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Old 06-11-2013, 03:17 AM   #1
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Volek and Phinney: The Sad Saga of Saturated Fat

The Sad Saga of Saturated Fat
14 MAY / 2013 / By Jeff Volek And Steve Phinney
Here’s a fascinating paradox. Over the last 4 decades, nutrition policy makers have increasingly exhorted us to eat less saturated fat. As a result of this unremitting message, the general population believes this single nutrient, if not overtly toxic, will at least cause wide-spread bodily damage. Additionally, foods that naturally contain saturated fat (e.g., beef, pork, dairy, eggs, and tropical oils) have been branded ‘unhealthy’. The paradox here is that as the drum-beat against saturated fats has increased, the actual science supporting this message has fallen into shambles. So here’s our question: should we all just be good citizens and swallow this advice, even if the science behind it no longer pasts muster?

Two generations of researchers have tried to prove that eating saturated fat causes heart disease. Rather than growing stronger, as would be the case if this hypothesis were rock-solid, increasingly the scientific data is painting a picture more akin to ‘low fat Swiss cheese’ (i.e., not much there besides the holes). Take, for example, multiple recent meta-analyses of large populations followed carefully for decades, examining what they eat and what they die of [1-4] All show no consistent association between dietary saturated fat intake and risk for heart disease or death from all causes. In fact some of these studies show just the opposite – an inverse association of dietary saturated fat intakes and atherosclerosis or stroke. Interestingly, they also suggest that one’s risk for a coronary event increases when dietary saturated fat is reduced and replaced by carbohydrate.

Here’s the problem as we see it. By continuing to provoke fear about the harmful effects of saturated fat, the likely response is that people will seek out foods low in fat and higher in carbohydrate. And in reality, that’s exactly what appears to be happening. According to a government-funded survey [5], Americans have decreased their consumption of saturated fat and replaced those calories with an even greater amount of carbohydrate. This dietary flip-flop of trading away saturated fat and replacing it with carbohydrate has occurred in the same time interval as rates of obesity and diabetes have rocketed skywards. This might be coincidence, or more likely it’s an extremely unfortunate unintended consequence.


Okay, so what we’re essentially doing here is telling you that much of what we’ve been taught about dietary fat is wrong. How could this be – that all those wise policy-makers backed up by legions of academic scientists have gotten this all wrong? That’s a long story, and a good place to start would be to read ‘Good Calories, Bad Calories’ by the investigative journalist Gary Taubes [6]. In short, 50 years ago diseased coronary arteries were found to contain buildups of cholesterol and saturated fat. Professor Ancel Keyes of the University of Minnesota hypothesized that too much of these two nutrients in the diet were the cause – i.e., his hypothesis was built on the flawed concept that ‘you are what you eat’. Then came well-done studies showing that blood levels of saturated fats predict future cases of heart disease [7-10] and diabetes [11-14], thus appearing to support Keyes’ hypothesis. But this works only if you believe this flawed sound-bite; a concept that doesn’t pass the ‘red face test’ (as addressed in our prior blog post).

Obviously, the key question here is: “what’s the precise relationship between dietary saturated fat and blood levels of saturated fat?” For people who believe ‘you are what you eat’, the answer is easy; and it follows from that easy answer that no one wants to accumulate saturated fat on their hips or lining their arteries. This is so instinctively logical that most people (including many prominent nutrition researchers) haven’t bothered to question it. Simply put, the current national policy imperative ‘don’t eat saturated fat’ is based solely on a sound-bite. The scientific evidence, however, clearly shows that dietary intake of saturated fat compared to serum levels of saturated fat show little if any correlation. Thus our advice in our last post that we banish this flawed sound-bite and replace it with: ‘you are what you save from what you eat’.

If dietary saturated fat intake has little to do with saturated levels in our blood, then what does? There is, in fact, sound evidence that increasing the proportion of carbohydrate in your diet is a major determinant of increased serum saturated fat levels. We know this because two respected research groups [15,16] fed humans carefully measured diets either high in carbohydrate or moderate in carbohydrate. In both studies, blood levels of saturated fats went up dramatically on the high carb diets (even though they were very low in fat).

On it’s surface, this looks like a paradox. But with a little thought, it actually makes sense. A high carbohydrate intake has two effects in the body that promote higher levels of saturated fat. First, carbohydrates stimulate the body to make more insulin, which inhibits the oxidation of saturated fat. Thus, when insulin levels are high, saturated fat tends to be stored rather than burned as fuel. Second, a high carbohydrate intake promotes the synthesis of saturated fat in the liver. This is particularly problematic for individuals with insulin resistance (characterized as ‘carbohydrate intolerance’ in our recent book [17]).

