Good Calories, Bad Calories Wrap Up

It’s hard for me to say how much to change diet based on GCBC. It does a pretty job of motivating a change away from a low-fat diet, but I also didn’t fact check any of the studies cited.

I think the best take-away is that making huge, sweeping decisions based on incomplete research is fraught with peril. Human health is a very complicated system, and suggesting that people make huge changes based on a few studies (as the US gov’t did), seems like a great way to make things worse instead of better.

After reading GCBC, I’m even more convinced that making big decisions without all the facts is a bad idea. And I don’t think we have all the facts now. GCBC makes a pretty good case that current and recent thinking about heart disease is incorrect. It also makes a pretty good case that obesity is a function of the types of things you eat, not just how much. Some of the other claims in the book, especially about cancer and Alzheimer’s, seem less well supported. The only thing that I’m really convinced of is that I need to do my own research regarding my health, and I can’t just take a doctor’s word for anything.

Am I going to make any changes to my diet based on reading this book? I may cut down on sugar intake a bit, though I already have pretty low sugar intake because I’m terrified of getting diabetes. I think I mainly still agree with Michael Pollan’s advice:

Eat food. Not too much. Mostly plants.

Although maybe the “mostly plants” part of that advice is mistaken, and my diet will be:

Eat Food. Not too much.

Fat Tissue Acts Like Capacitance

Batteries, as everyone knows, provide the power for most of the electrical gadgets that people use everyday. Batteries provide energy to a circuit by harnessing a slowly occurring chemical reaction.

Capacitors are equally important in electronics, but are less well-known outside the field. Capacitors are often used to “bypass” a power supply by providing energy faster than a battery can. Since batteries get power from a chemical reaction, they may not be able to respond fast enough if power requirements change quickly (for example when the transistors in a microcontroller switch states). To deal with the slowness of the battery, capacitors are charged from the battery and can be discharged when fast power is needed. One of the impacts of this is that capacitors get slightly discharged and recharged very often.

Until reading GCBC, I had always assumed that fat cells act more like a battery than a capacitor. It turns out that this isn’t the case. Fat cells do store energy in the form of fat (triglycerides), but they also release it fairly often. Fatty acids are constantly moving into and out of fat cells depending on how much energy is needed by the body. Fat cells will take in free fatty acids and tri-glycerides from the blood when blood sugar is high, and release fatty acids into the blood when blood sugar is low. This allows them to buffer energy levels from food.

According to GCBC, the flow of fatty-acids into and out of fat cells is governed by a molecule called glycerol phosphate. When glucose is metabolized in a cell, glycerol phosphate is produced. The glycerol phosphate is then released into the bloodstream, where it can be taken in by fat cells. The more glycerol phosphate in a fat cell, the fewer fatty acids the fat cell releases into the bloodstream.

Right after someone eats a meal containing carbohydrates, blood sugar rises. As the blood sugar is metabolized, glycerol phosphate is produced that causes fat cells to hold onto more of their fatty acids. This is good, because glucose is providing fuel for the body and fat isn’t needed for fuel. After a while, much of the glucose has been metabolized and glycerol phosphate levels fall. The fat cells then start releasing fatty-acids for the other cells in the body to use as fuel. That allows people to survive for long periods between eating.

Fat cells act like capacitors, continually storing up and releasing energy (in the form of fatty acids). It’s the metabolism of glucose, through glycerol phosphate, that manages this storage and release of energy.

Obesity

My father, when he was dealing with diabetes, also was overweight. That became kind of a big deal as his health faded. He kept trying to lose weight by exercising. He spent five years doing Tae Kwon Do with me (we got our black belts together), then kept up a pretty regular walking habit after that. I don’t think he ever lost any weight at all.

Since my dad’s death from diabetes and heart disease, I’ve been convinced that if he’d only tried a bit harder he would have lived longer. That if he’d dieted more or exercised more strenuously he could have lost weight, and then managed his diabetes better. This is kind of an upsetting opinion to hold, since it basically means that I’m blaming my dad for dying on me.

