Dietary fat is confusing. We cannot make general statements declaring ‘monounsaturated fat is good’ or ‘polyunsaturated fat is bad’ because, based on our current classification system, there are exceptions to every rule. Kurt Harris, author of the PaNu blog, has written a comprehensive piece describing each category of dietary fat while proposing another, perhaps clearer, labeling system. Read his informative article here.

Check out this article on gluten sensitivity in the Wall Street Journal.

Another great question from Evan:

So my Girlfriend said that the Paleo diet is too low sugar to be sustainable over a long period of time. Especially in the case of attempting to uphold a sustained level of higher level cognition and learning in the brain. what is an ‘appropriate’ amount of sugar for humans to consume?
I was also told that HFCS is GOOD because it’s actually partially broken down and can save your body energy (not to say that I’m actually believing what my source told me)
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Your girlfriend is correct in that our brain does prefer to run on glucose; however the misconception lies in the assumption that because our brain needs glucose, then we must get it from our diet. This is false; we are perfectly capable of producing all the glucose our brain needs to ‘uphold a sustained level of higher level cognition and learning’ from amino acids and glycerol (and, our brain can use ketones when glucose becomes scarce) without eating any carbohydrate at all.

Therefore, I disagree with the blanket statement that ‘the paleo diet is too low in sugar to be sustained over a long period of time’, however–and here’s the important distinction–our bodies are not capable of synthesizing enough glucose to support brain function AND that which is necessary to fuel intense, chronic, anaerobic exercise–the work demand of, say, crossfit.

If you are sedentary, or only participate in low-intensity, aerobic exercise (i.e. walking), then you are capable of burning fat to fuel you during periods of low-intensity movement thereby sparing precious glucose that you’ve manufactured from protein to keep your brain functioning. If you participate in metcon workouts, sprints, any fast-twitch muscle movements, or endurance events that depend on muscle glycogen (cycling, marathon) then your demand for glucose will be higher and must be supplied by glucose from the diet.

How much do you need? That depends on your sport and goals, but for the average 3x/wk crossfit athlete who would like to perform well and remain lean, somewhere around 80-100 grams/day of starchy carbs (with the majority consumed following exercise) is a good rule of thumb. Basically, eat as many carbs as you need to do the exercise you want to do.

Now, the second part of Evan’s question: High-fructose corn syrup. In the previous paragraph, I was talking about glucose—an essential monosaccharide that is the primary sugar found in starchy carbohydrate. Fructose—also a monosaccharide—is a completely non essential sugar; there is not a single reaction or process in our bodies that requires fructose. HFCS is composed of glucose and fructose (just like sucrose, or table sugar) somewhere in the range of 55 to 90 % fructose. It is ‘partially broken down’ in that it occurs in a slurry form with weak, easily broken bonds which allows the fructose and glucose to enter the portal vein very rapidly.

The sugars are carried immediately to the liver where 80 % of the fructose (and only 20% of the glucose) is extracted before the blood continues on to systemic circulation. This is our first clue that fructose is potentially a bad molecule: the liver extracts almost all of the fructose—just like it extracts almost all the ethanol when we drink alcohol. The liver is in charge of dealing with toxins before they can reach the rest of the body and the liver must deal with fructose just as it deals with ethanol.

We have a huge capacity to store glucose in the form of liver and muscle glycogen, however we have no way to store fructose, so we try to burn it off quickly yet 30 % of the fructose we ingest ends up as fat. This is because the fructose molecule enters glycolysis (energy-producing reaction) at a later point, following a key rate-limiting enzyme step. This means that there is no regulation as to how much energy is being produced because there is no enzyme keeping tabs on the fructose. It’s like a nozzle on a hose: With glucose, the stream is controlled by a dial on the hose matching the amount of glucose entering the energy-producing pathway to the amount of energy demand at the other end. With fructose, there is no dial on the hose; it is open full-bore all the time regardless of the body’s energy demand on the other end.

What happens when you have excess energy constantly entering a system that is not utilizing said energy? The liver has to protect itself by exporting all the by-products in the form of fat and when the the liver cannot continue to match the rate of export with the generation of new fat, fat droplets begin to accumulate in the liver. This is exactly what happens in the liver of an alcoholic, but with fructose we call it Non-Alcoholic Fatty Liver Disease.

So, Evan, your source stating that ‘HFCS is good because it saves your body energy’ is an understatement: HFCS is bad because it creates a huge energy surplus that, when consumed chronically, causes damage by overwhelming the liver’s capacity to deal with the fructose toxin. Now, if you are someone who can utilize the extra energy generated by fructose (by participating in regular exercise), consuming up to 25 grams of fructose/day is probably no problem for the normal, healthy person. Fructose can also be used to generate extra energy in the liver for a boost immediately before exercise (such as a small piece of fruit right before activity). But for the most part, fructose should be treated as alcohol; a toxin that is best minimized or consumed in small doses.