Insulin resistance makes it harder for muscles to take up and use blood sugar. If it has a hard time getting into muscles to be burned, for the only alternative for this excess blood sugar is to go to the liver for conversion into body fat. This combination of decreased oxidation and increased synthesis of saturated fat therefore results in accumulation of saturated fats in the blood and tissues. The culprit then is clearly not dietary saturated fat per se, but rather consumption of more carbohydrate than an individual’s body can efficiently manage. This threshold of carbohydrate tolerance varies from person to person, and it can also change over a lifetime. Thus the skinny model promoting her particular version of a low fat diet may actually thrive on it herself, but that doesn’t mean that it’s right for you if you weren’t born to be skinny. And of course, it also may not be right for her when she’s 50 after her metabolism has changed.

So, you may be asking, if consumption of saturated fat is not associated with harmful effects on the body, does this mean that this class of fats is completely off the hook? Our response is that the science of nutrition is pretty complex, so beware of black and white answers. Whereas dietary saturated fat intake is unrelated to risk for chronic disease, higher saturated fat levels in the blood do appear to pose a problem. As we noted, there is a lot of variation between individuals in their responses to any one diet. Thus there is an unmet need for tests that will guide individuals to the correct amounts of both carbohydrates and saturated fat to match their personal metabolic tolerances.

In addition to the studies mentioned above in which high carbohydrate feeding increased blood levels of saturated fats, we have also conducted a pair of studies [18, 19] comparing moderate carbohydrate to very low carbohydrate diets. Because these were not very low calorie diets, the low carb diets were naturally pretty high in fat, containing 2-3 fold greater intakes of saturated fat than the moderate carbohydrate diets used as controls. The results were pretty striking – compared to low fat diets, blood levels of saturated fat were markedly decreased in response to the low carbohydrate, high fat diets. Our data indicates that this occurred because the low insulin levels accelerated the oxidation of all fats (and particularly saturated fat); plus the relative paucity of dietary carbohydrate meant there wasn’t much of it to be converted into saturated fats. Thus, from the body’s perspective, a low carbohydrate diet reduces blood saturated fat levels irrespective of dietary saturated fat intake.

Now once we post this explanation of how saturated fats got such a bad rap, we know that we will get angry pushback from those advocates of low fat, high carb diets asking about all of the studies in rats and mice showing that high fat diets are bad for ‘you’ (by which they mean those rodents – not you personally). To that we offer two answers. First, rodents make lousy surrogates for human metabolism. A myriad of drug and nutrient studies show dramatically different responses between mice and men. Second, most researchers who study ‘high fat diets’ in mice use 40-60% fat and 20-40% carbs (leaving about 20% for the protein). Even at 20% carbs, this is still way too much to allow a mouse to adapt to fat burning like humans do when they get their carbs at or below 10% of dietary energy. As a result, at huge tax-payer expense, these many ‘intermediate carb’ studies tell us nothing useful about the human response to a well-formulated low carbohydrate diet.

And so we end this sad saga about poor, downtrodden saturated fats on a hopeful note. Yes, dietary saturated fat continues to be scapegoated as the presumptive cause of many health problems in developed countries. However we now know that nutrition policy makers have indicted the wrong nutrient for the crime of raising blood saturated fat levels. If we can just banish the phrase ‘you are what you eat’, however, perhaps the nutrition establishment would broaden their perspective to consider how other offenders determine blood saturated fat levels and contribute to overall health and disease.

There is convincing evidence that dietary carbohydrate exerts an important influence on how the body processes saturated fat. Thus, saturated fat, whether made in the body or eaten in the diet, is more likely to accumulate when aided and abetted by high levels of dietary carbohydrate, particularly in insulin resistant individuals (as in type-2 diabetes or metabolic syndrome). Especially in these substantial segments of our population, a one-size-fits-all recommendation to aggressively lower saturated intake with the expectation of lowering blood saturated fat levels is intellectually invalid and likely to backfire. Given our current epidemics of obesity and diabetes, we can’t afford to continue diet policies based on a tragically flawed, simplistic sound-bite.
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Old 06-11-2013, 03:59 AM   #2
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That is the most cogent, approachable piece on saturated fat I've ever read. It's 4am, I haven't been to sleep yet, and I followed it easily.