Good Calories, Bad Calories calls into question all of the conventional wisdom about obesity and weight gain. If the story in GCBC is right, then no amount of calorie restriction or exercise would have helped my dad. I find myself really wanting to believe it because it would mean my dad was a victim of poor medical advice, not poor self-control.

Low Calorie Diets Don’t Work

One of the most common findings in obesity research, according to GCBC, is that obese people tend to eat about the same amount as lean people. People who are obese aren’t overeating, at least not compared to non-obese people. Perhaps obese people just have different physiology than non-obese people, and need even fewer calories. If this was the case, then calorie restriction should lead to weight loss.

Not surprising to anyone, calorie restriction diets don’t work. There are a number of studies showing this fact. Ansel Keys even did a number of semi-starvation diet studies in which he reduced the calorie intake of subjects by a third or more. These subjects lost maybe 20 pounds, but also experienced other severe effects.

Subjects complained constantly of being hungry. They grew lethargic. They grew depressed. One subject in the study was enrolled in a psychiatric clinic halfway through because he was talking about hurting himself and others. Another subject actually did engage in self-harm near the end of the study.

The subjects didn’t even keep the weight off afterwards. Once the study ended, subjects ate as much as possible. When calorie restriction ends, people tend to eat until they have regained any lost weight and more. In several studies, participants who were later allowed an unrestricted diet complained that they didn’t feel full even after eating 8000 calories a day.

Several experiments on overfeeding have also been done. Subjects are given from 1000 to 8000 more calories per day than their standard diet. On these overfeeding diets, weight gain varies dramatically by person. Some people put on less than 10 pounds, others put on 30. After the studies end, subjects generally return to the weight that they had been at before the diet. This seems to indicate that diet by itself is not the most important factor in a person’s weight.

Standard calorie restriction dieting is not just ineffective, it also seems to be directly harmful to mental health.

Exercise Doesn’t Work

No studies have ever shown exercise can help reduce weight. A meta-study cited in GCBC estimated that, depending on type of exercise, weight can be expected to change by -3.2oz to 1.2oz. In other words, it may go up or down, but not by much.

I’m used to thinking of fast and slow metabolism being relevant to a person’s weight, but apparently this isn’t so. People who are overweight don’t just have more fat, they often have more connective tissues and muscle, which increases metabolism. The metabolism of overweight people tends to be higher than that of lean people, not lower. Furthermore, metabolic rates differ greatly between people even of the same weight. People of different weights may still have similar metabolic rates. So it seems that trying to raise metabolism by exercising won’t cause weight loss.

Low Carbohydrate Diets Often Work

Quite a few studies are described in GCBC that led to significant weight loss, and carbohydrate restriction was common among them all. Several studies were on diets of 800-1200 calories, mostly fat and protein. These were apparently pretty effective. Other studies were on unlimited calorie diets that limited carbohydrates to only 80 or 100 calories per day. These unlimited calorie diets were also effective at leading to people losing weight.

From the mid 1800’s to the mid 1900’s, it was apparently well known that low carbohydrate, high fat and protein diets would help someone to lose weight. It wasn’t until dietary fat became demonized for heart disease that it also came to be seen as the main cause of bodyfat. Several popular modern diets also subscribe to basically the same mechanisms, including the Atkin’s diet and the first stage of the South Beach Diet.

Interestingly, many of the larger studies on low carbohydrate diets didn’t work for everyone. Some studies had subjects that only lost weight if they ate no carbohydrates at all; some studies showed only half the people in the study lost weight. While low carb diets seem like the best bet for someone wanting to lose weight, they don’t seem like a sure thing.

Set Points

There’s a common theory that the body has a “set-point” for weight that it wants to stick to. No matter how you change behaviour, your body will try and stick to its set point. If you eat less, your body will try and do less and you’ll feel sluggish and tired. If you exercise more, your body will feel hungrier. So for an obese person to reduce their weight, the most effective thing to do would be to change that set point.

