Dr. Michael Greger's "How Not to Diet" aims to guide readers toward sustainable weight loss through a plant-based, whole-foods approach. The book has garnered significant attention, evidenced by its popularity and the enthusiastic support it received during a Red Pen Reviews fund drive. This review delves into the book's core claims, evaluating their scientific accuracy and overall effectiveness.
The Core Principles of "How Not to Diet"
"How Not to Diet" revolves around a vegan diet, or something close to it, emphasizing minimally processed plant foods as the cornerstone of healthy and sustainable weight loss. The book's recommendations are based on seventeen “key ingredients,” which Dr. Greger identifies as the factors “most effectual for weight loss.” Due to the sheer volume of information presented, this review will focus on three central claims:
- An anti-inflammatory diet aids in weight loss.
- Diet-derived pollutants ("obesogens") contribute to weight gain.
- Higher fiber diets promote weight loss.
Scientific Accuracy: A Mixed Bag
Overall, "How Not to Diet" received a scientific accuracy score of 2 out of 4, indicating that its claims are weakly supported by the available evidence. While some claims are well-founded, others lack sufficient scientific backing.
Claim 1: Anti-Inflammatory Diet and Weight Loss
This claim received a score of 1 out of 4, signifying poor support from current research. The premise that an anti-inflammatory diet promotes weight loss is appealing, but the evidence is limited. While some studies suggest that inflammation in the brain might lead to weight gain, it's plausible that such inflammation is merely a consequence of the same factors that cause weight gain.
The book asserts that identifying pro-inflammatory and anti-inflammatory foods is straightforward: observe the impact of specific foods on C-reactive protein and other inflammatory markers after consumption. However, these markers do not reliably predict weight gain. Although inflammatory markers are linked to obesity, a prospective cohort study in Finland found that no major inflammatory marker predicted weight gain or obesity development over seven years. Similarly, a meta-analysis of 60 studies in 2021 revealed that changes in C-reactive protein did not predict subsequent weight loss. Furthermore, a Mendelian randomization study found that genetically elevated levels of various inflammatory markers and mediators had no impact on BMI. Ironically, in individuals with autoimmune diseases, medications that inhibit interleukin-6 or TNF-a (both of which promote inflammation) can lead to weight gain. There is a lack of human studies examining the relationship between changes in hypothalamic inflammation and weight changes.
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"How Not to Diet" characterizes whole plant foods as generally anti-inflammatory compared to animal-sourced and processed foods, aligning with evidence suggesting that dietary patterns centered around minimally processed, whole, plant-based foods (such as the DASH and Mediterranean diets) tend to lower markers of systemic inflammation.
The book suggests that fiber is "strongly anti-inflammatory," but research does not consistently support this. A 2022 meta-analysis of randomized controlled trials found that supplementing with an average of 11 grams of soluble fiber daily for at least 12 weeks led to weight loss but had no effect on the inflammatory marker CRP.
The book implies that full-fat dairy products are inflammatory, stating that saturated fat is inflammatory and that dairy foods are a major source of saturated fat.
These inconsistencies may arise from the book's reliance on the Dietary Inflammatory Index (DII), a model that aims to determine the inflammatory or anti-inflammatory properties of various foods and food components. However, the DII's methodology is flawed, as it is partially based on petri dish studies and animal experiments, does not weight studies according to sample size, and does not weight effect sizes.
In summary, there is evidence that the overall whole foods, plant-rich dietary pattern recommended in How Not to Diet may help reduce inflammation. Yet many of the individual dietary recommendations for reducing inflammation (e.g., eliminating dairy foods, increasing fiber, or drinking green tea) are not well-supported by evidence.
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Claim 2: "Obesogens" and Weight Gain
This claim also received a score of 1 out of 4, indicating weak support from current evidence. "How Not to Diet" identifies several food-derived "obesogens," chemicals that supposedly promote obesity.
One example is organotins, tin-based chemicals found in seafood, especially "Halibut, swordfish, and canned tuna." While studies confirm that seafood can be a major source of organotins, the impact on obesity is uncertain. The only human study linking organotins to weight gain involved 110 newborn boys, finding that infants born to mothers with higher placental levels of TBT (a major organotin) gained slightly more weight in the first 3 months after birth. However, evidence suggests that eating fish may promote weight loss, contrary to what would be expected if the organotins in seafood had a substantial impact on weight gain. A network meta-analysis of randomized controlled trials found that eating fish resulted in an average weight loss of 1.85 pounds (0.84 kg). However, a large meta-analysis of cohort studies found a high seafood intake (>3 times per week) during pregnancy was associated with a higher risk of childhood obesity.
Another obesogen cited is DDT, a pesticide now banned in the United States and restricted in many other regions. "How Not to Diet" claims DDT is found "mostly in meat, particularly fish," which appears to be mostly true in many regions of the world. Research on DDT exposure and weight gain primarily involves infants and children. In the CHAMACOS cohort, boys (but not girls) born to mothers with higher serum levels of DDT were more likely to become obese during childhood. However, a similar study found no clear relationship between umbilical cord DDT levels and the risk of childhood obesity. A prospective cohort study of 90 people found that having higher blood levels of DDE, but not DDT, was associated with a higher BMI when participants were assessed 18 years later.
