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Nutrition Past and Future

35 How To Become Insulin Resistant (The Paleo Way) 1

 
Mark Sisson sells us on meat and fat just like any other low carb promoter. Low carb is said to be the most effective way to curb excessive insulin production. He offers a version of the nonsense low-carb hypothesis on heart disease here. “Low-fat eating requires you to consume excessive carbs,” he explains. “This leads to excessive insulin production and,” he says, “kick-starts the cycle that eventually leads to heart disease. Anyway you slice it, consuming too many carbs leads to high triglycerides.”Carbs cause heart disease? Maybe in his Paleo fantasies but not in reality. It is clear that he is describing the hyperinsulinemia and broken carbohydrate metabolism of metabolic syndrome. Insulin is produced in excess in that context because it is no longer efficient or effective. Given the choice between avoiding carbohydrates because we are too dysfunctional to process them normally and simply maintaining normal and healthy carbohydrate metabolism, it seems to me we should prefer the latter. Let’s not so easily accept Mark Sisson’s low-carb low standards. Instead, let’s ask how we might maintain insulin sensitivity so that we can consume healthy carbs without a second thought.

In healthy people, insulin in the presence of amino acids and carbohydrate stimulates muscle protein synthesis. If you chug down a recovery shake with carbs and protein after a workout, this is why you do that. Sisson is not just a broscientist but also a supplement creator and salesman. You'd think he would know better.

I’m going to open this examination of the effects of animal foods on glucose disposal and insulin efficiency by showing you the study that is most often used to argue that saturated fat does not harm insulin sensitivity. In this trial, these researchers did not detect any detriment to peripheral insulin sensitivity after the consumption of saturated fat. Peripheral insulin sensitivity means muscle insulin sensitivity.

Here is an example of the use of this one by low carbers. The low-carb advocacy organization called the Nutrition and Metabolism Society links to this on their “Research on Fats” page, right above an article by the notorious and incoherent cholesterol denier Uffe Ravnskov.

In this study, the researchers used an intravenous glucose tolerance test to provoke an insulin response. They did not have their participants consume carbohydrate through their mouths. An interesting fact about this study that is often overlooked by the fat promoters is that one of the low-fat diets performed the best here.

This study also investigated cardiovascular risk factors. Dr. Dayspring should note that saturated fat reduction lowered concentrations of both LDL-C and ApoB. If that’s his priority in preventing heart disease he might want to read this over and attempt to construct a less discordant set of beliefs about nutrition.

This study does not exonerate animal foods from a role in promoting insulin resistance. It is just one study, and it is a study that showed harm to cholesterol from saturated fats and it showed a benefit to a low-fat diet. It’s amazing how often the studies the low-carbers like actually make their ideas look bad once you read them. This one also only addressed saturated fat, which is just one possible promoter of insulin resistance to be found in animal foods. There are others, as you will see. In the previous videos you have already seen what you need to see to know that healthy carbs promote insulin sensitivity. Whether it is the saturated fat or something else in animal foods that harms insulin sensitivity is another matter for consideration. In this video, we’ll look at other factors to try to explain the research we saw in An Evolved Fuel System.

Here is one way animal foods might ruin your carbohydrate metabolism that you may not have known about. I’m not going to linger on this but foodborne illness can lead to all sorts of problems, including pancreatic injury and diabetes. This journal article by Rita Suri and colleagues links the hemolytic uremic syndrome that can be caused by E. coli-associated diarrhea to type 1 diabetes in children. What this means is that once a child is unlucky enough to be sickened by the bacteria in animal waste, later that child can become an insulin-dependent diabetic as a result. This terrible complication can arise years after the initial illness caused by E. coli. Plants don’t normally harbor E. coli. E. coli always traces back to some kind of animal waste.

These authors state that at least one third of survivors of diarrhea-associated hemolytic uremic syndrome may be left with permanent diabetes.

What interests me more than that is the effect of excess protein on insulin sensitivity, and that will be my main focus in these videos. I have argued that there is no reason to consume more protein than your body needs since excess protein is simply converted to glucose anyway, generating unnecessary metabolic waste and causing dehydration. It makes more sense to get that glucose efficiently from nutrient-rich carbs instead. Now I’m going to show you that that excess protein pushes you toward the insulin-resistant condition people like Mark Sisson and Loren Cordain will tell you they are trying to help you avoid. This is Loren Cordain making his argument for high levels of protein consumption. Cordain at one time wanted his gimmicky Paleo hypothesis to be taken seriously by health professionals so he distanced himself from high-fat diets. Instead, he decided to advocate for high-protein diets, diets so high in protein, they are potentially dangerous. You can see here that he states that a key advantage of lean meats and fish over plant foods is their much greater quantity of branched chain amino acids. Loren Cordain may not be aware of the research of Christopher Newgard.

