Here are episodes 1, 2, and 3:
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Here are the shownotes for the first three episodes.
I'm starting the podcast with coffee, because I start my day with coffee.
Why I drink coffee and won't apologize for it, but why I'm skeptical of the large body of literature associating coffee consumption with reduced disease risk.
Do we drink coffee by choice? Sort of. I discuss why our genes may play a role in our coffee consumption and may be the ultimate influence on the risk of diseases that ultimately cannot be changed by coffee consumption.
Research on coffee's association with health and disease
Genetic polymorphisms related to coffee consumption: Rs2472297, Rs4410790, Rs762551
How to Do a Proper Self-Experiment and Why Your "n" Doens't Technically Equal 1 (How to do a randomized controlled trial on yourself)
Update 5/7/16: Inspired by the recent Thrive Market article on how to make cold brew coffee, I have started making my own as my default form of coffee (see my pic on Instagram). It is less acidic than hot-brewed coffee and can be served both hot and iced. Compared to hot-brewed coffee (including iced coffee) I find that it tastes much better with less sweetener. I typically use about 5 grams of honey or unrefined sugar but I use zero sweetener in cold brew. One batch makes a concentrate that can be diluted to 13 12-oz cups of coffee, so making it in batches that can be kept in the fridge is an enormous time-saver. The Thrive article was inspiring, but the idea of using its suggestions to buy individual pieces of equipment (ball jars, mesh sieve, cheesecloth, etc) was thoroughly uninspiring, so I bought this simple kit from Amazon.
002: As the Cholesterol Consensus Crumbles, the Stance Against Saturated Fat Softens
Is it really true that saturated fatty acids (SFAs) are the "bad fats" and polyunsaturated fatty acids (PUFAs) are the "good fats"?
Christopher Ramsden uncovered previously unpublished data undermining the conventional wisdom that we should replace saturated fats with polyunsaturated vegetable oils to lower cholesterol and prevent heart disease.
The public health establishment dismissed the findings. Here's my take.
For links to related references, see my associated blog post.
003: The Sugar Conspiracy -- Trading One Nutritional Boogeyman for Another
In his April 7, 2016 piece in The Guardian, "The Sugar Conspiracy" Ian Leslie argues that the politics of nutrition has blinded us to the fact that sugar is more deserving than saturated fat of the status of dietary arch-villain and that the politics continue but the status of sugar and saturated fat are starting to switch.
But we need to move beyond nutritional boogeymen, not switch one for another.
Our sense of history and physiology -- key concepts about the historical role of Ancel Keys, the rate at which sugar is converted to fat in a process called de novo lipogenesis, and whether insulin's stimulation of fat storage can offer a plausible explanation of obesity -- get distorted when we try to make a public enemy out of sugar, just as they do when we make a public enemy out of saturated fat.
It's time for a more nuanced view.
- Wikipedia page on Ancel Keys
- 1961 Time Magazine cover Physiologist Ancel Keys
- rates of de novo lipogenesis in humans
- "response to massive carbohydrate overfeeding in man"
- Stephan Guyenet's AHS13 slides on insulin and obesity
- Stephan Guyenet on why insulin isn't making us hungry
- low-carb vs low-fat study discussed at the end of the Guardian article
- 2-3x RDA for protein spares lean mass during fat loss
- 1.5x RDA for protein 100% spares lean mass and 3x RDA allows lean mass gain during fat loss when accompanied by resistance exercise