LinkYouTubeFacebookInstagramTwitterLinkedInTikTokLinkLink

Dr. David Ludwig, MD, PhD

David S. Ludwig, MD, PhD, is a practicing endocrinologist, researcher, and professor at Harvard Medical School and Harvard School of Public Health. He received a PhD and an MD from Stanford University School of Medicine and completed an internship and residency in pediatrics and a fellowship in pediatric endocrinology at Boston Children's Hospital.

Dr. Ludwig also directs the New Balance Foundation Obesity Prevention Center at Boston Children’s Hospital. His research focuses on the effects of diet on hormones, metabolism and body weight. He developed a novel “low glycemic load” diet (i.e., one that decreases the surge in blood sugar after meals) for the treatment of obesity-related diseases. In addition, his group has done some of the original studies linking sugar-sweetened beverages and fast food to excessive weight gain, heart disease and type 2 diabetes.

Described as an “obesity warrior” by Time magazine, Dr. Ludwig has fought for fundamental policy changes to restrict junk food advertising directed at young children, improve the quality of national nutrition programs, and increase insurance reimbursement for obesity prevention and treatment.

Dr. Ludwig is Principal Investigator on numerous grants from the National Institutes of Health, has published over 150 scientific articles, and served for 10 years as Contributing Writer for JAMA. He has also written several books for the public, including 'Ending The Food Fight' (2007), 'Always Hungry?' (2016) and the cookbook 'Always Delicious' (2018).

Books by Dr. David Ludwig, MD, PhD

Video Presentations of Dr. David Ludwig, MD, PhD

"The Carbohydrate-Insulin Model of Obesity" - Dr. David Ludwig

David S. Ludwig, MD, PhD, is a practicing endocrinologist, researcher, and professor at Harvard Medical School and Harvard School of Public Health. He received a PhD and an MD from Stanford University School of Medicine and completed an internship and residency in pediatrics and a fellowship in pediatric endocrinology at Boston Children's Hospital.

Dr. Ludwig also directs the New Balance Foundation Obesity Prevention Center at Boston Children’s Hospital. His research focuses on the effects of diet on hormones, metabolism and body weight. He developed a novel “low glycemic load” diet (i.e., one that decreases the surge in blood sugar after meals) for the treatment of obesity-related diseases. In addition, his group has done some of the original studies linking sugar-sweetened beverages and fast food to excessive weight gain, heart disease and type 2 diabetes.

Described as an “obesity warrior” by Time magazine, Dr. Ludwig has fought for fundamental policy changes to restrict junk food advertising directed at young children, improve the quality of national nutrition programs, and increase insurance reimbursement for obesity prevention and treatment.

Dr. Ludwig is Principal Investigator on numerous grants from the National Institutes of Health, has published over 150 scientific articles, and served for 10 years as Contributing Writer for JAMA. He has also written several books for the public, including 'Ending The Food Fight' (2007), 'Always Hungry?' (2016) and the cookbook 'Always Delicious' (2018).

Harvard School of Public Health - Nutrition Seminar Series 2021

Dr David Ludwig's lecture on the Carbohydrate-Insulin Model of Obesity for the Nutrition Seminar Series, Harvard School of Public Health.

"Always Hungry?" - Dr. David Ludwig

Diet doesn't have to mean deprivation, and weight loss doesn't have to be temporary. 

Based on the over 150+ scientific studies I've conducted, and several hundred other referenced in the book, Always Hungry? turns dieting on its head with a three-phase program that ignores calories and targets fat cells directly. The recipes and meal plan include luscious high fat foods (like nuts and nut butters, full fat dairy, avocados, and dark chocolate), savory proteins, and natural carbohydrates. The result? Fat cells release their excess calories and you lose weight-and inches-without battling cravings and constant hunger.

Forget calories. Forget cravings. Forget dieting. ALWAYS HUNGRY? reveals a liberating new way to tame hunger and lose weight... for good.

"Do Calories Count? The Carbohydrate-Insulin Model of Obesity" - with Dr. David Ludwig

Do foods with the same calories have the same metabolic effect? Dr. David Ludwig did a study to help us better understand the role of calories.