The book focuses heavily on Bisphenol A (BPA), a chemical used to make certain types of plastic, stating that "ninety percent of exposure" to BPA is from "our diets," including canned and packaged food. A meta-analysis of observational studies found that higher levels of BPA (measured in urine) were associated with a higher risk of obesity, abdominal obesity, and overweight. However, there are very few prospective studies on BPA, making it difficult to establish a cause-and-effect relationship between high BPA levels and fat gain. Higher BPA levels may simply indicate the consumption of more canned foods and drinks (like soda), which are major sources of BPA.
"How Not to Diet" suggests that phthalates, chemicals used in plastic production, might be another obesogen. Phthalates have been studied for their potential to cause obesity, but current evidence (mostly lower-quality observational studies) appears inconsistent.
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The book also suggests that polycyclic aromatic hydrocarbons (PAHs) may contribute to weight gain. A 2023 meta-analysis found that specific PAHs are associated with a higher risk of obesity. The main routes of exposure to naphthalene and phenanthrene, the two PAHs most clearly associated with obesity in that meta-analysis, seem to be airborne contamination and occupational exposure, rather than from the diet.
Finally, "How Not to Diet" suggests that certain pesticides found in conventional agriculture may promote obesity, making organic plant foods preferable. The strongest evidence referenced is a prospective cohort study from 2017, which found that people who reported eating more organic food were less likely to become overweight or obese over the next several years. However, it's hard to be certain that eating less nonorganic food is actually responsible for the effect. The book singles out the pesticide atrazine as a likely mediator of the effect of nonorganic food on obesity risk, and there is indeed some research in rodents and at least one study of industrially-exposed workers suggesting this chemical can promote obesity with high exposures. But whether atrazine is readily found in nonorganic food in large enough amounts to promote obesity is not well-supported by evidence. Atrazine is almost always undetectable or in very low concentrations in food (the US and EU limit the amount of atrazine allowed in food).
In summary, the existing research tends to provide only weak and inconclusive evidence that the chemicals and pesticides mentioned in the How Not to Diet are found in high enough concentrations in our food supply to be a major culprit in weight gain.
Claim 3: Higher Fiber Diets and Weight Loss
This claim received a score of 4 out of 4, indicating strong support from current evidence. Eating a diet high in fiber-rich foods does appear to help with weight loss, an effect attributable to the fiber itself and possibly to common characteristics of fiber-rich foods (e.g., lower calorie density). While the book may overstate the size of the effect, it does not warrant a lower score for the claim.
Numerous trials have found that weight loss occurs when people take fiber supplements. For example, a meta-analysis of 27 randomized controlled trials that lasted at least 12 weeks found that supplementing with soluble fiber (from things like inulin and flaxseed powder) led people to lose an average of 2.75 pounds.
The reasons why eating more fiber can cause weight loss are not yet entirely clear, but a few compelling explanations exist. Fiber inhibits the absorption of macronutrients (like fat and carbohydrates), resulting in fewer calories being absorbed. Fiber may also slow stomach emptying, potentially sending greater fullness signals to the brain, promoting satiety.
"How Not to Diet" specifically recommends increasing fiber-rich foods (as opposed to just taking fiber supplements). This advice could result in other changes to the diet that promote weight loss independently of fiber. Most notably, efforts to increase intake of fiber-rich foods could lead to reduced consumption of ultraprocessed foods (UPFs), which are usually lower in fiber and more calorically-dense. UPFs are a subcategory of processed food typically defined as foods made mostly of substances derived from food (flour, sugar, oil, etc.) as well as additives (like flavorings), with minimal amounts of unprocessed food. A few examples of UPFs are soda, potato chips, and most commercially available candy and pastries, foods which have been linked to weight gain.
Additional Insights and Considerations
Beyond the three key claims, "How Not to Diet" delves into various other aspects of weight management, including the importance of meal timing, the impact of the gut microbiome, and the role of sleep. The book also offers practical advice in the form of "21 Diet Tweaks," which encompass strategies such as incorporating specific spices and vinegar, "front-loading" calories, and following the 20-minute rule.
The book emphasizes that it’s not what you eat but what you absorb, so you can lose more weight on a high-fiber diet eating the exact same number of calories simply because some of those calories get trapped and never make it into your system.
"How Not to Diet" challenges conventional wisdom by debunking statements like "A calorie is a calorie" and "Weight loss revolves around eating less and exercising more" or "You need to count calories to lose weight". Concepts like calorie density, fiber, and the influence of your gut microbiome are thoroughly reviewed in Dr. Greger’s latest work along with how sleep, food processing, and timing of our meals can all affect how to lose weight-and keep it off.
Dr. Greger shares valuable information in a clear and accessible manner, peppered with humor and wit.