AIDS, the common cold, and measles are examples of diseases that are known to be contagious. A recent article in PLoS Computational Biology describes another medical condition that is contagious--obesity.
Obviously, obesity is not commonly thought of as a transmissible condition. Perhaps if you believe that you should feed a cold and starve a fever, there might be a contagious element to obesity, but that's stretching it. However, one of the authors of the PLoS article, Nicholas A. Christakis, had observed in an earlier article in the New England Journal of Medicine that members of the Offspring Cohort of the Framingham Heart Study were 57% more likely to become obese if they had a friend who became obese during a certain interval.
Obesity and social networks
Christakis and his colleagues showed the phenomenon of the person-to-person spread of obesity in a graphic that can be viewed here. While the obesity of siblings and the obesity of spouses had an effect on the obesity of participants in the Offspring Cohort, the most important social network tie for transmission of obesity was mutual friendship. Interestingly, geographic separation did not diminish this phenomenon.
An infectious model for obesity
In 1971, the obesity of the Offspring Cohort of the Framingham Heart Study was 14%. By the year 2001 it was 29% and was continuing to increase. (Obesity was defined as a BMI of 30 or more.) In 2010, in the PLoS article Infectious Disease Modeling of Social Contagion in Networks, Hill et al. took the information from the 7500 members of the Offspring Cohort and used it to formulate an infectious disease model of obesity that they called SISa.
As described in the SISa model, the infectious equation for obesity includes a spontaneous appearance factor. Some percentage of people will spontaneously or automatically become obese in a particular year. In the Offspring Cohort, the rate of spontaneous obesity began at 0.8% in 1971 and has increased to 1.9% in 2001.
The infectious disease model of obesity also includes a remission factor that describes percentage of people who transition from obesity to a BMI below 30. The remission factor was unchanged over 30 years and was about 4% per year.
Finally the model includes an interpersonal transmission rate. That rate has increased over the years, from 0.12% for each obese friend in 1971 to 0.5% per obese friend in 2001. In other words, if a member of the Offspring Cohort had more than four obese friends, he or she would have an increased likelihood of being obese in the next year.
Transmission of obesity
In a news story in Science Daily, Dr. Hill speculated that the non-social transmission of obesity may result from unhealthy foods or increasingly sedentary lifestyles. (She did not rule out possible dietary causes such as consumption of HFCS, industrial oils or grains.) For the Offspring Cohort, the non-social transmission rate seems to have leveled off at about 2%. However, the social-network transmission of obesity continues to increase and has several interesting aspects.
It appears that the more obese friends a person has, the more likely that person is to become obese. It is the absolute number of obese friends that matters, not the percentage of friends who are obese. Conversely, the number of normal-weight friends seems to have no effect on a person's ability to avoid obesity or to recover from obesity once it occurs.
The authors speculate that the increasing prevalence of obesity provides a positive feedback mechanism. People will have more friends who are obese and will become inclined to think that obesity is "normal." When they themselves start gaining weight, they may see no reason to avoid the weight gain because several people they know and respect carry an increased amount of weight.
Interventions
If we live in a society that is becoming increasingly obese, and we want to remain at or attain a normal weight, do we want to avoid making friends who are obese? Obviously not. Perhaps it will be enough to know that having obese friends can subtly influence us to believe that obesity is normal or even necessary for us to fit in with our peers. With a certain amount of effort, perhaps we can learn to accept friends who are obese without compromising our own pursuit of a journey to good health.
10 comments:
Hi Stargazey,
I have been reading through your posts today after I visited Paul Jaminet's blog and I find them interesting. I enjoy wasting my time on paleo blogs. ;)
I have been low carbing for the last 2 and a half years and I managed to lose weight and maintain it. However, I couldn't reach the desired weight (about 4 kgs to go and some abdominal fat - I am 42, female and had two kids) and there are some hormonal problems. Theoretically speaking, is it possible that low carbing leads to calorie restriction and reduced T3 which leads to high LDL, hairloss, acne, dry skin, constipation, certain infections, etc.? That is my experience and although I went to see an endocrinologist (in August this year) it wasn't a lucky visit as I didn't come out more informed and she didn't give me a prescription for T3 either. She just wants me to take Lipitor.
Do you have any ideas?
I haven't lost almost any weight this year (about 2 kgs in January and about 2 also in July, the latter I put back on). I wonder if my conversion to T3 is permanently damaged or it will reverse to normal if I eat more calories (I used Fitday a few times and it came at around 1400 kcal a day)
At this point I don't know what to do next. After reading The Perfect Health Diet blog I started taking more vit C, NAC, eating more starchy carbs in the hope to improve my health. (some strange skin issues)
Thanks a lot.
Hi, lightcan and welcome!