GCBC suggests that the set point is due to fat cells taking in energy at a different rate than they release it. Since fat cells support us between meals, we need enough fat to release energy for us when we’re exercising or not eating. If someone has fat cells that very easily release energy, they may need less fat in order to manage the between meal times. The opposite is also true; if someone has fat cells that have difficulty letting go of energy already absorbed, they may need more fat to release the required amount of energy over time.

According to GCBC, changing the amount of energy released by fat cells is as simple as changing how many carbohydrates you’re eating. If you eat a lot of carbs, it somehow messes with the system that allows fat cells to take in and release energy. Switching to low carb diets changes the set point, so you don’t even have to change the total number of calories you’re eating. This is a pretty cool system, so I’m going to save discussion of it for its own post.

If body weight is governed by a set-point that’s a function of diet, exercise, and biology, then that has a big impact on what kinds of diets and exercise people should do. Set point theory basically means that temporary diets or temporary exercise regimens (just until the weight is lost) are guaranteed to be a failure. Any weight a person wants to lose will require a permanent change in lifestyle.

Fat-Shaming Culture

“Theories that diseases are caused by mental states and can be cured by willpower are always an index of how much is not understood about the physical terrain of the disease.”
– Susan Sontag

Much of weight gain seems to be governed by hormones and genetics. Weight gain takes on a different character in men and women, as well as in different stages of life (childhood vs puberty vs adulthood). There also appear to be huge individual differences in how people put on weight that have nothing to do with lifestyle choices.

While a calorie may be a calorie, the human body is not a furnace. We don’t burn the food we eat for fuel, we break it down and convert certain molecules into other molecules for storage and metabolism. The body is better at doing this with different types of foods, and different people’s bodies respond differently.

The constant focus on the self-discipline aspects of obesity have created an environment in which, if someone is fat, they are automatically assumed to have personal failings as well. I’m a bit ashamed that it took a rebuttal of 50 years of medical advice to convince me to treat people with respect regardless of their size. Reading GCBC has drastically changed my mind about how much someone can affect their own weight through their behavior. I’m now much more comfortable with the idea that people who are overweight are not running down a path to destruction of their own volition.

That’s certainly the image I had of my father during the last years of his life. I had conceptualized his health decline as something entirely his own doing, which made it a lot harder for me to empathize with him in life or to deal with his death. After reading GCBC, I’ve gained the understanding that it wasn’t as easy as just making a simple dietary change or exercising a bit more. This new understanding has been crucial to me letting go of a lot of the sadness and blame that I’ve been feeling.

GCBC on Cancer, Alzheimer’s, and aging

I have a family history of both alzheimer’s and cancer. The conventional wisdom on both of these seems to be that they’re pretty lifestyle independent. There’s not a lot I can do to avoid them, since I don’t smoke and I drink only moderately. Having watched several family members succumb to Alzheimer’s, I would do a lot to avoid the same fate myself.

Alzheimer’s

Good Calories, Bad Calories lays much of the blame for Alzheimer’s on, you guessed it, carbohydrates. It seems the diabetics are twice as likely to get Alzheimer’s as non-diabetics, and diabetics who take extra insulin are four times as likely to get it. GCBC consistently uses this type of thing as evidence that they share the same cause.

Alzheimer’s disease is associated with the presence of compounds called amyloids in the brain. These amyloids are misfolded protiens that are toxic to nerve cells. They also form plaques in the brian which can kill nerve cells.

The human body has an enzyme that can clear out the amyloids. The enzyme is IDE, which is Insulin-Degrading Enzyme. As expected from the name, IDE primarily degrades insulin. If there’s a ton of insulin around, there might not be enough IDE to degrade the amyloids as well. That’s certainly the claim GCBC makes.

Since high carbohydrates can lead to high insulin levels, they may also be responsible for Alzheimer’s.

Cancer

Along with diabetes and obesity, cancer appears to increase greatly as societies westernize. The reason for this is commonly held to be environmental pollutants, but apparently many missionary doctors have noticed cancer increasing as diets change. Indiginous people living in their traditional ways have less cancer than indiginous people in the same location who have switched to western diets. Sugar consumption also apparently correlates extremely closely with breast cancer incidence across countries.

