the same amount of energy from carbohydrates (particularly refined starches and sugars) for saturated fats leads to similar effects on insulin sensitivity and HbA1c (a measure of blood sugar control). In contrast, replacing these carbohydrates with polyunsaturated or unsaturated fats tends to improve insulin sensitivity and HbA1c.

Following the claim that sugar causes insulin resistance and type 2 diabetes, Metabolical argues that lowering insulin is needed to treat metabolic disease: “Every diet that reduces insulin burden by improving insulin sensitivity… reduces the burden of metabolic disease… The difference between success and failure for both obesity and NCD reversal is whether you get insulin down and keep it down.” (p.199). And therefore, Metabolical recommends reducing sugar or carbohydrate intake as the primary intervention for insulin resistance or diabetes: “…if you’re insulin resistant (one in two people), you likely need to restrict refined carbohydrate and sugar in order to reduce four of the eight subcellular pathologies (glycation, oxidative stress, mitochondrial dysfunction, and insulin resistance). However, if you already have type 2 diabetes (one in ten people), you might have to eschew carbohydrate completely for a time…” (p.202).

To support this, Metabolical cites a Virta Health study to indicate the effectiveness of a low-carb treatment diet for diabetes (p.151). The study shows that a low-carb diet with strong support can be helpful for managing diabetes. However, it doesn’t show that this happened independent of calorie intake. Low-carb diets generally cause people to eat fewer calories, even if they aren’t deliberately restricting, and participants in the intervention (continuous care) group on average lost 14 kg (30 lbs). They also received intensive support and education that the other group (usual care) did not get, and the study was not randomized. This study is consistent with the leading idea that insulin resistance and type 2 diabetes risk mostly revolve around calorie intake and body fatness (although low-carb diets also have the added benefit for managing established diabetes that they reduce the amount of glucose the body has to deal with).

The book also claims that a study by the author (but doesn’t actually cite it), shows that sugar causes diabetes: “We then published our landmark fructose restriction study (see Chapter 20) in the journal Obesity in 2016, which demonstrated causation between sugar consumption and metabolic syndrome.” (page 50). Adolescents were provided with study food for 9 days. This diet reduced their self-reported sugar intake from 28% to 10%. The difference was made up with starch. After the diet, glucose tolerance and hyperinsulinemia both improved. However, importantly, participants lost weight on the diet. 33/43 participants could not eat all of the food to achieve weight maintenance. Therefore, this study doesn’t demonstrate that the metabolic benefits are independent of weight loss. And, there was no control group, which makes the findings harder to interpret. Of note, the low-sugar diet also included processed foods such as hot dogs, pizza, bean burritos, baked potato chips, and popcorn, the types of foods the book argues cause metabolic disease.

Strong evidence indicates that weight loss drives improvements in metabolic health, including insulin resistance and diabetes. For example, total meal replacement diets with at least 40% of energy from carbohydrates lead to remission of type 2 diabetes and improvements in insulin sensitivity. The chances of remission and improvements in insulin sensitivity increase with the amount of weight loss. Trials with lower-carb diets or low GL or GI diets do not appear to be more effective in improving metabolic outcomes such as type 2 diabetes, insulin resistance or blood sugar control, compared with higher-carb or high GL or GI diets. And, in contrast to the claim made, the effect of changing sugar intake on diabetes development or insulin resistance would not appear to be strengthened by factoring for energy intake or weight change.

In summary, consumption of refined carbohydrates/sugar probably contributes to insulin resistance and type 2 diabetes, but they don’t appear to be its primary cause, and their effects appear to occur mostly via calorie intake. Some evidence suggests a direct effect of sugar on metabolic health. However, the evidence demonstrating adverse effects of sugar on diabetes or insulin resistance tends to use large amounts of liquid fructose, tends to be confounded by an increase in calorie intake, are not compared to a low-sugar diet providing the same amount of calories, and don’t necessarily represent the types of food people usually consume. Importantly, other macronutrients (e.g. types of fats) can also affect the risk of developing metabolic disease to a similar or greater extent to carbohydrate/sugar consumption. Evidence to date largely supports that the effect of sugar on metabolic outcomes is mediated by excess energy intake. The limitations mentioned above limit the ability to conclude any direct link between sugar and metabolic outcomes.

