## [Weight Science: Evaluating the Evidence for a Paradigm Shift | Nutrition Journal ](https://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-10-9) I was pointed to this paper as a good defense of [Health at Every Size](https://en.wikipedia.org/wiki/Health_at_Every_Size) (see [[2023-05-02#[Red Pen Reviews: Anti-Diet: Reclaim Your Time, Money, Well-Being, and Happiness Through Intuitive Eating](https://www.redpenreviews.org/reviews/anti-diet/)|Red Pen Reviews: Anti-Diet: Reclaim Your Time, Money, Well-Being, and Happiness Through Intuitive Eating]] for a critical take). It's claims include: Overweight and moderately obese live longer that normal weight: > Except at statistical extremes, body mass index (BMI) - or amount of body fat - only weakly predicts longevity [32]. Most epidemiological studies find that people who are overweight or moderately obese live at least as long as normal weight people, and often longer [32–35]. Obesity is associated with health risks, but is not causal: > While it is well established that obesity is associated with increased risk for many diseases, causation is less well-established. Epidemiological studies rarely acknowledge factors like fitness, activity, nutrient intake, weight cycling or socioeconomic status when considering connections between weight and disease. Yet all play a role in determining health risk. When studies do control for these factors, increased risk of disease disappears or is significantly reduced [61]. (This is less true at statistical extremes.) It is likely that these other factors increase disease risk at the same time they increase the risk of weight gain. Weight loss increases your chance of premature death: > Most prospective observational studies suggest that weight loss increases the risk of premature death among obese individuals, even when the weight loss is intentional and the studies are well controlled with regard to known confounding factors, including hazardous behavior and underlying diseases [91–96]. Recent review of NHANES, for example, a nationally representative sample of ethnically diverse people over the age of fifty, shows that mortality increased among those who lost weight [97]. Weight loss does not work in the long term: > Long-term follow-up studies document that the majority of individuals regain virtually all of the weight that was lost during treatment, regardless of whether they maintain their diet or exercise program [5, 27]. The pursuit of weight loss has many contraindications: > Research identifies many other contraindications to the pursuit of weight loss. For example, dieting is known to reduce bone mass, increasing risk for osteoporosis [108–111] Health improvements can be achieved without weight loss: > As indicated by research conducted by one of the authors and many other investigators, most health indicators can be improved through changing health behaviors, regardless of whether weight is lost [11]. The authors go on to argue that weight loss is not an appropriate intervention and that health can be improved without weight loss. This is the most comprehensive defense of HAES that I've come across. The critical review I linked to above addresses some but not all of these claims. I'm trying to learn more about this with an open mind, so I will continue looking into these claims, but I currently do not assign it a high probability of being true. ## [@sguyenet: A simple general theory to explain the obesity epidemic](https://twitter.com/sguyenet/status/1654316831589699584) > A simple general theory to explain the obesity epidemic, and some other problems of modern society: We've gotten too good at satisfying our own innate preferences. [[Stephan Guyenet]] offers a hypothesis: Some foods stimulate eating, while other foods inhibit eating. Pringles, for example, will keep me coming back for more until I'm uncomfortably full, whereas eating black beans is much less likely to result in a binge. As food becomes abundant and cheap, it's easy to fill our pantries with foods that stimulate eating. For whatever reason, that tends to be our preference. This process might be part of the explanation for the obesity epidemic. > We're wired to prefer foods and food environments with more phagostimulatory properties [stimulates eating] and fewer phagoinhibitory properties [inhibits eating]. And as we gain greater control over our food and environment via technology and affluence, we increasingly satisfy those preferences. > As we increasingly satisfy our preferences, we unintentionally create a more fattening diet and environment for ourselves. Guyenet says he doesn't have strong evidence for it: > I don't have strong evidence to support this theory (technically, hypothesis) and I'm not sure how you'd test it directly. We do at least have [evidence](https://pubmed.ncbi.nlm.nih.gov/31105044/) that ultra processed foods cause increased caloric intake: > Energy intake was greater during the ultra-processed diet (508 ± 106 kcal/day; p = 0.0001), with increased consumption of carbohydrate (280 ± 54 kcal/day; p < 0.0001) and fat (230 ± 53 kcal/day; p = 0.0004), but not protein (-2 ± 12 kcal/day; p = 0.85). Weight changes were highly correlated with energy intake (r = 0.8, p < 0.0001), with participants gaining 0.9 ± 0.3 kg (p = 0.009) during the ultra-processed diet and losing 0.9 ± 0.3 kg (p = 0.007) during the unprocessed diet. Limiting consumption of ultra-processed foods may be an effective strategy for obesity prevention and treatment.