Newgard has found that the presence of these very branched chain amino acids is linked to insulin resistance in humans. Here he describes his 2009 investigation that implicated them.

Newgard tells us that obese and insulin resistant subjects had a greater pool of branched chain amino acids in their bodies than normal subjects, and these may have been derived from their diets.

Newgard states here that consistent elevations of branched chain aminos may cause hyperinsulinemia and subsequent pancreatic beta-cell dysfunction. Dr. Newgard is truly cutting-edge, but researchers from long ago were also concerned about the effects of excess protein on carbohydrate metabolism.

You can see here that in 1922, Russell Wilder noted that diabetic patients do poorly on high-protein diets.  He said that one reason for this was that excess protein is converted into glucose through gluconeogenesis, thereby raising blood sugar.

But this was an inadequate explanation for what was wrong with excessive protein intake. Protein additionally seemed to harm what he called “the sugar-utilizing mechanism.”

He wrote, “The sugar tolerance of the diabetic patient is depressed by high calorie, luxus diets, but much more markedly depressed by protein than by isocaloric amounts of fat. This protein effect is not primarily due to the sugar and ketogenic substances, which the ingestion of protein throws on the metabolism, but to some other more specific action of protein the result of which is to interfere with the mechanism of sugar utilization.”

One might expect excess dietary protein to raise blood sugar through gluconeogenesis, which is the process through which your liver turns protein into carbs. Why doesn’t the glucose made from that excess protein raise blood sugar more? The answer can be found in the very insulin-stimulating nature of protein. The pancreas is overworked in response to that protein as it secretes more insulin, and that insulin clears sugar from the blood. It seems to balance out, but over time these demands on the beta cells may be costly. This study from 2005 by Frederic Tremblay and colleagues noted this effect.

Today we know that increased gluconeogenesis is a characteristic feature of type II diabetes and obesity. When high-protein diet gurus tell you to consume more protein than you need, they are asking you to make your liver function more like a diabetic’s liver and less like a healthy person’s liver.

Low carbers ignore this problem of overly-stimulated insulin production and try to sell you on meat as a way to control your blood sugar. They may point to trials that suggest that high-protein diets stabilize blood sugar. Shane Bilsborough and Timothy Crowe  responded well to this line of reasoning in their article about low-carb diets. They noted that “protein foods such as meat and fish elicited a greater peak insulin concentration than white pasta.”

It seems a little funny to me that in his sales pitch for diets based on meat, Sisson may have identified one of the very worst aspects of meat. Meat is just terrible for your insulin action. It’s apparently worse than refined pasta products.

A high-protein diet can lead to elevated insulin levels for up to eight hours after a meal, as we learned from this study described by Bilsborough and Crowe.

Using data from the insulin index of foods created by Susanne Holt in 1997, Bilsborough and Neil Mann published this very curious chart comparing the amount of insulin response in relation to glucose caused by protein-rich foods. Given that insulin’s role in the body is to remove glucose from the blood and allow it to be used by cells, this exaggerated response to low-carb foods seems rather odd. This apparent over-reaction in insulin production causes high-protein diets to appear to be effective for glycemic control. Over time, such stresses may expose the failings of this strategy. It is often claimed that protein doesn’t cause a strong insulin response, but those who say this don’t seem to consider that the insulin response protein does cause is so disproportionate.

What they also overlook is that while in most healthy people total insulin release may not seem excessive, diabetics respond to high protein consumption with an especially exaggerated insulin response. Think about what this means in practice. The people who are most likely to try a high-protein diet out of sheer desperation may be the people most harmed by such diets.

The branch chain amino acids valine, leucine, and isoleucine are among the most insulin-stimulating amino acids. Should it be surprising that Newgard found them to be associated with insulin resistance?

It is this potential for high amino acid concentrations to contribute to insulin resistance that caused these researchers to be concerned about the long term effects of high-protein diets.

