Showing posts with label overweight. Show all posts
Showing posts with label overweight. Show all posts

Tuesday, 10 May 2016

Princess Health and Why some dogs (and humans) are born hungry. Princessiccia

Princess Health and Why some dogs (and humans) are born hungry. Princessiccia

The brain is the central regulator of appetite and body fatness, and genetic variation that affects body fatness tends to act in the brain. One important site of variation is the POMC gene, which codes for a signaling molecule that suppresses food intake. A new study shows that Labrador retrievers often carry an inactive version of the POMC gene, causing them to be highly food motivated, obesity-prone-- and perhaps more easily trainable.

Read more �

Saturday, 9 January 2016

Princess Health and Always Hungry? It's Probably Not Your Insulin.. Princessiccia

Princess Health and Always Hungry? It's Probably Not Your Insulin.. Princessiccia

David Ludwig, MD, recently published a new book titled Always Hungry? Conquer cravings, retrain your fat cells, and lose weight permanently. The book is getting widespread media coverage. Ludwig is a professor of pediatrics at the Harvard Medical School and a professor of nutrition at the Harvard School of Public Health. He's a pediatric endocrinologist, but his primary focus is research, particularly the impact of nutrition on hunger, calorie expenditure, and body weight. Although I sometimes disagree with how he interprets evidence, he has made significant and useful contributions to the scientific literature in these areas, and I also support his efforts to find policy solutions to curb the intake of sweetened beverages and other junk foods. In the grand scheme of things, he's an ally in the fight to improve the American diet.

Ludwig has written several high-profile op-ed pieces in recent years, both in the popular press and in scientific journals (1, 2). He argues that our understanding of eating behavior and obesity may be all wrong, and that our focus on calories may be leading us away from the true cause of obesity: hormonal imbalance. And the primary culprit is insulin. You might recognize this idea, because it's similar to the one that science journalist Gary Taubes developed in his book Good Calories, Bad Calories.

According to this view, overeating is irrelevant. We gain fat because our insulin levels are too high, leading our fat tissue to take up too much fat, and other tissues to take up too much glucose, causing our blood energy levels to drop and resulting in fat gain, hunger, and fatigue. The ultimate cause of the problem is the rapidly-digesting carbohydrate and sugar we eat. This idea is encapsulated by Ludwig's quote, "Overeating doesn't make you fat. The process of getting fat makes you overeat" (3).

Here are eleven facts that may make you question this line of reasoning:
Read more �

Thursday, 10 December 2015

Princess Health and New Evidence Strengthens the Link Between Hypothalamic Injury, Obesity, and Insulin Resistance. Princessiccia

Princess Health and New Evidence Strengthens the Link Between Hypothalamic Injury, Obesity, and Insulin Resistance. Princessiccia

Obesity involves changes in the function of brain regions that regulate body fatness and blood glucose, particularly a region called the hypothalamus. My colleagues and I previously showed that obesity is associated with inflammation and injury of the hypothalamus in rodent models, and we also presented preliminary evidence that the same might be true in humans. In our latest paper, we confirm this association, and show that hypothalamic injury is also associated with a marker of insulin resistance, independently of BMI.

Introduction

Read more �

Monday, 16 November 2015

Princess Health and Carbohydrate, Sugar, and Obesity in America. Princessiccia

Princess Health and Carbohydrate, Sugar, and Obesity in America. Princessiccia

We like explanations that are simple, easy to understand, and explain everything. One example of this is the idea that eating carbohydrate, or sugar, is the primary cause of obesity. This lets us point our finger at something concrete and change our behavior accordingly. And it's true enough that it has practical value. But the world around us often turns out to be more complex than we'd like it to be.

The CDC recently released its latest data on the prevalence of obesity in the US, spanning the years 2013-2014 (1). These data come from its periodic National Health and Nutrition Examination Surveys (NHANES). Contrary to what many of us had hoped for after a slight decline in obesity in the last survey, the prevalence has once again increased. Today, roughly 38 percent of US adults have obesity. As a nation, we're continuing to gain fat, which is extremely concerning.

I decided to examine the relationship between obesity prevalence and our intake of carbohydrate and sugar over the years. The food intake data come from the USDA's Economic Research Service (2). For some reason, the data on carbohydrate don't extend beyond 2010. This probably relates to funding cuts at the USDA*.

Let's have a look at the data for carbohydrate:

Read more �

Friday, 16 October 2015

Wednesday, 26 August 2015

Princess Health and How Much Does Sugar Contribute to Obesity?. Princessiccia

Last week, the British Medical Journal published a review article titled "Dietary Sugars and Body Weight", concluding that "free sugars" and sugar-sweetened beverages contribute to weight gain. But what are "free sugars", and why does the scientific literature suggest that the relationship between sugar intake and body weight isn't as straightforward as it may initially appear?