GCBC draws a link between carbohydrates and cancer (you knew that would be true, right?). This time, the intermediate hormone that GCBC implicates is IGF, or insulin-like growth factor. Insulin-like growth factors are present in the body normally and apparently serve important signalling functions. When large amounts of insulin are present, it causes even more IGF to be present. The insulin binds to sites that would have been bound by IGF, leading to higher blood concentrations of IGF.

There’s some research showing that IGF (specifically, IGF-1) stimulates the growth of prostate and breast cancer tumors. Tumors will often have two to three times as many receptor sites for IGF as normal cells. GCBC makes a pretty strong claim that IGF is the main reason that people in western civilizations develop cancers. The theory seems to be that mutations occur all the time, but having high levels of IGF allows cells with cancerous mutations to thrive. The extra IGF tells the cells to proliferate and grow. And if the receptor sites on a tumor get filled up by insulin instead of IGF, that just allows the absorption of more glucose to fuel the cancerous growth.

Honestly this section of the book was the least convincing to me. It seems plausible, but the mechanism suggested by GCBC is a lot less fleshed out than the mechanisms suggested for heart disease.

General Longevity

IGF and insulin have also been linked to longevity. Slower growth leads to longer life in many species. There’s even a fairly strong link in many species between calorie restricted diets and longer life in several animals, including larger primates.

Animal studies on calorie restriction show that the longer lived animals have lower blood sugar levels, lower insulin levels, and very high sensitivity to insulin. The conclusion drawn by GCBC is that carbohydrate restriction is the main cause of longevity benefits, and carbohydrate restriction is necessary to get the calorie restriction used in these studies. One study has shown that feeding glucose to worms shortened their lives, though I haven’t seen any research about that in large animals.

The obvious implication from GCBC is that eating fewer carbs will lengthen your life. While carb restriction is definitely easier than calorie restriction, it still seems like a pretty severe diet change for most people. Given what GCBC has to say on premature dietary suggestions made in the past, I’m not making any huge changes now.

Metabolic Syndrome

The central health claim of GCBC is that carbohydrates cause a lot of the lifestyle related illnesses that are rampant in western civilizations. The metabolic link between carbohydrates and heart disease, diabetes, or cancer is complicated. Overall, it’s summed up in the book as metabolic syndrome, a disorder in how the body produces and uses insulin.

Modern medical literature seems to treat metabolic syndrome as just a description of several symptoms that tend to appear together. The main symptom is having fat in organs not best suited for storing fat; other symptoms include high blood pressure, insulin resistance, and low levels of HDL. Once someone has metabolic syndrome, their likelihood of developing heart disease or diabetes skyrockets.

According to GCBC, the symptoms of metabolic syndrome all stem from the blood-sugar spikes that come from eating processed carbohydrates. This is also the accepted cause of diabetes, and GCBC makes the claim that diabetes is just a more advanced form of metabolic syndrome. If this is so, then the fact that diabetics are so much more likely to develop heart disease than non-diabetics can help explain the link between carbohydrates and heart-disease.

In order to understand how metabolic syndrome develops from eating carbohydrates, we have to understand how two different forms of sugar are metabolized in the body. Most sugars are made up of about half glucose and half fructose.

Glucose

Glucose is the fuel for cells in the body. When glucose is consumed, it eventually makes its way to the blood stream. As far as I can tell, glucose is the only sugar that counts as blood sugar. Once in the blood stream, insulin in the blood allows the glucose to be taken into a cell. The glucose can then be metabolized by mitochondria to provide the cell with the energy it needs to stay alive and do its thing.

This is why the pancreas produces insulin after you eat. Blood sugar is going up, so the body needs insulin in order to use the glucose.

Fructose

Fructose is digested much differently than glucose. It can’t be processed anywhere except the liver.