In 1962, researchers investigating the effects of high-protein feeding on cholesterol levels made an unexpected discovery. The substitution of egg whites in place of sugar in the menus of their participants did not affect their cholesterol levels, but it did raise their triglycerides. Sugar didn’t raise triglycerides the way egg whites did. Even more intriguing was the fact that even after their diets were returned to a lower protein level, their triglycerides remained elevated. This study strongly suggests an induced metabolic dysfunction from high-protein feeding.

With a less extreme intervention used on vegetarians, Frank Sacks also produced an increase in triglycerides using higher-protein diets. The amount of extra protein added to their diets was only 27 grams, so the effect wasn’t as great, but it was still there.

Of course, high triglycerides are associated with insulin resistance.

Mark Sisson knows that proteins cause a disproportionate release of insulin. So what has he said about this? When he talks about insulin in the context of meat, he says insulin is a good thing. It’s primal, whatever that means. The body knows what it is doing. Concluding, he says, “Now, pass the bacon.” Do you see how much trouble these fad diet salesmen have with logical consistency? Do you see how they use pandering and predictable drivel to mask that? Maybe the body does know what it’s doing but the brain is another matter entirely.

He recently attempted to assure his followers that the low-carb diet he promotes isn’t harmful for insulin sensitivity. Read this and you will see he is plainly doing his best to deflect and dodge here. No, low-carb is fine because you are “Going Primal,” whatever that means, so you must be getting sunshine and losing weight and reducing inflammation. Can you imagine Sisson attempting to critique one of the many studies that make low carb look bad? “They forgot to include the sunshine!,” he might say. Let's try to focus,  Mr. Sisson. One variable at a time. And then notice his need for a huge caveat as he says low-carb improves insulin sensitivity as long as you are losing weight, but then he could say that about any diet, couldn’t he? You need weight loss to happen to make low carb seem better than awful. But can you lose weight forever? Does “Going Primal” mean you are losing weight until you disappear? Go ahead and dodge and deflect, Mr Sisson. It’s embarrassing but I’m sure it pays well.

Regarding his point about inflammation, by now you’ve already seen one study in which low-carb increased inflammation. This was hardly a new discovery about low-carb. Notice the authors here connected the high cortisol of the low carb diet with the possibility of insulin resistance.

Mark Sisson knows you don’t want a lot of extra cortisol floating around in your body. I wonder what he makes of that study. Maybe he would fault their methodology for its lack of sunshine.

In this study, men on a high-protein diet had significant elevations of uric acid in their blood. The authors warned that if such an unusually high measurement were sustained, that might predispose individuals to metabolic syndrome. “High-protein” here meant around 26% of calories from protein, which is the approximate level that Sisson recommends. When you hear the words “metabolic syndrome” you should think “insulin resistance.” There is a lot of evidence that meaty, high-protein diets raise uric acid and therefore raise the risk of insulin resistance.

In this trial in healthy women, two diets were used. One produced much higher serum uric acid levels than the other. The one that produced higher uric acid levels was called the acid diet. The one that produced lower uric acid levels was called the alkaline diet.

Here you can see the diets. The acid diet is the one on the bottom. That’s the one that caused the higher uric acid levels. You can see from what I‘ve highlighted how much more meat and fish were in that one. I also highlighted a few other dietary components to show you that both diets used high-fat foods like mayonnaise and butter. The difference here really was the protein quality. Vegetable protein from tofu did not lead to higher uric acid levels.

High meat consumption appears to be associated with high uric acid levels at the population level as well, according to this study. Vegetable protein was not associated with higher uric acid levels here, either.

In this study conducted in Shanghai, proteins from animal sources including seafood were associated with a higher prevalence of hyperuricemia, which is excessive uric acid in the blood. Soy products apparently decreased the risk of hyperuricemia.

The authors of that earlier study were right to link elevated uric acid with metabolic syndrome. In this recent study, hyperuricemia measured in young adults predicted insulin resistance 15 years later. Based on this, the authors here concluded that “hyperuricemia in the midtwenties (sic) is an independent marker for predicting diabetes and prediabetes in the subsequent 15 years.” This suggests that if you eat the Paleo way, you will be rewarded for that with a higher risk of diabetes years down the road. And that, it could be argued, will make you more Paleo. More on that in just a bit.