Note: at one point, the book mentions that fructose as whole fruit is protective of diabetes and heart disease: “Our ancestors didn’t have the health implications associated with fructose because they ate the whole fruit”(p.259-60). However, this isn’t emphasized in most of the book’s discussions about sugar. Generally, the book implicates sugar from all dietary sources as harmful, without distinguishing between the sugar found in whole fruits and other forms of dietary sugar.

Overall (average) score for claim 2

2.0 out of 4

Claim 3

Sugar is addictive.

Supporting quote(s) and page number(s)

Page 9: “We have the data to show that sugar is addictive and keeps us coming back for more.”

Page 60: “Another reason that patients can’t or won’t alter their diets is that they’re abusing sugar- the food additive that’s most addictive”

Page 78: “fructose… is addictive”

Page 276: “Oh, and by the way, sugar is addictive.”

Page 282: “Human imaging studies also support the contention that sugar, and specifically the fructose molecule, is addictive.”

Page 283: “Animal studies also show that sugar, and specifically the fructose molecule, is addictive. … it’s now obvious- sugar is addictive”

Page 285: “…sugar isn’t a food… and a sizable percentage of the population is addicted.”

Page 352: “Education alone hasn’t solved any substance abuse. It didn’t solve alcohol and it didn’t solve tobacco. It didn’t solve heroin or crystal meth or cocaine. And it’s not going to solve sugar. …Remember, we’re dealing with an inherently addictive compound in sugar, and it’s been infused into the majority of processed foods.”

Page 354: “Sugar is clearly abused, because it’s addictive in a percentage of the population.”

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

2 out of 4

This claim received a score of 2 out of 4, meaning that it is weakly supported by current evidence. Metabolical argues that sugar is inherently addictive. The book discusses substances in food and drink that may be addictive (Chapter 21). These include salt, caffeine, fat, and sugar. Metabolical says that only sugar and caffeine have addictive properties in Western diets, but sugar is the most addictive (p.280-286). The book argues that salt and fat are not addictive. The evidence we reviewed suggests that some foods may trigger addiction-like eating behavior in some people, but this is not just about sugar (or caffeine), and some of the most problematic foods don’t even contain sugar at all.

Food addiction is the idea that we can be addicted to food, similar to how people develop addictions to drugs. Whether someone has food addiction has been most commonly determined using the Yale Food Addiction Scale (YFAS). YFAS is based on behavioral characteristics suggestive of addiction. It’s modified from the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) definition for substance-use disorders. Estimates using YFAS place food addiction prevalence at around 20% and 15% in the US). Food addiction is more common in people with eating disorders, or living with overweight/obesity (24.9%).

The concept of food addiction is controversial. There is disagreement whether food addiction is useful or a valid concept. This is because we have to eat food to live, and others have suggested that food (substance) addiction is actually a behavioral eating addiction.

Not all foods are equally associated with being addictive. Food addiction has been most closely associated with highly processed, or ultra-processed foods, rather than minimally processed foods such as fruits or vegetables. The foods that are most associated with addiction-like eating behavior are typically combinations of carbohydrate and fat, and they often don’t contain sugar at all (e.g., French fries, pizza). Ultra-processed foods are highly varied in their qualities. There could be a number of factors that make them have addictive-like properties. For example, their high fat, salt, and sugar content, non-nutritive sweetener content, and other characteristics (such as packaging, energy density, or palatability) have all been implicated in food addiction. 

Some ultra-processed foods have similarities with addictive substances (e.g. drugs), being substance dense, and rapidly delivering the substance in question. In particular, ‘hyper-palatable foods’ containing combinations of fat, carbohydrates (sugar and non-sugar components) and salt, are suggested to have addictive properties. These combinations are not typically seen in minimally processed foods.

Metabolical however, does not consider all these factors to be addictive. Instead, Metabolical claims that sugar is the addictive component of food, and cites a study to support this. In the study, participants completed the YFAS, and then rated 35 foods varying in nutrient content on how much they are associated with addictive-like eating behaviors. The authors found that the extent of processing of a food was a large predictor of whether a food exhibited higher ratings of addictive-like behavior. For example, foods such as chocolate, ice cream and french fries were more frequently described as problematic than cucumber, beans and broccoli.