Since it can’t be used in most of the body, fructose doesn’t cause an insulin spike or count as blood sugar. Instead, it get’s converted into triglycerides in the liver, which VLDL then transports to fat cells for storage. Remember from the post on fat that VLDL is highly associated with heart disease. Turns out VLDLs probably cause heart disease because they lead to physically smaller LDLs. Those smaller LDLs can make their way into damaged areas of an artery wall and cause plaques.

Furthermore, when the liver has high levels of fructose in it, it focuses on the fructose and ignores all the glucose. This means that the blood glucose levels stay higher longer, in turn prompting the pancreas to produce even more insulin.

Insulin

So glucose directly causes insulin to rise. Fructose causes it to rise indirectly, by decreasing glucose metabolism in the liver. Why does that matter?

What I didn’t know before reading this book is that insulin is not just used to allow uptake of glucose. It’s also used to regulate fat storage within the body. Higher levels of insulin cause fat to be stored, rather than burned for energy. If insulin is high for long enough, organs in the body will start to put on fat. That’s exactly the primary symptom of metabolic syndrome mentioned above.

Chronic high insulin levels cause body tissues to become less sensitive to insulin. That’s when diabetes type 2 develops. Your body is still make insulin in response to the blood sugar floating around, but your tissue ignores it more. In order to overpower the insulin resistance, type 2 diabetics often have to take insulin injections.

Metabolic Syndrome in Action

To sum up the first half of the book, metabolic syndrome is the true cause of many of the diseases of western civilization. The symptoms of metabolic syndrome, according to GCBC, are all caused by eating too much sugar and simple carbohydrates. High levels of fructose will lead to heart disease through the formation of small LDLs. High levels of glucose will lead to insulin resistance, which in turn leads to diabetes and fat in places it shouldn’t be.

That’s about all there is to it, and that’s about exactly the opposite advice that I got about the effect of diet on health up until reading this book.

Everything Bad is Good for You

GCBC is pretty contrarian in it’s health advice. It doesn’t come out and say you should change your diet in any specific way, but it does call into question a lot of the things I had always assumed were indisputable.

Salt

The most surprising part of GCBC for me was the very weak link between salt and high blood pressure. The medical wisdom seems to be that if you eat salt, your body will have to hang on to more water in order to keep your blood at the right pH. The research cited in GCBC seems to show that this does happen, but not actually all that much.

The best you can hope to do by halving your salt intake is about 2-5mmHg lowering in blood pressure. Given that the safe range of blood pressure is 100-140mmHg systolic and 60-90mmHg diastolic, a change of 5mmHg doesn’t seem that significant. Salt probably won’t push you out of the healthy range, so there must be something else going on.

The alternative proposed in GCBC is that eating lots of carbohydrates is actually what causes hypertension. The idea is that eating carbohydrates causes insulin spikes, which causes the kidneys to retain salt (regardless of salt in diet), which causes the body to retain water, which causes high blood pressure.

This is a pretty long chain of cause and effect, but apparently cutting out carbohydrates has been shown to work as well as using diuretics to reduce blood pressure. Hypertension is also often associated with insulin-resistance, which implies some kind of effect from carbohydrates.

Fat

The other controversial suggestion in GCBC is that eating fatty foods doesn’t cause or contribute to heart disease. In fact, a huge chunk of the book is spent in support of this assertion. You should read the whole book if you want all the details, but the main idea seems to hinge on a confusion of what cholesterol is and how it works in the body.

The historical perspective has been that eating fat leads directly an increase in blood cholesterol. Blood cholesterol then builds up in arteries, forming plaques. These plaques create bottlenecks in arteries that can then be blocked, leading to heart attacks. That story is the main impetus for the huge push to lower fat intake over the past 50 years.

According to GCBC, the science of cholesterol has progressed significantly from where it was in the mid-1950s.

It turns out that cholesterol is a critical ingredient in cell membranes, some hormones, and other functions. Our bodies will make it when we need it, but if we get it in our diets then our bodies will just use that instead. It gets made in the liver or taken in from food and transported by blood to the various tissues of the body. However, cholesterol doesn’t dissolve well in water. It turns out it needs to be transported in the blood by lipoprotiens.