This is the Primitive Nutrition channel so you can be certain that I looked for a way the evolution angle might help us understand hyperuricemia. It has been argued in this paper that high uric acid may have been advantageous in the past for the purpose of regulating blood pressure. Uric acid would have helped to keep blood pressure high enough while our ancestors lived in low-salt environments.

With that in mind, I find this study to be quite interesting. In Motherwell, Scotland, mothers who had been given advice to consume low-carb, high-protein diets during pregnancy seemed to program into their children a tendency toward high blood pressure. This was discovered after the researchers caught up with their children once they reached 27 to 30 years of age. Both meat and fish consumption by the moms during pregnancy were associated with elevations of blood pressure here. Perhaps there was an elevation of uric acid in those mothers during their pregnancies from eating all that meat. Once again, we see a delayed effect from eating lots of meat, except here we are talking about high blood pressure but without an explicit linkage to hyperuricemia.

Let’s return to those branched chain amino acids. Bodo Melnik has written a provocative paper about the hormone-stimulating potential of milk proteins. He notes the much higher protein content of cow’s milk in comparison to human milk. He reports that among all mammalian species, the average protein content is lowest in human milk.

Melnik states that leucine is the amino acid that is most stimulating of insulin. We have already seen that branched-chain amino acids are insulin-stimulating.

You can see here how much more leucine there is in cow’s milk than human milk.

Melnik referenced a study demonstrating that the ingestion of cow’s milk protein in 8-year-old boys resulted in increased insulin secretion and insulin resistance. He also connected whole cow’s milk consumed in infancy to childhood obesity because cow’s milk is so growth-stimulating.

Leucine and a hormone called insulin-like growth factor 1 work together to promote unregulated and undesirable growth processes, he says.

Weirdly, Loren Cordain is listed as a co-author along with Melnik for this paper here, in which it is proposed that the branched-chain amino acid leucine is linked to prostate cancer. One suggested way to avoid this hypothesized leucine problem is said to be – what else? – adherence to a Paleo diet. The restriction of dairy protein is also suggested. The most obvious alternative strategy – a lower-protein vegan diet – is not suggested.

This is hard for me to figure out. Loren Cordain advises retirees to eat lean meats precisely because they are so high in leucine along with the other branched chain amino acids.

He states that the high amounts of branched chain amino acids in meat are a reason he considers vegetarian diets to be inadequate.

If you look at the foods highest in leucine, you will see Paleo favorites like eggs, chicken, fish, and game meat. Soy proteins are listed near the top as well but those are artificial foods and no one consumes soy protein in serving sizes as large as the serving sizes used for meat.

We already saw that Melnik says that human milk is low in protein, right there in the middle of the paragraph.

At the same time, Loren Cordain has described the Paleo Diet as extremely high in protein, 33% protein here. Why are these guys writing a paper together?

Why are they concerned about the excess leucine in dairy but not the high quantities of leucine in meats? They say the answer is that animal-sourced proteins beside dairy do not impact IGF-1 because of ecological observations like what you see here. Does this settle it? Something about meat keeps it from increasing IGF-1? Not so fast. I think they may be avoiding other ecological studies that contradict this, perhaps because they are too invested in Paleo diet nonsense.

Generally high intakes of protein were found to be associated with higher IGF-1 in this study. Milk proteins were not the only proteins associated with elevated IGF-1. Fish and poultry were linked to higher IGF-1, as well. Why not target those in their paper?

If you watch my “Define Healthful” videos, you will see that for any proposed benefit of Paleo, a vegan diet probably performs even better. This consistent observation makes it perfectly clear that Cordain is a pseudoscientist, backfilling excuses for his goofy fad diet. This issue with IGF-1 also reveals his skewed priorities. Is he really trying to help you avoid cancer and insulin resistance through lower IGF-1? This study shows us a better approach. Some people restrict their caloric intake for years in an effort to live longer. This probably doesn’t work but let’s ignore that for now. It has been proposed that caloric restriction extends life in part by lowering IGF-1. But in this study, it was found that caloric restriction does not actually lower IGF-1. Instead, it was found that what really does lower IGF-1 is a low-protein diet. Based on this, the authors stated that reduced protein intake may become an important component of the anti-cancer toolbox.

Here you can see some of their methods. Who represented the low-protein group? The researchers studied vegetarians, especially low-protein, raw food vegans.