Furthermore, both the glycemic load (GL) and fat content of foods were strong predictors of problematic food ratings (salt was not added to models due to collinearity with fat). GL was particularly predictive for people with a high YFAS score. However, GL was a stronger predictor of problematic food ratings than sugar or net carbohydrate, suggesting other influential factors (e.g. lack of fiber). Another review cited in the book to argue that only sugar and caffeine have hedonic properties in food and drink actually concluded that processed foods with sweeteners (sugar and non-nutritive sweeteners) and fats had the greatest addictive potential. However, the focus of this review was to try and define what food addiction is, rather than to find the addictive properties of foods.

The most problematic foods for addictive-like eating identified in the study above are all combinations of fat and carbohydrate, either savory (starch, fat, salt) or sweet (sugar, fat). These combinations have been used to create a formal definition for highly palatable foods (termed hyper-palatable foods). These foods are also suggested to potentially be addictive. However, it’s important to note that the potentially addictive properties of food aren’t all about sugar– savory foods with no added sugar can also be “addictive”.

Most evidence on sugar addiction comes from lab and rodent studies, or cross-sectional data from imaging/clinical studies looking at responses to foods. For example, evidence of addiction to sugar, including withdrawal symptoms, has been reported in rats. A review paper cited in Metabolical and co-written by the book’s author (p.277) even states that sugar addiction has not been demonstrated in humans. In fact, they state that fat and salt content may be driving the addictive potential. Other reviews have also concluded that there is insufficient evidence to support addiction to sugar per se in humans. That said, sugar could contribute to the addictive potential of certain foods, just probably not in the dominant way portrayed in Metabolical.

In summary, the claim that sugar per se is addictive is weakly supported. There is evidence that some people may display aspects of food addiction, and some foods may have addictive-like properties. However, there is uncertainty around the concept of food addiction itself. If one accepts the idea that foods can be addictive, there is then further uncertainty as to what food properties drive addiction. People eat foods, not isolated nutrients, and the evidence suggests that the “addictiveness” of some foods is likely to result from a combination of factors including sugar, starch, fat, salt, and other food properties.

Overall (average) score for claim 3

2.0 out of 4

Overall (average) score for scientific accuracy

2.0 out of 4

Reference 1

Reference

Chapter 22: Food Fraud, reference 1. Oceana. Oceana Finds Seafood Fraud Persists, More Than 20% of Samples Mislabeled, 2019.

Associated quote(s) and page number(s)

Page 287: “It’s estimated that 20 percent of the seafood sold is mislabeled,”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2 out of 4, meaning that it weakly supports the claim.

The reference is a web page from Oceana, a non-governmental organization. It is a press release of a report into mislabelling of seafood. The actual report and fact sheets are in a link within the text of the press release. This is not a peer-reviewed publication.

The report suggests that 1 in every 5 fish is mislabelled. But, it is unlikely that the approach used to obtain samples of fish is representative of the overall fish market. For example, the report only considered 449 samples from 27 cities in 25 US states.

Importantly, these samples were of seafood types not covered in the Seafood Import Monitoring Program reports. Indeed, as has been noted elsewhere, the report aimed to select fish species with previously known high rates of mislabelling. Therefore, the sample is non-random and likely an overestimate of mislabelling.

Other issues include inconsistency in determining mislabelling, with some species being cross-referenced using generic common names, and others with scientific species names. For example, the report used specific scientific naming for labeling types of yellowtail fish, but vague information for labeling seabass, with no consideration for the type. This leads to inconsistency in determining the rate of mislabelling.

Reference 2

Reference

Chapter 13: Food in the Time of Corona, reference 7.  Viner and Whittaker. Lancet: 395(10239): 1741–1743.

Associated quote(s) and page number(s)

Page 195: “But the mind-boggling fact about COVID-19 is that it affects every organ in the body. For instance, a syndrome of inflammation of the blood vessels, called Kawasaki disease, has affected young children in New York City and Italy,”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2 out of 4, meaning that it weakly supports the claim.

The reference is a Comment in the Lancet journal, reporting of ‘Kawasaki-like disease’ in 10 children in Italy, during COVID-19.