Each lipoprotien serves as a carrier for a bunch of cholesterol (or some other fatty molecule). Lipoprotiens come in different sizes and types, smaller ones holding less cholesterol. The less protien you have, the smaller your lipoprotiens. This is what the so called HDLs, LDLs and VLDLs are. They’re not cholesterol at all, they’re the cholesterol transport mechanisms.

HDLs transfer fatty molecules away from cells that don’t want them by interacting with a binding site on the outside of the cell. HDLs are not associated with having heart disease.
LDLs transfer fatty molecules to the cells that want them. Cells that want fatty molecules will create receptacles on their membrane that will accept LDL molecules. LDLs are associated with having heart disease.
IDLs apparently get turned into large LDLs, which aren’t that likely to give you heart disease.
VLDLs apparently get metabolized into small LDLs. VLDLs themselves are associated with heart disease. The small LDLs that are created from VLDL are also associated with heart disease.

I think GCBC didn’t quite get this right. You need both HDL and LDL because they do different jobs. What GCBC does seem to be right about is that LDL (and thus IDL and VLDL) itself is associated with heart disease, but cholesterol doesn’t seem to be. I don’t think there’s much scientific dispute about this now, but I do think that medical researchers are trying to cover their asses for all that talk about cholesterol 50 years ago. Why else would the wikipedia cholesterol page spend 10 long paragraphs talking about LDL and HDL with only a small note at the beginning stating that they aren’t actually cholesterol?

So if fat affects cholesterol (which it does seem to), then what does it do to the amount of IDL and VLDL? It seems like what we want is probably IDL instead of VLDL to protect ourselves from heart disease. The claim in GCBC is that eating carbohydrates leads to lots of VLDL and not much IDL. Eating fat will have a small effect on cholesterol, but no effect at all on IDL and VLDL levels.

So the takeaway according to GCBC is don’t worry too much about fat in the diet.

Nutrition and Politics

My dad developed diabetes when he was in his twenties, and struggled with it for the rest of his life. Throughout my childhood, I had a bunch of conversations with him about what diabetes was and how he was dealing with it. As I got older, I watched his health decline faster and faster. He died suddenly of diabetes related heart failure while I was in grad school.

Since then, I’ve read a lot more about nutrition and health. The more I learn, the more I believe that my dad was treated using the best advice politicians could give. GCBC goes into some detail about how politics played a huge part in how heart disease and diabetes were treated historically, and how a lot of evidence about the origins of those diseases was ignored.

Large portions of GCBC are spent explaining the history of nutrition science in excruciating detail. Study after study is held up and compared to everything else. After slogging through all of that, the takeaway seems to be that one guy was sure he was right, and everyone else fell in line and stopped studying (or believing studies about) other hypotheses.

Ansel Keys first popularized the idea that cholesterol was the main cause of heart disease after WWII. He then found a link between eating high fat diets and having lots of cholesterol. Nevermind that no causal studies were performed, he was convinced. The next fourty years saw the production of a number of not very convincing studies that were used to inspire huge changes in the American diet.

Once Keys had convinced a critical mass of scientists and politicians, everyone who questioned the idea that cholesterol was to blame was treated with derision in an epic example of groupthink. A government panel released a report called “Dietary Goals for the United States”, which recommended a diet for all Americans based on Keys’ cholesterol ideas.

The motivation for all of this seemed to be the mass prevention philosophy of Geoffrey Rose. The idea was that, even though all the studies on dietary fat hadn’t shown much impact for a given person, the impact on society was huge. For example, it was estimated that you could live an extra 4 months if you completely cut saturated fat out of your diet. That may not be much for you, but if everyone did that the effect would be huge.

Since 4 months of additional lifetime might not be enough to convince someone to completely cut saturated fat out of their diet, Rose explicitly advocated creating social pressure to be healthy. Social pressure, unfortunately, is often highly resistant to scientific evidence. This effectively meant that future scientific discoveries would have a very difficult time changing anything.