Read more �

Thursday, 13 August 2015

Princess Health and A New Human Trial Undermines the Carbohydrate-insulin Hypothesis of Obesity, Again. Princessiccia

Princess Health and A New Human Trial Undermines the Carbohydrate-insulin Hypothesis of Obesity, Again. Princessiccia

The carbohydrate-insulin hypothesis of obesity states that carbohydrates (particularly refined carbohydrates and sugar) are the primary cause of obesity due to their ability to increase circulating insulin, and that the solution to obesity is to restrict carbohydrate intake. Numerous studies have tested this hypothesis, more or less directly, in animals and humans. Despite the fact that many of these studies undermine the hypothesis, it remains extremely popular, both in the popular media and to a lesser extent among researchers. A new human trial by Kevin Hall's research team at the US National Institutes of Health offers very strong evidence that the carbohydrate-insulin hypothesis of obesity is incorrect. At the same time, it offers surprising and provocative results that challenge prevailing ideas about diet and weight loss.



Read more �

Tuesday, 14 October 2014

Princess Health and Obesity ? Diabetes. Princessiccia

Princess Health and Obesity ? Diabetes. Princessiccia

A new study adds to the evidence that the prevalence of type 2 diabetes is rapidly increasing in the US, and our national weight problem is largely to blame.

The Centers for Disease Control (CDC) currently estimates that a jaw-dropping 33 percent of US men, and 39 percent of US women, will develop diabetes at some point in their lives (1). Roughly one out of three people in this country will develop diabetes, and those who don't manage it effectively will suffer debilitating health consequences. Has the risk of developing diabetes always been so high, and if not, why is it increasing?

In the same issue of the Annals of Internal Medicine as the low-carb vs. low-fat study, appears another study that aims to partially address this question (2).

Read more �

Thursday, 18 September 2014

Thursday, 4 September 2014

Princess Health and What about the Other Weight Loss Diet Study??. Princessiccia

Princess Health and What about the Other Weight Loss Diet Study??. Princessiccia

The same day the low-fat vs low-carb study by Bazzano and colleagues was published, the Journal of the American Medical Association published a meta-analysis that compared the effectiveness of "named diet programs". Many people have interpreted this study as demonstrating that low-carbohydrate and low-fat diets are both effective for weight loss, and that we simply need to pick a diet and stick with it, but that's not really what the study showed. Let's take a closer look.

Johnston and colleagues sifted through PubMed for studies that evaluated "named diet programs", such as Ornish, Atkins, LEARN, Weight Watchers, etc (1). In addition, the methods state that they included any study as low-carbohydrate that recommended less than 40% of calories from carbohydrate, was funded by the Atkins foundation, or was "Atkins-like". These criteria weren't extended to the low-fat diet: only studies of name-brand low-fat diets like the Ornish diet were included, while the meta-analysis excluded low-fat diet studies whose guidelines were based on recommendations from government and academic sources, even though the latter group represents the majority of the evidence we have for low-fat diets. The inclusion criteria were therefore extremely asymmetrical in how they represented low-carb and low-fat diets. This fact explains the unusual findings of the paper.

The abstract immediately activated my skeptic alarm, because it states that at the one-year mark, low-carbohydrate diets and low-fat diets both led to a sustained weight loss of about 16 pounds (7.3 kg). Based on my understanding of the weight loss literature, that number seems far too high for the low-fat diet, and also too high for the low-carbohydrate diet.

Read more �

Monday, 1 September 2014

Princess Health and Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence. Princessiccia

Princess Health and Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence. Princessiccia

A new high-profile study compared the weight loss and cardiovascular effects of a low-carbohydrate diet vs. a low-fat diet. Although many studies have done this before, this one is novel enough to add to our current understanding of diet and health. Unlike most other studies of this nature, diet adherence was fairly good, and carbohydrate restriction produced greater weight loss and cardiovascular risk factor improvements than fat restriction at the one-year mark. Yet like previous studies, neither diet produced very impressive results.

The Study

Lydia A. Bazzano and colleagues at Tulane University randomly assigned 148 obese men and women without cardiovascular disease into two groups (1):
  1. Received instructions to eat less than 40 grams of carbohydrate per day, plus one low-carbohydrate meal replacement per day. No specific advice to alter calorie intake. Met regularly with dietitians to explain the dietary changes and maintain motivation.
  2. Received instructions to eat less than 30 percent of calories from fat, less than 7 percent of calories as saturated fat, and 55 percent of calories from carbohydrate, plus one low-fat meal replacement per day. No specific advice to alter calorie intake. This is based on NCEP guidelines, which are actually designed for cardiovascular risk reduction and not weight loss. Met regularly with dietitians to explain the dietary changes and maintain motivation.
Participants were followed up for one year, with data reported for 3 month, 6 month, and 12 month timepoints. This study actually measured body fat percentage, but unfortunately did so using bioelectrical impedance (like on some bathroom scales), which is essentially meaningless in this context.