Thanks, emel.
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Old 06-12-2013, 08:48 AM   #3
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Excellent find.Thanks for posting it.
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Old 06-12-2013, 11:08 AM   #4
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Spurred by a teaser from a podcast with Phinney, I read that mayonaise is non-preferred as a fat source. I suspected it was because it is usually made from soybean oil. During my digging, I found a tidbit about ideal fats, by Volek, on the Atkins blogs:

Quote:
Finally, Dr. Volek in another study investigated whether the quality of fat mattered on a low carbohydrate diet when individuals are not losing weight. His team found that a very low-carbohydrate diet that is supplemented with omega-3 fatty acids (EPA and DHA) results in an even better fatty acid composition profile in the blood. This is very preliminary, but may indicate that a controlled-carbohydrate diet that emphasizes monounsaturated fat and omega-3 fatty acids and slightly lower saturated fatty acid consumption is an ideal way to eat when an individual is no longer losing weight.
colette_heimowitz : Fascinating medical research updates from Atkins Science Board members
but you may have to be a member to see it.
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Old 06-12-2013, 11:15 AM   #5
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And then here's a passage about keto-adaption, from ketotic.org. I like it because it mentions the timing of the thing. How often do we see folks giving up just when a low carb routine is getting fired up for fat loss?

Note the quotes from my pals Volek and Phinney midway through, which is why I pasted it here instead of starting a new post:

Quote:
What is keto-adaptation?

Keto-adaptation is the process of shifting your metabolism from relying mostly on glucose for fuel, to relying mostly on fat-based sources of fuel. Not only does fat oxidation itself increase, but your body starts producing enough ketones that they can be used as a significant source of fuel as well. Ketones are derived from partially metabolized fat, and they can be used in many of the same tissues of the body as glucose can, including much of the brain. The benefits of using fat and ketones rather than glucose for fuel are many, and are the main subject of this site. However, it takes time for the metabolism to adjust to producing and using ketones at a significant rate. Even though changes are evident within days of carbohydrate restriction, improvements continue for weeks.

In brief:

Carbohydrate-based fueling is a self-perpetuating cycle: it runs out quickly, and every time you eat more carbs you delay adaptation to fat-burning.
Fat-based fueling is sustainable, because it allows access to a very large store of energy without you frequently stopping to refuel. Blood sugar is maintained though precise internal processes without wild swings. These two together create a desirable flow of even, stable energy, mood, and alertness.
There is a delay between first reducing the amount of carbohydrates that you eat, and having a smoothly running fat metabolism. In the intervening days, you may feel slow, or even unwell. These symptoms can be minimized by making sure to eat lots of fat, staying hydrated, and using salt liberally. Other electrolytes may also be helpful to add -- homemade broth makes a good supplement. Keep carbs consistently low, or you will never adapt and the process will go on indefinitely.


Carbohydrate-based fueling is a self-perpetuating cycle.

The body can store only relatively small amounts of glucose, in the form of glycogen. About 100 grams can be stored in the liver, and about 400 grams can be stored in the muscles. Muscle glycogen can only be used by the muscle it is stored in — it can't go back to the bloodstream — so the liver glycogen is the only source that can be used to keep blood sugar stable, and provide fuel for the brain. If you are not making use of ketones for fuel, then this is not enough glucose to get through a typical day, let alone a day when you are doing something strenuous. If you depend on glucose metabolism, then you have to frequently replenish your glycogen stores or you will begin to feel tired, physically and mentally.

There are basically two ways to get the necessary glucose, and only one of them involves eating it. The first is to eat carbohydrate. Unfortunately, every time you ingest more than a small amount of carbohydrate, it stops all progression toward keto-adaptation. So this strategy is a Catch-22. It makes you continually dependent on dietary carbohydrate. It locks you in, because supply is limited, but restocking prevents other fuels from becoming available.

The other way to get glucose is to let the body make its own on demand out of protein. This process is called gluconeogenesis. Gluconeogenesis is the reason that eating carbohydrate is not necessary, even though some amount of glucose is manufactured and used internally. This is analogous to any other internally produced nutrient, such as vitamin D, which we don't need to ingest, because the body makes it in response to sun exposure, or to a hormone, like adrenaline, that we make and use every day, but don't need to get from food.

One of the benefits that comes directly from this physiological mechanism is that on a keto diet you will no longer need to eat so often. Skipping a meal does not become an emergency, or even a problem. A lot of people have problems with mood, cognition, and wakefulness if they don't eat frequently. On a keto diet your blood sugar will naturally become steady, and the advice to eat every 3 hours to prevent hypoglycemia will become irrelevant.

What exactly happens during keto-adaptation?

In their recent book The Art and Science of Low Carbohydrate Living, Volek and Phinney describe two stages of keto-adaptation. In the first few days of a keto diet, your body is still running on glycogen stores. This is the toughest part of the process, because in order to break the vicious cycle of glucose-based metabolism, you have to avoid eating carbohydrates, even though your glycogen stores are dwindling. Fat metabolism is still not optimized, and ketone production hasn't become significant.