For an excellent video explaining this entire process, check out Dr. Robert Lustig: ‘Sugar, the Bitter Truth’ here.

Or an abridged version here.

Evan said…
In my Paleo thus far I haven’t included lots of starchy vegetables, mostly because I A.) don’t know very many and B.) don’t know how to prepare them.

Thanks, Evan. Let’s talk about ‘safe starches’: those that are composed primarily of glucose and fiber and do not appear to have gut irritating antinutrients like lectins or saponins.

This list is not comprehensive, but it will get you started:

Roots/Bulbs/Tubers: Beets, carrots, celeriac (celery root), garlic, green onions, horseradish, kohlrabi, leeks, onions, parsnips, potatoes, radishes, rutabaga, shallots, turnips, yam, maca, jicama, ginger, cassava, manioc, yucca, taro, water chestnut, artichoke, fennel.

Squashes are a ‘safe starch’ too: Acorn, kabocha, butternut, delicata, pumpkin, hubbard, spaghetti. As are green plantains.

You’ll have to ask around to find a lot of these–your average grocery store probably won’t carry the more obscure varieties. Try farmers markets and Asian grocery stores (Uwajimaya is a good bet).

Cooking: Beets, parsnips, rutabaga, taro, yucca, yam, plantains are all delicious when roasted. Chop, put some coconut oil/butter/lard in a pan in the oven at 375 degrees, add salt/pepper/spices (get creative!) and mix frequently. They will get soft in ~ 30 minutes or so. You can also dice into small chunks and cook on your stove top in a covered pan, or slice thin, put on cookie sheet and make ‘chips’.

Squashes cook well when roasted in the oven.

Here’s a great recipe for celery root soup.

Kohlrabi, radishes, jicama, and fennel are all delicious raw: Jicama and kohlrabi need to be peeled first.

Artichokes are best when steamed.

Anyone else found tasty ways to cook up safe starches?

Check out this great article.
Could it be that the mainstream ‘low-fat’ movement is losing momentum?!

My favorite line from the piece:

‘If you work out the numbers, you come to the surreal conclusion that you can eat lard straight from the can and conceivably reduce your risk of heart disease.’

Sing it, Gary Taubes.

Check out this spot on Nightline featuring Art De Vany and Robb Wolf.

When the topic of ‘your crazy diet’ comes up, how often do you hear: “You eat eggs everyday? That’s a lot of cholesterol. That can’t be healthy, you should stop”.

By acknowledging this statement, your ‘concerned friend’ is admitting that they think the ‘saturated fat (or cholesterol) causes heart disease’ myth exists. (The myth states: 1. dietary saturated fat (or cholesterol) raises blood cholesterol, and 2. elevated blood cholesterol increases your risk of having a heart attack, 3) therefore, if you eat a lot of saturated fat (or cholesterol) you are more likely to have a heart attack). I don’t believe in this myth, and I will write a post about this soon so that you can be armed with a few catchy phrases to help quiet your ‘concerned friends’ next time the topic of ‘your crazy diet’ comes up.

But first, a couple visuals so that you can happily enjoy your daily eggs and sleep soundly at night knowing that your arteries aren’t hardening with every drippy egg yolk that passes your lips.

First, this article is great.

(Side note: notice how the first sentence is stated as FACT. More soon on why this myth has persisted for so long).

In summary, our body needs cholesterol and will synthesize whatever we don’t get from our diet. But, as this study points out, we have a wide range of mechanisms that are inducible, or genes that can cause enzymes to be manufactured at a greater rate in order to adapt to what we’re eating. Protein is one example: why is kidney function the same on a 5% or 40% animal protein diet? Because we upregulate all the enzymes necessary to get rid of urea, a by-product of protein metabolism, that our kidneys must dispose of to prevent nitrogen toxicity. Humans are highly elastic in this regard, and capable of changing in response to the diet. As the egg case-study shows, same goes for cholesterol:

“The patient had extremely efficient compensatory mechanisms — namely, a marked reduction in the efficiency of cholesterol absorption, greatly increased synthesis of bile acids, and apparently reduced cholesterol synthesis relative to his cholesterol absorption.”

Second, check out this visual (click on image for larger view):

Based on the longitudinal Framingham Heart Study, we see that there were no significant differences between the blood cholesterol levels in ‘low’ (0-2 eggs/wk), ‘medium’ (3-7), and ‘high’ (7-14) egg eaters, and there was no association between number of eggs consumed and heart attack risk.

Stay tuned for more myth-debunking…