The paper does not strongly support that COVID-19 leads to Kawasaki disease. Instead, it highlights key differences between Kawasaki disease and the observed ‘Kawasaki-like disease’: “These differences raise the question as to whether this cluster is Kawasaki disease with SARS-CoV-2 as the triggering agent, or represents an emerging Kawasaki-like disease characterized by multisystem inflammation”. There is no mention of New York City in the Comment or in the original study. And, as a discussion of a small case series in Italy, the Comment is greatly limited in being able to draw a causal link between COVID-19 and development of the disease.

Reference 3

Reference

Chapter 21: Food Addictions, reference 23. Paoli et al. Eur J Clin Nutr. 2013:67(8):789-96.

Associated quote(s) and page number(s)

Page 281: “So-called high-fat foods preferred by people are almost always also high in carbohydrate (e.g., potato chips, pizza, donuts) – then add sugar, and preference for high-fat foods goes up even more. Conversely, if you take the carbs out and just eat the fat (as in low-carb and ketogenic diets), people eat less.”

Note: a separate reference was provided for “as in low-carb”.

Criterion 2.1. Does the reference support the claim?

4 out of 4

This reference received a score of 4 out of 4, meaning that it offers strong support for the claim.

It is a review of therapeutic uses of very-low-carbohydrate, ketogenic diets. The review suggests there is strong evidence that ketogenic diets can be used for weight loss. This could be from a reduction in appetite and lower energy intake, or from improvements in metabolic efficiency. The review suggests that ketogenic diets may lead to eating less, but that ketogenic diets may have metabolic advantages to support a calorie deficit.

Reference 4

Reference

Chapter 28: The Case for Real Food, reference 3. U.S. Census Bureau. “Historical Households Tables”, 2019.

Associated quote(s) and page number(s)

Page 367: “In 2018, there were 127.6 million households in the US,”

Criterion 2.1. Does the reference support the claim?

4 out of 4

This reference received a score of 4 out of 4, meaning that it strongly supports the claim.

The reference is a link to the US Census Bureau. This is a trusted government page. The page does not directly provide support for the claim, but requires clicking on the first Excel file on the page. This reports that in 2018, there were 127.6 million households in the US.

Reference 5

Reference

Chapter 16: What and How Fetuses, Infants and Toddlers Eat, reference 17. Cohen et al. Am J Prev Med. 2018 Jun;54(6):727-735.

Associated quote(s) and page number(s)

Page 233: “Project Viva examined the associations between pregnancy, cognition, and childhood sugar consumption in the form of sugar sweetened beverages, other beverages (diet soda, juice), and fruit. Among 1,234 mother-child pairs enrolled, a mean maternal sucrose consumption of 50 grams/day consistent with the upper limit of current USDA guidelines – negatively impacted mid-childhood cognitive testing. Also of note, prenatal diet soda consumption was shown to negatively impact mid-childhood verbal scores as well.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2 out of 4, meaning that it weakly supports the claim.

It is a prospective observational study of 1,234 mother-child pairs (a subset of the Viva Health study). It reports associations between maternal and childhood sugar consumption and childhood cognition scores.

Maternal food intake was based on a food frequency questionnaire (FFQ). The FFQ asks how frequently people consume a given portion size of a food item. This FFQ contained about 140 foods, and was asked during the first and second trimester. Fruit intake was determined from 13 items, soda from 3 questions, diet soda from 3 questions, and fruit juice from 5 questions. Fructose and sucrose intake were calculated from all FFQ items.

Cognitive tests were performed by research staff when children were on average 3.7 (early childhood) and 7.7 (mid-childhood) years old. Tests included the Kaufmann Brief Intelligence Test and Peabody Picture Vocabulary Test.

Maternal sucrose consumption averaged 49.8 grams/day. As sucrose consumption increased, this was significantly associated with some childhood cognition scores decreasing, but not all. Out of 4 mid-childhood cognition outcomes, only 2 were significant. Another 2 early-childhood outcomes were also not significant. Out of 36 analyses of maternal sugar/sources of sugar intake and childhood cognition, only 5 demonstrated a significant association. These findings were after taking into account important confounders, including maternal age, BMI, education, ethnicity, smoking status, income and child’s sex. Other adjustments such as for maternal intelligence, did not alter the final models.

