Tuesday, November 29, 2011

Another Simple Food Weight Loss Experience

Whole Health Source reader Sarah Pugh recently went on a six-week simple food (low reward) diet to test its effectiveness as a weight loss strategy, and she was kind enough to describe her experience for me, and provide a link to her blog where she discussed it in more detail (1). 

Consistent with the scientific literature and a number of previous reader anecdotes (2), Sarah experienced a reduction in appetite on the simple food diet, losing 15 pounds in 6 weeks without hunger.  In contrast to her prior experiences with typical calorie restriction, her energy level and mood remained high over this period.  Here's a quote from her blog:
Well, it looks like the theory that in the absence of nice palatable food, the body will turn quite readily to fat stores and start munching them up, is holding up. At the moment, the majority of the energy I use is coming from my insides, and my body is using it without such quibbles as the increased hunger, low energy, crappy thermo-regulation or bitchiness normally associated with severe calorie restriction.
I can't promise that everyone will experience results like this, but this is basically what the food reward hypothesis suggests should be possible, and it seems to work this way for many people.  That's one of the reasons why this idea interests me so much.

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Saturday, November 26, 2011

A Brief Response to Taubes's Food Reward Critique, and a Little Something Extra

It appears Gary Taubes has completed his series critiquing the food reward hypothesis of obesity (1).  I have to hand it to him, it takes some cojones to critique an entire field of research, particularly when you have no scientific background in it.

The food reward hypothesis of obesity states that the reward and palatability value of food influence body fatness, and excess reward/palatability can promote body fat accumulation.  If we want to test the hypothesis, the most direct way is to find experiments in which 1) the nutritional qualities of the experimental diet groups are kept the same or at least very similar, 2) some aspect of diet reward/palatability differs, and 3) changes in body fat/weight are measured (for example, 2, 3, 4, 5, 6, 7, 8, 9).  In these experiments the hypothesis has both arms and one leg tied behind its back, because the most potent reward factors (energy density, sugar, fat) have nutritional value and therefore experiments that modify these cannot be tightly controlled for nutritional differences.  Yet even with this severe disadvantage, the hypothesis is consistently supported by the scientific evidence.  Taubes repeatedly stated in his series that controlled studies like these have not been conducted, apparently basing this belief on a 22-year-old review paper by Dr. Israel Ramirez and colleagues that does not contain the word 'reward' (10). 

Another way to test the hypothesis is to see if people with higher food reward sensitivity (due to genetics or other factors) tend to gain more fat over time (for example, 11, 12, 13, 14, 15, 16).  In addition, studies that have examined the effect of palatability/reward on food intake in a controlled manner are relevant (17, 18, 19, 20, 21, 22), as are studies that have identified some of the mechanisms by which these effects occur (reviewed in 23).  Even if not all of the studies are perfect, at some point, one has to acknowledge that there are a lot of mutually buttressing lines of evidence here.  It is notable that virtually none of these studies appeared in Taubes's posts, and he appeared largely unaware of them. 
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Monday, November 21, 2011

The Super Committee Failure—What’s Next?

The stock market today was shocked, simply shocked, that the Super Committee didn’t come up with a debt deal.I don’t know why. Republicans can’t vote for more taxes unless they're willing to get “primaried” from the right and risk losing their seat. Ditto for Democrats who would face the same punishment from their base if they voted to change the sacred defined benefit entitlements without at

Sunday, November 20, 2011

Two Recent Papers by Matt Metzgar

This is just a quick post to highlight two recent papers by the economist and fellow health writer Matt Metzgar.

The first paper is titled "The Feasibility of a Paleolithic Diet for Low-income Consumers", and is co-authored by Dr. Todd C. Rideout, Maelan Fontes-Villalba, and Dr. Remko S. Kuipers (1).  They found that a Paleolithic-type diet that meets all micronutrient requirements except calcium (which probably has an unnecessarily high RDA) costs slightly more money than a non-Paleolithic diet that fulfills the same requirements, but both are possible on a tight budget. 

The second paper is titled "Externalities From Grain Consumption: a Survey", with Matt Metzgar as the sole author (2).  He reviews certain positive and negative externalities due to the effects of grain consumption on health.  The take-home message is that refined grains are unhealthy and therefore costly to society, whole grains are better, but grains in general have certain healthcare-related economic costs that are difficult to deny, such as celiac disease.

There are a lot of ideas floating around on the blogosphere, some good and others questionable.  Composing a manuscript and submitting it to a reputable scientific journal is a good way to demonstrate that your idea holds water, and it's also a good way to communicate it to the scientific community.  The peer review process isn't perfect but it does encourage scientific rigor.  I think Metzgar is a good example of someone who has successfully put his ideas through this process.  Pedro Bastos, who also spoke at the Ancestral Health Symposium, is another example (3).

Thursday, November 3, 2011

Does High Circulating Insulin Drive Body Fat Accumulation? Answers from Genetically Modified Mice

The house mouse Mus musculus is an incredible research tool in the biomedical sciences, due to its ease of care and its ability to be genetically manipulated.  Although mice aren't humans, they resemble us closely in many ways, including how insulin signaling works.  Genetic manipulation of mice allows researchers to identify biological mechanisms and cause-effect relationships in a very precise manner.  One way of doing this is to create "knockout" mice that lack a specific gene, in an attempt to determine that gene's importance in a particular process.  Another way is to create transgenic mice that express a gene of interest, often modified in some way.  A third method is to use an extraordinary (but now common) tool called "Cre-lox" recombination (1), which allows us to delete or add a single gene in a specific tissue or cell type. 

Studying the relationship between obesity and insulin resistance is challenging, because the two typically travel together, confounding efforts to determine which is the cause and which is the effect of the other (or neither).  Some have proposed the hypothesis that high levels of circulating insulin promote body fat accumulation*.  To truly address this question, we need to consider targeted experiments that increase circulating insulin over long periods of time without altering a number of other factors throughout the body.  This is where mice come in.  Scientists are able to perform precise genetic interventions in mice that increase circulating insulin over a long period of time.  These mice should gain fat mass if the hypothesis is correct. 

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