Another noticeable effect in the first days is water loss. One of the inefficiencies of glycogen storage is that it needs to be stored with water. It takes about 3 or 4 grams of water to store a gram of glycogen [1] . This means that as you deplete your glycogen stores you could lose up to 2 kg of water! Not only that, but high circulating insulin levels cause water retention by inhibiting sodium excretion (see e.g. [2]). The keto diet lowers insulin levels and increases insulin sensitivity, allowing excess fluid to be released. These combined effects are the origin of the claim that the weight lost on keto diets is due to water loss. In the very beginning, this is true, but subsequently, of course, it is not.

When glycogen runs out, you start producing ketones, and some are excreted in the urine. This is easy to measure, and some keto dieters use it to know if they are hitting a low enough level of carbohydrate restriction. This also marks the beginning of the second stage of keto-adaptation. Ketones are now becoming available for fuel, but they haven't yet risen to their stable adapted level. There is an interesting interplay between ketone use in the muscles and the brain. When ketone levels are low, the muscles tend to use them directly for fuel, but as levels increase, the muscles use them less, turning to fat for fuel instead. The brain, on the other hand, uses ketones proportionally to their concentration in the blood. This means that at low levels of ketones, the brain's supply is not much affected, because the muscles intercede, but above some threshold, the brain's supply rapidly becomes much higher. At this point, the brain can rely on ketones, and since it is no longer susceptible to running out of fuel, the need to eat frequently throughout the day to maintain mental function disappears. The muscles in turn now rely on fat: they finally have access to a virtually unlimited supply of energy, which is particularly valuable for athletes.

Much confusion has been generated by scientists not recognizing one or both stages of keto-adaptation. A few studies have been publicized claiming that low carbohydrate diets worsen mental or physical performance (e.g. [3], [4]). On reading the details, it turns out that the testing was done in the first few days of carbohydrate restriction. Obviously, these studies are not valid criticisms of the keto diet, except as measurements of the initial adaptation cost. They do not reflect the longer-term outcome.

How to make keto-adaptation as quick and painless as possible

As noted above, the difficult part of keto-adaptation is the first stage. There are two reasons. The first is that glucose is less available, but fat and ketone metabolism haven't effectively taken over. The best strategy for coping with this is to eat a lot of fat. Even if you eventually wish to get most of your fat from your fat stores, you do not normally need to restrict it in the diet, and especially not now. Fat is an important source of essential fatty acids and nutrients. Moreover, ingesting fat with protein helps to moderate the insulin response. A keto diet is not a high protein diet, it is a high fat diet. Do not fear it. Eat plenty of fat during keto-adaptation to ensure you have energy available.

The second difficulty is a result of the sodium excretion and transient rapid water loss we mentioned. If care is not taken to replenish sodium and water, both sodium and potassium are sometimes lost too rapidly. This can cause tiredness, weakness, and headaches. Be sure to get enough sodium: about 5 grams per day, or 2 teaspoons of table salt, will help prevent these symptoms.

Adequate potassium may be necessary to preserve lean mass [5], and magnesium deficiency can lead to muscle cramps, as well as fatigue and dizziness. Both of these minerals are abundant in meat, but are easily lost though cooking: into the water, if the meat was boiled, or the drippings otherwise. In addition to taking care to preserve the liquid from meat, acute effects can be cut short through supplementing potassium and magnesium by capsule. We recommend regularly drinking broth.

Finally, keep your dietary carbohydrates low. The worst scenario is to eat some every few days -- you will set yourself back, and be in perpetual limbo. Now is not the time to experiment with your carbohydrate tolerance, or eat foods you aren't sure about the content of. Commit to a very low level of carbohydrate intake, and stay with it consistently for at least long enough to get ketone production in full force. Most people we have talked to, if they experienced any discomfort at all, felt fully functional within 4 or 5 days. However, metabolic changes continue for at least two weeks and often more [6]. We recommend a 30 day trial at near zero levels of carbohydrate, to give yourself a chance to experience a completely keto-adapted state.

Last edited by emel; 06-12-2013 at 11:16 AM..
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Old 06-20-2013, 08:06 AM   #6
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sorry, I started a thread that is pretty redundant in light of this one.
As I said in that other thread;

Phinney and Volek actually state on page 40 of the art and science book that,
"Yes, it has been shown that saturated fats in animal or human diets can raise blood cholesterol under some circumstances."
they then go on to poo poo the importance of this....but I applaud their clarity.
I agree that their whole message is that dietary fat is good not bad.
But human dietary metabolism is proving to be (to me at least) a very YMMV paradigm.
I have been vlc for almost 10 months and my LDL and trigs went way up....Clearly, for me at least, it's not JUST the carbs. I am not going back to a carb based woe...too many other benefits from lc...I think my challenge is to find the balance between lc and some fat restriction to optimize my health.
This is challenging, but I am actually enjoying experimenting with my diet.
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