The authors then took into account that there were 36 analyses. They adjusted for the fact that they made lots of statistical comparisons and this can increase the risk of false positives. When this was done, the associations between sugar intake and cognitive outcomes weren’t significant, and only one association remained significant. This was an inverse association between higher maternal diet soda consumption and lower mid-childhood cognition.

The language in the claim (“negatively impacted”) implies causality. However, this single observational study is limited in being able to make a causal link between sugar intake and childhood cognition.

Reference 6

Reference

Chapter 8: Checkpoints Alpha, Bravo, Charlie: Nutrient-Sensing and Chronic Disease, reference 11. Erkin-Cakmak et al. J Clin Endocrinol Metab. 2019; 104(7):3003-3011.

Associated quote(s) and page number(s)

Page 129: “But on the other hand, when a cell has too much ATP, AMP-kinase gets turned off. Mitochondria aren’t burning, and the cell will divert the pyruvic acid to make structural components. Anything that impairs AMP-kinase will drive fat synthesis and worsen insulin resistance. And what food impairs AMP-kinase the most? Sugar, of course.”

Note: this is one of two references for: “Sugar, of course”.

Criterion 2.1. Does the reference support the claim?

1 out of 4

This reference received a score of 1 out of 4, meaning that it weakly supports the claim.

This reference is a non-randomized trial of children living with obesity and metabolic syndrome. The author of Metabolical, Robert Lustig, is one of the study’s authors.

51 children were provided with study food for 9 days. The diet lowered their self-reported sugar intake from 28% to 10% of energy intake, and fructose from 10% to 4%. The difference was replaced with starch. The researchers then looked at the impact of the 9 days of lower sugar and fructose on fat synthesis, insulin sensitivity and other measures. 43 completed the trial, but only 20 were analyzed in this study as they had suitable data at baseline (day 0) and day 10.

The researchers found that from day 0 to day 10, fat synthesis had dropped, with reductions in liver fat and circulating insulin. However, the claim is that sugar impairs AMP-kinase activity. The paper reports measures of fat synthesis and insulin levels. But, the study did not measure AMP-kinase, so it does not provide evidence that the change in fat synthesis and insulin was caused by a change in AMP-kinase.

And, despite the study intending to hold calorie intake constant, 15/20 children lost weight, with an average loss of 1.1kg over 9 days. The lack of a control group limits the ability to determine whether these changes were due to changes in sugar intake per se. So, the study’s findings could just be from weight loss.

Reference 7

Reference

Chapter 19: reference 6. Rivers and Kantor. Nutr Rev. 2020;78(10):787-797.

Associated quote(s) and page number(s)

Page 260: Metamucil is a soluble fiber (psyllium), but has no insoluble fiber. Furthermore, thus far Metamucil hasn’t succeeded as a stand-alone therapy for type 2 diabetes. It has been shown to improve cholesterol and insulin, but only after a healthy diet was instituted. It did nothing to reverse the effects of a bad diet, and the FDA refused to approve even a qualified health claim.”

Criterion 2.1. Does the reference support the claim?

0 out of 4

This reference received a score of 0 out of 4, meaning that it contradicts the claim.

The paper is a US Food and Drug Administration (FDA) review of a health claim for psyllium husk to reduce the risk of type 2 diabetes.

The claim states that the FDA did not approve a qualified health claim. However the reference says the opposite. A health claim was not approved for psyllium husk, but a qualified health claim was. This allows the use of the following: “Psyllium husk may reduce the risk of type 2 diabetes, although the FDA has concluded that there is very little scientific evidence for this claim”, or “Psyllium husk may reduce the risk of type 2 diabetes. FDA has concluded that there is very little scientific evidence for this claim.”

The claim was that psyllium did ‘nothing’ to reverse the effects of a bad diet. The FDA review concluded that 1 of 6 moderate-high quality randomized controlled trials showed a benefit on glucose and insulin resistance. In this study, psyllium husk was compared with guar gum and a standard diet. The significant improvements in insulin and cholesterol with psyllium husk were after participants were advised on a healthy diet. This was before they got randomized to one of the groups, and compared with the group that continued to follow the healthy diet advice only.

Reference 8

Reference

Chapter 25: Real Food is Good for the Planet, reference 2. Food and Agriculture Organization: Tackling Climate Change through Livestock, 2013.

