The success of the human species can be attributed to many factors, but one in particular logically trumps all others: our ability to survive on a large variety of food sources. Evolutionary speaking, our species lived off of everything from an almost entirely plant-based diet, to one based entirely off of animals. This means that our species has evolved eating a wide range of macronutrient compositions, from high carbohydrate consumption in warmer, tropical regions, to extremely high-fat, low-carb diets in arctic regions.
Unfortunately, many officials in the field of nutrition today do not have this understanding, leading to flawed, polarized recommendations that may not be best for each individual. When health officials are adamant about their specific diet, it sends a message that, if this doesn’t work for you, then you are doing something wrong and there is nothing left to do. Often, the topic of these types of diets involves macronutrient composition, such as whether to eat more fat or more carbohydrates, which sends the message that, to be healthy, you have to eat a certain amount of fat vs. carbohydrate vs. protein.
As a matter of fact, when discussing the best diet for any health-related topic, macronutrient composition is almost always at the forefront of the discussion, and discussing problems such as metabolic syndrome and insulin resistance is no exception.
While traditionally, U.S. based organizations (e.g. AHA, USDA) have long been advocates of low-fat, high-carbohydrate diets, some organizations (e.g. American Diabetic Association) have started to recognize the important role fat plays in a healthy diet. Moreover, other nations, such as the UK, have started to recognize that a low-carb, high-fat diet can also work to avoid insulin resistance.
Of course, what matters for our discussion today is what is found in the scientific literature. Unfortunately, when we turn to the science, we see the same arguments over low-carb high-fat (LCHF) vs. high-carb low-fat (HCLF) diets, with some researchers strongly advocating for one over the other, while other researchers argue the exact opposite. So what are we left to do?
I consider it my job to clear this up. To do that, I want to make it as simple, or as complicated, as you want it. Therefore, with this article, I will start simple, giving you the broad advice you need, and then continue on with my scientific models for those that are interested.
Starting out simple, here are the basic facts: with a broad examination of the nutrition literature, including the exploration of macronutrient composition, one simple conclusion can be drawn: the specific macronutrient composistion does not matter, as many dietary styles work well to prevent and/or reverse insulin resistance and diabetes, with individual variability.
Yes, that means that both an LCHF diet and an HCLF diet work to prevent or reverse insulin resistance, along with many macronutrient combinations in between (see references 4-11).
However, in each circumstance (experiment, clinical trial, case study, etc.), some people do better on one diet than others.
This means that, across the pipulation, all types of diets work, but success will vary depending on the individual. Thus, at a population level, both an LCHF and an HCLF diet work, but at an individual level, one may be better than the other.
So, the simple message remains clear: when it comes to nutrition basics, what matters is that you build a diet based on real, whole foods. This means taking attention away from macronutrient composition, and instead putting it on the quality of the food you are choosing to consume.
So, are you living your life based on a real, whole foods diet? Have you gotten the industrial not-so-foods out of your life, at least, for the vast majority of your days? Good, let’s keep moving forward.
Now, I don’t take any of the above statements to mean that macronutrients are irrelevant and that we should quit discussing them; rather, I only mean that the idea of one “ideal macronutrient composition” for all of our health problems is ridiculous.
We are omnivores, designed to eat a full range of foods (as a species), and that means that, as a species, what works is either an LCHF diet, or an HCLF diet, or ones in between.
But, what is important for us to dig into, today, is this topic of insulin resistance.
I have previously written at length about the pathophysiology of insulin resistance, including the key factors that lead to damaged insulin signaling, and in turn, the large number of diseases that manifest in response to this dangerous condition.
Today I will use my previously discussed models of insulin resistance, so for a full understanding of these models, it will help to have read my previous articles in this series. If you have not read these, don’t worry, I will briefly review these models and dive into how the foods we eat play their role. If you are familiar with my models, or want to jump straight to the dietary information, feel free to skip down to where I begin discussing macronutrients and insulin resistance.
Let’s begin with a review of insulin resistance:
Insulin resistance is a problem of excess fat accumulation. For example, when an individual’s fat storage is at capacity, any excess fat spills over into the blood and later into other tissue, such as the liver. Once there it can interfere with the functioning of the insulin receptor, which causes the failure of those cells to effectively respond to glucose. The failure of these cells to respond effectively to insulin is termed insulin resistance and is a very dangerous state to be in.