Results

Read more �

Wednesday, 25 June 2014

Princess Health and Fat and Carbohydrate: Clarifications and Details. Princessiccia

Princess Health and Fat and Carbohydrate: Clarifications and Details. Princessiccia

The last two posts on fat and carbohydrate were written to answer a few important, but relatively narrow, questions that I feel are particularly pertinent at the moment:
  • Was the US obesity epidemic caused by an increase in calorie intake?
  • Could it have been caused by an increase in carbohydrate intake, independent of the increase in calorie intake?
  • Does an unrestricted high-carbohydrate diet lead to a higher calorie intake and body fatness than an unrestricted high-fat diet, or vice versa?
  • Could the US government's advice to eat a low-fat diet have caused the obesity epidemic by causing a dietary shift toward carbohydrate?
However, those posts left a few loose ends that I'd like to tie up in this post. Here, I'll lay out my opinions on the relationship between macronutrient intake and obesity in more detail. I'll give my opinions on the following questions:
  • What dietary macronutrient composition is the least likely to cause obesity over a lifetime?
  • What dietary macronutrient composition is best for a person who is already overweight or obese?
  • Is fat inherently fattening and/or unhealthy?
From the beginning

Read more �

Wednesday, 11 June 2014

Princess Health and Has Obesity Research Failed?. Princessiccia

Princess Health and Has Obesity Research Failed?. Princessiccia

I frequently encounter the argument that obesity research has failed because it hasn't stopped the global increase in obesity rates. According to this argument, we need to re-think our approach to obesity research because the current approach just isn't working.

Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*. What gives? Maybe if we just scrapped the whole endeavor we'd be better off.

Let's take a closer look at this argument and see how it holds up.

Why Do Research?

There are two fundamental reasons why we do research:
  1. To gather accurate information about the natural world. This information is intrinsically valuable because we like knowing how the world works, and it may eventually have practical value that's not immediately obvious.
  2. Practical applications. We want to solve problems and improve our lives.
If we want to determine whether or not obesity research has failed, we should evaluate it using those two metrics.

Has Obesity Research Gathered Accurate Information?

Read more �

Wednesday, 21 May 2014

Princess Health and A New Understanding of an Old "Obesity Gene". Princessiccia

As you know if you've been following this blog for a while, obesity risk has a strong genetic component. Genome-wide association studies (GWAS) attempt to identify the specific locations of genetic differences (single-nucleotide polymorphisms or SNPs) that are associated with a particular trait. In the case of obesity, GWAS studies have had limited success in identifying obesity-associated genes. However, one cluster of SNPs consistently show up at the top of the list in these studies: those that are near the gene FTO.

As with many of the genes in our genome, different people carry different versions of FTO. People with two copies of the "fat" version of the FTO SNPs average about 7 pounds (3 kg) heavier than people with two copies of the "thin" version, and they also tend to eat more calories (1, 2).

Despite being the most consistent hit in these genetic studies, FTO has remained a mystery. As with most obesity-associated genes, it's expressed in the brain and it seems to respond somewhat to nutritional status. Yet its function is difficult to reconcile with a role in weight regulation:
  • It's an enzyme that removes methyl groups from RNA, which doesn't immediately suggest a weight-specific function.
  • It's not primarily expressed in the brain or in body fat, but in all tissues.
  • Most importantly, as far as we know, the different versions of the gene do not result in different tissue levels of FTO, or different activity of the FTO enzyme, so it's hard to understand how they would impact anything at all.
An important thing to keep in mind is that GWAS studies don't usually pinpoint specific genes. Typically, they tell us that obesity risk is associated with variability in a particular region of the genome. If the region corresponds to the location of a single gene, it's a pretty good guess that the gene is the culprit. However, that's not always the case...

Read more �

Tuesday, 29 April 2014

Princess Health and Fat vs. Carbohydrate Overeating: Which Causes More Fat Gain?. Princessiccia

Princess Health and Fat vs. Carbohydrate Overeating: Which Causes More Fat Gain?. Princessiccia

Two human studies, published in 1995 and 2000, tested the effect of carbohydrate vs. fat overfeeding on body fat gain in humans. What did they find, and why is it important?