Associated quote(s) and page number(s)

Page 334: “However, pinning our problems on cow farts and burps is a bit of hyperbole because this is a symptom and not a cause of the problem. According to the Food and Agriculture Organization (FAO), livestock- including cows, pigs, sheep, and other animals are responsible for about one-seventh (14.5 percent) of global greenhouse gas (GHG) emissions. Ten percent of that is methane production due to natural sources (e.g., decaying vegetation and bacteria in swamps). But human activity makes up a whopping 75 percent.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2 out of 4, meaning that it weakly supports the claim.

The reference is a link to a landing page of the Food and Agriculture Organization (FAO) for the Animal Production and Health Division (NSA). The FAO is considered a credible source. The landing page provides no detail on global greenhouse gas (GHG) emissions from livestock.

It is only after clicking through two separate links is there a statement which says: “Livestock supply chains account for 14.5 percent of global greenhouse gas (GHG) emissions.” (from ‘Livestock and Climate Change’: https://www.fao.org/livestock-environment/en/ and then onto ‘Livestock Environmental Assessment and Performance (LEAP) Partnership’: https://www.fao.org/partnerships/leap/en/). There is no other detail on how this value was obtained by the FAO.

There is no obvious support for the subsequent claims regarding methane production and human activity, even after clicking on links on the webpage (and are not supported by any other references).

Note: At some point previously, the link did appear to contain some relevant information. However, the page also states that enteric fermentation of ruminants is responsible for 39% of the 7.1 gigatons of greenhouse gas emissions produced annually by livestock. It also says 10% is from livestock manure, not vegetation and swamp bacteria. Therefore some of the statements are not supported.

Reference 9

Reference

Chapter 17: Food Classifications, reference 1. Moubarac et al Curr Obes Rep. 2014 Jun; 3(2): 256-72.

Associated quote(s) and page number(s)

Page 242: “First, let’s review the public classification systems used to convey nutrition information/disinformation.”

Criterion 2.1. Does the reference support the claim?

1 out of 4

This reference received a score of 1 out of 4, meaning that it is largely irrelevant to the statement.

The paper is a review of the classification systems for food processing.

There isn’t a claim actually being made in the quote. At best, it could be considered that the reference is meant to be a review of all public classification systems used to convey nutrition information/disinformation. If so, the paper is not a review about classification systems for nutrition information/disinformation.

The review includes only five classifications about food processing. The review does not consider other dimensions of nutrition information/disinformation. For example, systems about macronutrients/micronutrients or food group content, such as Nutri-score, UK front of package label multiple traffic lights, Mediterranean diet adherence, or classifications for national dietary guideline adherence. Although, the 5 classifications in the review do attempt to capture nutrition information.

Reference 10

Reference

Chapter 22, reference 3. Food Navigator. Milk in India Found to Be Most Highly-Adulterated Food Product Despite FSSAI Assurances of Safety, 2019.

Associated quote(s) and page number(s)

Page 288: “Dilution/adulteration. Something is added to the food to disguise or extend it. Milk is a common vehicle. In 2019 in India, milk was determined to have lower fat levels than advertised because the cows are inadequately fed.”

Criterion 2.1. Does the reference support the claim?

1 out of 4

This reference received a score of 1 out of 4, meaning that it does not convincingly support the claim.

The reference is a link to an online news website, Food Navigator, reporting on adulterated foods in Delhi. It is not peer-reviewed, and not considered to be credible evidence. The strongest support for the claim of lower fat levels was in a quote in the article from another newspaper, from a ‘government officer’. Even so, nowhere does the article state that this is due to inadequate feeding. There is no indication as to the proportion of milk in India that may have lower fat levels than advertised, as this only refers to Delhi.

Overall (average) score for reference accuracy

1.9 out of 4

Summary of the health-related intervention promoted in the book

The key recommendations made in Metabolical are to choose “Real Foods” and to avoid all processed food. There are few specific recommendations around the types of “Real Food” food groups to consume. Much of the guidance centers on avoiding sugar.