"Quality Calories & Quality Science" - with Dr. David Ludwig

In the messy world of nutritional science, some researchers rise above the others in their attempt to produce high quality and useful data. Dr. Ludwig exemplifies that role. As a practicing pediatric endocrinologist, he has seen first hand the rise in obesity, type 2 diabetes, fatty liver and other previously rare complications in adolescents. 

As a result, he has made it his mission to help us better understand the role of calories, the importance of quality of calories, and the importance of the quality of the science we read. Is a calorie just a calorie? Why are so many scientific studies not helpful in answering this question, and what can we do about that? Dr. Ludwig answers these questions and more.

Scholarly Articles from Dr. David Ludwig, MD, PhD

The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted DietsWhen lean people adopt carbohydrate-restricted diets (CRDs), they may develop a lipid profile consisting of elevated LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) with low triglycerides (TGs). The magnitude of this lipid profile correlates with BMI such that those with lower BMI exhibit larger increases in both LDL-C and HDL-C. The inverse association between BMI and LDL-C and HDL-C change on CRD contributed to the discovery of a subset of individuals—termed Lean Mass Hyper-Responders (LMHR)—who, despite normal pre-diet LDL-C, as compared to non-LMHR (mean levels of 148 and 145 mg/dL, respectively), exhibited a pronounced hyperlipidemic response to a CRD, with mean LDL-C and HDL-C levels increasing to 320 and 99 mg/dL, respectively, in the context of mean TG of 47 mg/dL. In some LMHR, LDL-C levels may be in excess of 500 mg/dL, again, with relatively normal pre-diet LDL-C and absent of genetic findings indicative of familial hypercholesterolemia in those who have been tested. The Lipid Energy Model (LEM) attempts to explain this metabolic phenomenon by positing that, with carbohydrate restriction in lean persons, the increased dependence on fat as a metabolic substrate drives increased hepatic secretion and peripheral uptake of TG contained within very low-density lipoproteins (VLDL) by lipoprotein lipase, resulting in marked elevations of LDL-C and HDL-C, and low TG. Herein, we review the core features of the LEM. We review several existing lines of evidence supporting the model and suggest ways to test the model’s predictions.
Dietary carbohydrates: role of quality and quantity in chronic diseaseDavid S Ludwig and colleagues examine the links between different types of carbohydrates and health Carbohydrate is the only macronutrient with no established minimum requirement. Although many populations have thrived with carbohydrate as their main source of energy, others have done so with few if any carbohydrate containing foods throughout much of the year (eg, traditional diets of the Inuit, Laplanders, and some Native Americans).12 If carbohydrate is not necessary for survival, it raises questions about the amount and type of this macronutrient needed for optimal health, longevity, and sustainability. This review focuses on these current controversies, with special focus on obesity, diabetes, cardiovascular disease, cancer, and early death. The large brain of modern humans is energetically expensive, requiring a disproportionate share of dietary energy compared with that of other primates. The first hunting and gathering societies were characterised by greater consumption of not only animal foods but also plant foods with greater carbohydrate availability than leaves—including ripe fruit, honey, and eventually cooked starchy foods.34 The higher nutrient and energy density of this diet allowed for evolution of a smaller gastrointestinal tract, offsetting the energy demands of the brain.5 As a result of selective pressures related to dietary changes, two major gene adaptations occurred affecting carbohydrate digestion: average salivary amylase gene copy number (AMY1) increased more than threefold, with substantial variation among populations related to starch consumption6; and lactase persistence into adulthood developed in multiple geographically distinct populations, facilitating digestion of the milk sugar lactose.7 After our transition to an agrarian lifestyle in the Neolithic period, beginning 12 000 to 14 000 years ago, total carbohydrate intake increased substantially as grains became a dietary staple, but archaeological evidence shows that diet related problems also emerged, including endemic nutrient deficiencies, a decrease in mean height, …
Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trialObjective To determine the effects of diets varying in carbohydrate to fat ratio on total energy expenditure. Design Randomized trial. Setting Multicenter collaboration at US two sites, August 2014 to May 2017. Participants 164 adults aged 18-65 years with a body mass index of 25 or more. Interventions After 12% (within 2%) weight loss on a run-in diet, participants were randomly assigned to one of three test diets according to carbohydrate content (high, 60%, n=54; moderate, 40%, n=53; or low, 20%, n=57) for 20 weeks. Test diets were controlled for protein and were energy adjusted to maintain weight loss within 2 kg. To test for effect modification predicted by the carbohydrate-insulin model, the sample was divided into thirds of pre-weight loss insulin secretion (insulin concentration 30 minutes after oral glucose). Main outcome measures The primary outcome was total energy expenditure, measured with doubly labeled water, by intention-to-treat analysis. Per protocol analysis included participants who maintained target weight loss, potentially providing a more precise effect estimate. Secondary outcomes were resting energy expenditure, measures of physical activity, and levels of the metabolic hormones leptin and ghrelin. Results Total energy expenditure differed by diet in the intention-to-treat analysis (n=162, P=0.002), with a linear trend of 52 kcal/d (95% confidence interval 23 to 82) for every 10% decrease in the contribution of carbohydrate to total energy intake (1 kcal=4.18 kJ=0.00418 MJ). Change in total energy expenditure was 91 kcal/d (95% confidence interval −29 to 210) greater in participants assigned to the moderate carbohydrate diet and 209 kcal/d (91 to 326) greater in those assigned to the low carbohydrate diet compared with the high carbohydrate diet. In the per protocol analysis (n=120, P<0.001), the respective differences were 131 kcal/d (−6 to 267) and 278 kcal/d (144 to 411). Among participants in the highest third of pre-weight loss insulin secretion, the difference between the low and high carbohydrate diet was 308 kcal/d in the intention-to-treat analysis and 478 kcal/d in the per protocol analysis (P<0.004). Ghrelin was significantly lower in participants assigned to the low carbohydrate diet compared with those assigned to the high carbohydrate diet (both analyses). Leptin was also significantly lower in participants assigned to the low carbohydrate diet (per protocol). Conclusions Consistent with the carbohydrate-insulin model, lowering dietary carbohydrate increased energy expenditure during weight loss maintenance. This metabolic effect may improve the success of obesity treatment, especially among those with high insulin secretion. Trial registration ClinicalTrials.gov [NCT02068885][1]. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT02068885&atom=%2Fbmj%2F363%2Fbmj.k4583.atom
High Glycemic Index Foods, Overeating, and ObesityObjective.. The prevalence of obesity has increased dramatically in recent years. However, the role of dietary composition in body weight regulation remains unclear. The purpose of this work was to investigate the acute effects of dietary glycemic index (GI) on energy metabolism and voluntary food intake in obese subjects.Methods.. Twelve obese teenage boys were evaluated on three separate occasions using a crossover study protocol. During each evaluation, subjects consumed identical test meals at breakfast and lunch that had a low, medium, or high GI. The high- and medium-GI meals were designed to have similar macronutrient composition, fiber content, and palatability, and all meals for each subject had equal energy content. After breakfast, plasma and serum concentrations of metabolic fuels and hormones were measured. Ad libitum food intake was determined in the 5-hour period after lunch.Results.. Voluntary energy intake after the high-GI meal (5.8 megajoule [mJ]) was 53% greater than after the medium-GI meal (3.8 mJ), and 81% greater than after the low-GI meal (3.2 mJ). In addition, compared with the low-GI meal, the high-GI meal resulted in higher serum insulin levels, lower plasma glucagon levels, lower postabsorptive plasma glucose and serum fatty acids levels, and elevation in plasma epinephrine. The area under the glycemic response curve for each test meal accounted for 53% of the variance in food intake within subjects.Conclusions.. The rapid absorption of glucose after consumption of high-GI meals induces a sequence of hormonal and metabolic changes that promote excessive food intake in obese subjects. Additional studies are needed to examine the relationship between dietary GI and long-term body weight regulation. glycemic index, obesity, dietary carbohydrate, diets, insulin.