I've heard that low-carbing may cause a problem with T3 conversion, but it's also possible that your reduced ability to convert T4 to T3 is a result of something else. Did the doctor do a free T3 level? (The test is quite expensive, so it's not normally done as part of a blood panel.) If free T3 was normal, she probably didn't see a good reason to give you more.
As far as skin issues, are you getting enough omega-3 fatty acids and vitamin D?
Regarding the LDL, was it a calculated value or was it measured directly? The calculation method doesn't work properly for low-carbers because their triglycerides tend to be quite low. Also, particle size matters. Low-carbers tend to have large fluffy LDL, which is much less dangerous than the small dense LDL that high-carbers have.
Just a few ideas. I have a Ph.D., not an M.D., so please don't construe any of this as medical advice. Best wishes, though, as you look for solutions.
Hi,
I understand your position and I am glad that you could give your interpretation of the data. My LDL doubled on the high-fat diet and although it might be of the 'fluffy' variety (without a NMR or a VAP test we can only speculate) it is still high. Chris Masterjohn says if there is more of it, that is the cells don't need it and don't ask for it, it is more likely to oxidise. It is of course calculated but I don't think it makes that much of a difference.
2003 normal diet
LDL 2.82 trig 0.72 (mmol/l)
after 2 months on low carb, losing weight
LDL 4.7 trig 0.6
one year later
LDL 10.9 trig 0.7
I asked around on the web and I'm told not to worry.
I still have to get my results back and then I can tell you the exact numbers regarding fT3. I understand it's at the low end of the range.
I am taking vit D, avoiding omega 6 and sometimes taking omega 3. I took at least 2 g on a regular basis for the last 2 years.
Thank you for your kindness.
Fascinating post! The situation is a bit similar with smoking, I believe.
Dear lightcan,
We discussed your T3/FT3 amongst other things a year ago on my blog HERE. It was well below the Reference Range then.
Do you have recent test results and Reference Ranges?
Best wishes, Nige.
Ned--you're right about the smoking. In fact, Christakis and Fowler addressed it in the NEJM, The Collective Dynamics of Smoking in a Large Social Network. By the way, I'm enjoying your blog. Thanks for introducing me to it!
Nige--I followed the link and agree with your recommendation that lightcan needs to insist on an Rx for Cytomel (or the generic, liothyronine) until her free T3 gets into a normal range. Not that I'm a physician, but it seems strange that the specialist will put her on expensive statins rather than cheap liothyronine to bring her free T3 into the normal range. And I'm glad to see you're back to blogging!
Hi Stargazey,
This comment doesn't fit with your most recent post so you might not want to show it, but I came across some information that I hope you can interpret in a future post.
I eat VLC and use stevia because Dr. Bernstein recommends it in his book--I'm pre-diabetic due to impaired glucose tolerance. Now I read that stevia increases insulin production by acting directly on the beta cells. That doesn't sound good.
The Website http://zhion.com/blog11/?p=204 was the most credible I found trying to learn more. It's about a mouse study--not exactly applicable. And I also can't figure out how much glucose 16.7 mmol/L is equal to--any way to translate it into grams? That's the amount the study found the mice had to ingest for stevia to enhance their insulation secretion.
Can you determine whether stevia is good or bad? Is liquid sucralose better--I thought it was worse. Bottom line: I don't want to burn out any more beta cells than I already have.
I learn a lot on your blog. I hope you can help with this topic.
Thanks.
I was wondering if you could offer your thoughts on a problem i have:
what about blood glucose readings after a meal?
I've been low carbing for a while, but for the past few months i've been eating 30g carbs in the form of white rice a day (only carbs of the day) and my glucose levels go crazily high. Is this normal, or should my body have adapted to it by now?
Hi, Razamatazz! No it's not normal for your blood sugars to go that high if you're eating 30 grams of carbs every day. Your body may be entering the early stages of diabetes. Low-carbing can prevent or delay the onset of diabetes, but it doesn't always. To be safe, you should go to a carb-knowledgeable doctor to find out about that. (If you go to a conventional doctor, they might put you on the carb-heavy ADA diet plus medication and you'd end up even worse in the long run.) I hope you're able to get an answer that helps you.
I apologize jkim. Your comment has been trapped in my spam filter and I just found it there.
Just a few thoughts. You're right about the limited applicability of studies done in rodents as well as those done in cultured cells. All those studies can do is indicate that humans may experience similar results, but there is no guarantee of that. In the link you cite, there was a study done in humans, but there were only twelve subjects, so the statistics aren't strong enough to be sure about the results.
In any case, stevia, aspartame and sucralose have been used long enough that there are probably no terrible side effects produced by any of them. By contrast sugar and high fructose corn syrup have a very negative effect on insulin sensitivity in the long term and are very likely to promote obesity. If you need to eat something sweet, I'd recommend the artificial sweeteners.
1 mmol/L of glucose is the equivalent of 18 mg/dL. So 16.7 mmol/L would be the same as a U.S. blood sugar reading of 300 mg/dl.
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