We know that daily calorie intake has increased the US, in parallel with the dramatic increase in body fatness. These excess calories appear to have come from fat, carbohydrate, and protein all at the same time (although carbohydrate increased the most). Since the increase in calories, carbohydrate, fat, and protein all happened at the same time, how do we know that the obesity epidemic was due to increased calorie intake and not just increased carbohydrate or fat intake? If our calorie intake had increased solely by the addition of carbohydrate or fat, would we be in the midst of an obesity epidemic?

The best way to answer this question is to examine the controlled studies that have compared carbohydrate and fat overfeeding in humans.

Horton et al.

Read more �

Friday, 11 April 2014

Princess Health and More Graphs of Calorie Intake vs. BMI. Princessiccia

In the last post, a reader commented that the correlation would be more convincing if I graphed calories vs. average BMI rather than the prevalence of obesity.  It was a valid point, so I went searching for average BMI values from NHANES surveys.  I dug up a CDC document that contains data from surveys between 1960 and 2002 (1).  Because these data only cover five survey periods, we only get five data points to analyze, as opposed to the eight used in the last post.  The document contains BMI values for men and women separately, so I averaged the two to approximate average BMI in the general adult population.  It's also worth noting that I use the approximate midpoint of the survey period as the year.

First, a graph of average BMI over time.  It went up:



Now, let's see how well average BMI correlates with calorie intake:


The correlation between calorie intake and obesity prevalence was remarkable, but this correlation is simply incredible.  An R-squared value of 0.98 indicates that daily calorie intake and average BMI are almost perfectly correlated.

We can further deduce that each 100-calorie increase in daily food intake is associated with an 0.62-point increase in average BMI among US adults.  

Wednesday, 9 April 2014

Princess Health and Calorie Intake and the US Obesity Epidemic. Princessiccia

Between 1960 and 2008, the prevalence of obesity in US adults increased from 13 to 34 percent, and the prevalence of extreme obesity increased from 0.9 to 6 percent (NHANES surveys). This major shift in population fatness is called the "obesity epidemic".


What caused the obesity epidemic? As I've noted in my writing and talks, the obesity epidemic was paralleled by an increase in daily calorie intake that was sufficiently large to fully account for it. There are two main sources of data for US calorie intake. The first is NHANES surveys conducted by the Centers for Disease Control. They periodically collect data on food intake using questionnaires, and these surveys confirm that calorie intake has increased. The problem with the NHANES food intake data is that they're self-reported and therefore subject to major reporting errors. However, NHANES surveys provide the best quality (objectively measured) data on obesity prevalence since 1960, which we'll be using in this post.

Read more �

Wednesday, 2 April 2014

Princess Health and Uncovering the True Health Costs of Excess Weight. Princessiccia

Princess Health and Uncovering the True Health Costs of Excess Weight. Princessiccia

Is excess weight hazardous to health, or can it actually be protective? This question has provoked intense debate in the academic community, in some cases even leading researchers to angrily denounce the work of others (1). There is good evidence to suggest that excess body fat increases the risk of specific diseases, including many of our major killers: diabetes, heart attack, stroke, heart failure, cancer, and kidney failure (2). Yet strangely, the studies relating excess weight to the total risk of dying-- an overall measure of health that's hard to argue with-- are inconsistent. Why?
Read more �

Saturday, 22 February 2014

Princess Health and Why Do We Overeat?  A Neurobiological Perspective. Princessiccia

Princess Health and Why Do We Overeat? A Neurobiological Perspective. Princessiccia

I just posted a narrated Powerpoint version of my talk "Why Do We Overeat? A Neurobiological Perspective" to YouTube.  Here's the abstract:
In the United States, the "obesity epidemic" has paralleled a gradual increase in daily calorie intake.  Why do we eat more than we used to, and more than we need to remain lean-- despite negative consequences?  This talk reviews the neurobiology of eating behavior, recent changes in the US food system, and why the brain's hardware may not be up to the task of constructively navigating the modern food environment.
This is the same talk I gave at the University of Virginia this January.  I had a number of people request it, so here it is:
 
 
This is one of my favorite talks, and it was very well received at UVA.  If you find it informative, please share it!
 
 

Thursday, 13 February 2014

Princess Health and Mindless Eating. Princessiccia

Princess Health and Mindless Eating. Princessiccia

You think you're in control of your eating behavior-- but you aren't

In 2005, Brian Wansink's research group published a remarkable study that demonstrates the powerful unconscious influence of the food environment on our consumption (1).

Volunteers were invited to a test kitchen to eat bowls of tomato soup for lunch. Each person was given a bowl containing 18 ounces of soup-- but there was a catch. Half the volunteers were given custom-made soup bowls that partially refilled as they ate, such that the soup level dropped more slowly.
Read more �