There you see how much lower their IGF-1 was. Low protein diets appear to be better if you are looking for an anti-cancer strategy. Does this remind you of anyone else’s ideas about cancer prevention? Do C. Colin Campbell and his rats come to mind? Who do you think has a more coherent nutritional strategy for minimizing your chances of developing cancer, Cordain or Campbell? Do you think that the high-protein diet guru Loren Cordain is really interested in the issue of IGF-1? Or do you think he is just doing his best to pretend to be interested while he tries to sell diet books?

Do I need to make the answer even clearer to you? Cordain’s name was attached to an article about prostate cancer. Again, leucine is singled out as cause for concern.

But Cordain doesn’t seem to understand that many studies have found an association between red meat and prostate cancer.

Cordain and Sisson base their high-protein diet advice on their conjecture about our evolutionary history, and it’s that conjecture that overrides any contrary evidence. As with uric acid and blood pressure, insulin resistance and meat can be viewed through the prism of evolution, and it can lead us to a very different conclusion from the preferred interpretation of these Paleo salesmen. Now we tie together all the observations I’ve shown you so far about high uric acid, insulin resistance, and high blood pressure to show you why all these make the low-carber truly Paleo. These are all traits that may have been useful to our ancient ancestors. I find this 1994 paper by Brand Miller and Colagiuri called “The Carnivore Connection” to be most interesting. The hypothesis put forth here was updated in a more recent paper from 2011 so I’ll mostly focus on that one, but first, notice here this interesting comment from the original one. “Carnivorous animals like the cat which have evolved and reproduce well on a low carbohydrate diet, appear to be genetically insulin resistant. Moreover, they appear to develop non-insulin dependent diabetes mellitus when exposed to a high-carbohydrate diet.” Apparently carnivory is linked by evolution to insulin resistance. How do they explain this and what does this have to do with humans?

The idea behind the “carnivore connection” is that insulin resistance would have been a favorable trait for human survival at one time because humans of the past were in low-carbohydrate environments. That’s quite disputable but let’s hear them out. Their argument is that many of us have been, in a sense, selected to be insulin resistant. Our propensity for insulin resistance has run into our current preference for refined junk carbs, and the result is widespread diabetes. To support this view, the authors make many interesting observations. Low-carb, high-protein diets promote insulin resistance, especially during reproduction, because glucose is essential to fetal development. Glucose is also the required fuel of the brain. Insulin resistance would have helped our ancestors maintain a higher blood glucose concentration at critical times.

All this would have provided selective pressure for insulin resistance. In further support of their view, the authors stated that insulin-sensitive people do not tolerate high-protein diets well. Obese and insulin-resistant animals and people can tolerate high-protein diets, they contend.

Other interesting observations here are that insulin resistance would have been helpful during times of unstable food supply.

And that the epidemiology of diabetes seems to correlate with the timing of the introduction of agriculture.

These authors were aware of the importance of carbohydrate quality, which has changed for the worse in recent times.

It’s too bad they weren’t also aware of the metabolic costs of animal foods, because I think they stumbled at the finish line of this paper when they tried to interpret the meaning of their hypothesis for our present day diet choices. They stated that any diet that reduces blood sugar and insulin is a good thing, including high-protein, low-carb diets. I’m not sure how they would justify that opinion. A look back at the oldest representations of human bodies we have, coupled with a short investigation into modern nutrition science, should have pointed them toward a different conclusion.

The oldest depictions we have of women are the Venus figurines of the Upper Paleolithic.

And this is what they look like. Do you think that Paleo magazine would sell very well if they used cover models that look like these female forms from the Paleolithic? They look a tad bit softer than your typical cover model.

I’ll share these pictures I took of a couple casts of Venus figurines on display at the Smithsonian. If you saw a woman of today looking like this, would you be surprised to learn that she is insulin resistant? This is what I consider the real Paleolithic ideal: resistant to famine, resistant to insulin, built for short-term survival and reproduction, and most definitely not vegan.

It’s amazing to me that the low carber broscientists have chosen to plant their flag on the subject of insulin resistance. Sisson says insulin metabolism is the most important concept in his book, yet no one looking objectively at the research would recommend a high-meat, high-fat diet to improve insulin sensitivity. I have to admit, these guys are excellent salesmen. It wouldn’t even occur to me to convince people of something so ridiculous, yet somehow they pull it off.

I am nowhere near finished talking about diet and insulin resistance. I have much more for you, including some other research on saturated fat, in Part II.