“Real Food” is described briefly in places (as fresh produce, eggs and meat, p.305, green vegetables, p. 342, water, fresh fruit and vegetables p. 363). “Real Foods” are also described as foods that are high in (soluble and insoluble) fiber, and low in sugar. “Real Foods” also contain vitamins, polyphenols, polyamines, flavonoids, and other antioxidants (p.261).

Metabolical suggests that conventional foods are full of antibiotics, herbicides and pesticides, that also drive disease. The book suggests buying organic (p.296), but still warns that some organic foods contain sugar. The book also suggests grass-fed, pasture-raised animal foods over corn-fed foods as they are better for health (page 9). For example, by suggesting that omega-3 can only be obtained from eggs from pasture-raised chickens, wild fish and pasture-raised meat (and not corn-fed chicken eggs, corn-fed farmed fish, or corn-fed meat) (p.262-3 and 338-9).

In places, the book recommends specific restriction of sugar and or carbohydrate to treat metabolic conditions such as fatty liver, insulin resistance or diabetes (as noted in Criterion 1.1, claim 2).

Condition targeted by the book, if applicable

Common chronic diseases and conditions such as obesity, diabetes, insulin resistance, non-alcoholic fatty liver disease, hypertension, heart disease and cancer.

Apparent target audience of the book

The book is targeted to a general audience, with chapters on the diets of adults, adolescents, children, and toddlers.

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

3 out of 4

The intervention received a score of 3 out of 4, meaning it is likely to moderately improve the target condition compared to average diets. This is because the book generally recommends nutrient-dense foods over nutrient-poor, processed foods.

The lack of specific details on the foods to consume prevented a higher score being given. Furthermore, the book suggests there are no particular health concerns from red meat consumption (besides processed meat, p.73) and does not suggest limiting red meat intake (e.g., the book suggests that LDL-cholesterol is not of great concern for cardiovascular health, p.35/39). The book also suggests that higher saturated fat intake is not an issue for heart disease via elevating LDL-cholesterol (p.74, 187-9, 190-191, p.204). Therefore, people could follow the advice, and yet eat lots of red meat (e.g. as a ‘carnivore diet’), and potentially increase their risk of cardiovascular disease.

The advice regarding complete sugar/carbohydrate restriction per se could unintentionally also lead to avoidance of nutrient-dense foods beneficial for health.

Eating organic or pasture-raised, animal-based foods instead of conventionally raised animal-based foods is not expected to have a meaningful benefit on target conditions.

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

3 out of 4

The intervention received a score of 3 out of 4, meaning it is likely to moderately improve general health compared to current diets. As in criterion 3.1., this is because the book generally recommends nutrient-dense foods over nutrient-poor, processed foods.

It is unlikely that most people will be able to stick with the diet in the medium- to long-term (6+ months), given the requirement to completely eliminate all processed foods.

Consuming organic or pasture-raised, animal-based foods is not expected to have a meaningful benefit on general health.

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

2 out of 4

The diet received a score of 2 out of 4. The diet is likely to be adequate for essential nutrients, given the key recommendation to choose nutrient-dense “Real Foods” over nutrient-poor, processed foods, as typically consumed in current diets.

Consuming only “Real Food” is also likely to provide non-essential, health promoting nutrients above the levels obtained in current average diets. Despite the recommendations likely being adequate, the book offers very little guidance in terms of the quantities or diversity of “Real Foods” that should be consumed. This leaves a lot of uncertainty in how someone may follow the diet advice, and therefore whether the diet actually meets nutritional needs.

The fact that a person is eating minimally processed food doesn’t guarantee a nutritionally adequate diet. For example, the nutrient analysis of a nose-to-tail carnivore diet we did in our review of The Carnivore Code suggests that it’s inadequate for several essential nutrients, despite being a minimally processed diet. Likewise, a vegan diet of minimally processed foods is nutritionally inadequate without supplementation. Most people eating a varied diet will be fine with a little common sense, but as written, the book’s guidance leaves room for nutritional inadequacy in some scenarios.

Furthermore, the advice to completely avoid all processed foods may potentially lead to deficiencies for some groups of people, such as the elderly or children, if key micronutrients are not obtainable through “Real Food”. For example, fortified foods may help elderly people with low calorie intake and poor micronutrient absorption meet their needs for vitamins and minerals. 

Overall (average) score for healthfulness

2.7 out of 4