The science became political goals. The political goals led to social manipulations. After that, the early scientific ideas became dogma. Subsequent research on nutrition was interpreted in light of that dogma and very little advancement happened.

Or that’s the idea that GCBC espouses. I take less of a cynical attitude. It’s easy to make the right decisions with the benefit of hindsight. I’ve seen some talks that take a more conspiratorial view of things. I don’t think that these nutrition decisions were made optimally, but why ascribe to malice what can be explained by human nature?

Whatever the reason, the increasing incidence of heart disease and diabetes since “Dietary Goals for the United States” was released is only tragic.

Good Calories, Bad Calories

I’ve been hearing about Good Calories, Bad Calories for a while now. Several people have recommended it to me as a great source of nutrition wisdom. I was a bit pessimistic before reading it, since my understanding of nutrition has always been that most people (even the experts) aren’t really sure what’s going on.

After picking up a copy, I was surprised to find that it was mostly a chronicle of nutrition research over the past century and a half. I was definitely expecting more of a diet book. The author has his ideas about the healthiest way to eat, but a lot of the book is actually about all the different people who’ve researched aspects of nutrition throughout history.

I enjoyed reading the book, and I think that I have a much better sense of the details of nutrition now. I’m planning to write a blog post about a few of the major themes I see running through the book to cement my thinking on it.

These include:
1. The fact that large organizations (the AHA and the US gov’t) take half-formed scientific research as gospel. The result of that, according to GCBC, have been making people sick for a century.
2. Everything bad is good for you
3. Metabolic Syndrome is a thing
4. Aging and Cancer
5. Obesity

Rise: Support Your Health

I’ve been working hard for the past six months designing Rise, a new quantified self health tracker. It’s an accelerometer-powered device that sits on a person’s leg and helps them keep track of how much they’re sitting. Sitting, and being generally sedentary, have been linked to a whole host of health problems. Sitting too much can lead to blood clots in the legs in the short term, and diabetes and increased risk of heart disease in the long run.

The health problems that sitting causes are pretty simple to avoid: just sit less. Even getting up for just a few minutes every hour can have a marked impact on the health of the average office worker. So if it’s so easy to solve the sitting problem, then why did I spend so much time working on it?

It’s because sitting is insidious. People don’t notice how much they sit, and when they do notice it’s often because health problems are already starting to crop up. Rise, our sit tracker, will not only track how long a person has been sitting but send periodic alerts to let the wearer know its time to stand up and walk around for a bit. We’re building apps for both Android and iOS so that this is accessible to as many people as possible.

It’s been a fun project to work on, and a great extension of the research that I did when I got my Master’s. We’ve launched an IndieGoGo crowdfunding campaign to help turn the prototypes into final products. I’m excited to see how the campaign goes, and to see my work actually get out into the world and help some people. If you’re interested, you can check it out here.

The industrial revolution

From Makers: The New Industrial Revolution:

Although we think of factories as the “dark satanic mills” of William Blake’s phrase, poisoning their workers and the land, the main effect of industrialization was to improve health. As people moved from rural communities to industrial towns, they moved from mud- walled cottages to brick buildings, which protected them from the damp and disease. Mass- produced cheap cotton clothing and good- quality soap allowed even the poorest families to have clean clothing and practice better hygiene, since cotton was easier to wash and dry than wool. Add to that the increased income that allowed a richer and more varied diet and the improved access to doctors, schools, and other shared resources that came with the migration to cities, whatever ill effects resulted from working in the factories was more than compensated for by the positive effects of living around them. (To be clear, working in factories was tough, with long hours and poor conditions. But the statistics suggest that working on farms was even worse.)

It’s interesting that the industrial revolution seems to have led to a net increase in health even at the beginning. I had always thought that people who worked in factories experienced much worse health overall. Given that the switch to agriculture did have a negative impact on health, it seems that social changes have pretty un-intuitive consequences.