The New England Journal of Medicine published an childhood obesity article today describing a study that projects that between 55 to 60 percent of today’s children will be obese by the time they reach 35 years of age.
One child in 11 is currently obese in the U.S. (ages 2 through 5). Childhood obesity is the main risk factor for adult obesity (no surprise there) but obesity in childhood is also a major risk factor for adult depression.
We can’t blame genes for childhood obesity — genes haven’t changed much since the 1960s, when childhood obesity was almost unheard-of. And we can hardly blame a two year old for poor life choices.
We can, however, look at sugar consumption, between-meal snacking, juice and sugared beverage consumption, seed oil consumption, and high-carbohydrate meals, all of which have ballooned since the sixties. Poverty is also a major contributor — obesity, particularly childhood obesity, is disproportionately represented in low income communities. These communities have less access to fresh vegetables, and what they do have access to is subsidized high-carbohydrate, low fiber products of industrialized agriculture and processed food companies.
Parents often give children fruit juices in bottles or juice boxes to keep them busy, keep them from crying, or because they think juice is healthy. But fruit juice has had most of the healthy fiber removed, leaving little but sugar water and a bit of flavoring. Worse, many fruit drinks have added sugar. Both natural and added sugar creates addiction to sugar, which makes the child cry or whine when it is not present, causing the parent to give in to the addiction.
Try plain water. You can add a bit of lemon or other fruit to add a touch of flavor, without all the sugar.
Whether it takes the form of reduced calories, reducing one of the nutrient types (protein, fat, or carbohydrate), or fasting occasionally (not eating for a day or two), dietary restriction has been shown to have beneficial effects in all manner of organisms, such as yeast, worms, flies, mice, monkeys, and humans.
When studying lifespan, it helps to work with organisms that have very short lifespans, where the effects of an intervention can be seen in the researcher’s lifetime. This is why much of the work has been done in short-lived species such as yeast, fruit flies, tiny worms, and mice. In these organisms, we see common mechanisms that dietary restriction triggers to increase lifespan, and we see those same mechanisms at work in longer lived animals, such as humans, even if we haven’t had time to collect a lot of data on actual lifespans.
Complicating the picture in humans is that not many have signed up for a lifetime of dietary restriction.
But recent work has shown that intermittent fasting causes the same changes in mitochondria that constant dietary restriction causes. And it is these changes in the mitochondria that are responsible for the extended lifespans.
This is very good news, as skipping a few meals every now and then is something people can do easily, and many people are already doing it, for a number of reasons, not the least of which is that it is an effective weight-loss technique. That it might also make you live a longer and healthier life is definitely a plus.
This life-extension benefits of intermittent fasting happen even if the organism is not overweight, so it is separate from the health benefits of avoiding obesity.
Besides dietary restriction, the antibiotic rapamycin has also been shown to increase lifespan in yeast, fruit flies, and mice.
In studying the effects of rapamycin, a metabolic pathway called TOR (short for ‘Target Of Rapamycin’) was found. Rapamycin inhibits TOR. TOR, in turn, inhibits messenger RNA, the molecule that translates the DNA code into protein. So rapamycin increases messenger RNA, thus increasing protein production in cells.
It turns out that dietary restriction and intermittent fasting decreases protein production in cells (as you might expect), except for in the mitochondria, where it actually increases protein production.
It is this increase in mitochondrial protein production that is one of the keys to longevity.
Another key is autophagy, which is a kind of basic housekeeping that cells do (it means ‘eating oneself’). Older, damaged parts of the cell are recycled for their nutrients, and replaced by new undamaged parts.
As it turns out, dietary restriction increases autophagy, through a mechanism involving the TOR pathway.
We are beginning to see a pattern here.
A particular form of autophagy affects mitochondria. Unsurprisingly, it is called mitophagy. Youthful mitochondria fuse together, but as they age they can toggle into fragmented states. In their youthful, fused state, mitochondria extend lifespan by communicating with organelles in the cell called peroxisomes to control fat metabolism. This is described more fully in a recently published paper.
Thus lifespan and energy metabolism are closely linked.
The central molecule in metabolism is adenosine triphosphate (ATP).
ATP is the molecule created when we digest food. It is used in cells as an energy source, where its phosphates are removed one at a time, extracting energy from the molecule with each one. The resulting molecules are adenosine diphosphate (ADP) and adenosine monophosphate (AMP).
Because this molecule is central to all life, there are a lot of signalling molecules that interact with ATP and with AMP. One of these molecules is the enzyme AMP-activated protein kinase (AMPK).
The paper discussing mitochondria and lifespan points out that they could increase lifespan either by intermittent fasting, or by tinkering with an organism’s genes for AMPK.
As the name implies, AMPK is activated by AMP. As ATP is used to provide energy to cells, the depleted form, AMP, builds up, and activates AMPK. AMPK is thus a cellular energy sensor, responding to low levels of ATP (i.e. high levels of AMP).
Low glucose levels activate AMPK. So does low oxygen (hypoxia), since oxygen is needed to burn food to produce ATP. Inadequate blood supply (ischemia) can cause low glucose and oxygen levels, and thus activate AMPK. Changes in calcium levels caused by exercise also activate AMPK.
It is by activating AMPK that the hormone adiponectin increases glucose and fatty acid burning, an effect covered in detail in Gut Reactions.
My book, Gut Reactions: The Science of Weight Gain and Loss, deals with weight loss from dozens of angles, from genetics, food choices, exercise, psychology, and hormones, to advertising, cultural pressures, and childhood priming.
Walk past the diet section in a bookstore and you will find hundreds of books that each claim to have the solution to weight problems. Whether it’s a low-fat diet, a low carbohydrate diet, a Paleolithic diet, a gluten-free diet, or any number of other magical things to try, they all claim that your weight loss problem is simple, and has a simple solution.
The popularity of these diets is linked to the observation that they all seem to work. Why would all of these different approaches to weight control all have success? One reason is that they all limit your choices. When you are not able to eat everything in sight, you tend to eat less. Another reason is that each diet targets a different set of people, and work for that set, if not for others.
Of course, they all work until they don’t. Limiting your diet in this way is difficult to do for long periods of time.
There aren’t many things that we expect to work for all people all the time. People are different from one another. There are genetic differences, cultural differences, behavioral differences, psychological differences, and social differences, and they all play a part in the weight maintenance equation. Add to these differences age, gender, gut microbiology, and environment and it becomes clear that weight control is a personal thing, and the solutions might have to change not only with each individual, but also with time and setting.
Obesity is not one disease. There are many sub-types of obesity. Some people will have disorders in how their bodies manage energy balance, while others may have differences in how they respond to reward, making it hard for them to resist highly palatable foods. There are many ways to affect our body composition towards more fat, and that is what this book is about.