However, we have to be careful, because the statement above can be interpreted incorrectly. When I say “excess fat accumulation,” I don’t mean just the obvious – the fat you consume and the fat stored under your skin. That excess fat in your body can come from any macronutrient, and the fat in your body doesn’t have to be noticeable. Let me explain these.
First, excess fat in the body can come from any macronutrient. Obviously, it can come directly from the fat you consume, but it can also come from carbohydrates or even protein because the body easily converts these to fat. The easiest way to put on excess pounds of fat is to eat diets high in both fats and (processed) carbohydrates, because the processed carbohydrate will put your body in fat-storage mode, and then the excess fat will be forced into storage (more on this here).
Second, insulin resistance doesn’t always begin in overweight individuals – an important factor is the fat storage capacity of the individual. It is entirely possible for one individual to weigh 150 pounds but be at full fat-storage capacity, while another individual weighing 200 pounds has fat cells (adipose tissue) that keep expanding. Even though that second individual may be more upset about his/her weight, this person is actually in a better state, metabolically speaking. This person with a greater ability to expand fat storage has a body where fat is tucked away safely. Meanwhile, the lighter person at full-fat capacity is in a state where excess fat is spilling over into the blood, where it can go on to cause insulin resistance.
Taken together we can start to see the big picture: consuming excess energy from any macronutrient can put the body in a state of excess fat-storage. Whether or not this storage is “in excess” is dependent on the fat storage capabilities of the individual.
However, this still isn’t the whole picture, because the body is well-equipped to deal with excess energy. While it is all-too-common to hold the belief that the body is naturally unresponsive, and that our health and weight is a direct effect of how much we eat, this belief is far too simplified.
In a metabolically healthy individual, excess energy is not necessarily a problem because that excess fat simply gets burned up. If there is a surplus of energy in the body, the metabolism simply revs up, burning off those extra calories. Therefore, consuming excess calories, per se, is not enough to cause weight gain and insulin resistance (more on this here).
So then, what is key to causing excess fat storage? What is the missing link that is necessary for all of this to become a problem?
The answer, simply, is when fat oxidation (burning off that fat) gets halted. When excess fat does not get burned up, it has to stick around, where it can then cause problems. Once fat starts building up in the blood, it can begin to build up other places, such as the muscle, liver, and pancreas, where it can cause insulin resistance.
Now we have enough information to see the bigger picture: insulin resistance can be caused due to overeating and overstuffed fat cells, but the real problem is the failure to burn off that excess fat.
To better explain this, let’s take a look at some models of fat circulation. First we’ll take a look at a healthy model, in which fat is able to be efficiently oxidized.
Healthy Body vs. Metabolically Unhealthy Body
Here’s the healthy model, in which fat goes back and forth between the blood (circulation) and storage, before eventually being burned off (oxidation) in the mitochondria. In this model, fat is free to get stored safely away in adipose tissue or be burned off in the mitochondria.
(note: click to open the following images)
Moreover, if too much fat starts building up in adipose tissue, then the system simply shifts to burning more and storing less.
Remember, both of these situations are healthy – the body is fully equipped to deal with excess fat accumulation. However, this model can become disrupted when the body’s fat burning capabilities get disrupted. When this occurs, real problems start to occur, including insulin resistance.
One more thing to add in before we get into how diet impacts this. Fat cells don’t necessarily have to be full for insulin resistance to occur. The same problems that arise out of overfilled fat cells can occur by other means, resulting in the same situation (i.e. excess circulating fat). Briefly:
Inflammation:
- Inflammation plays a key role in fat homeostasis and insulin resistance. Inflammatory cytokines, produced by over-filled fat cells, are largely responsible for increased lipolysis (removal of fat from storage), and in turn, insulin resistance (1). However, inflammatory markers don’t have to come from adipose tissue, as simply infusing pro-inflammatory cytokines into the bloodstream is enough to cause insulin resistance (1).
- The chemical reactions that occur in the mitochondria to produce energy (ATP) naturally produce reactive compounds, coined reactive oxygen species (ROS). ROS can be dangerous when they go off and react with other molecules, such as the insulin receptor. The good news is that nature designed a brilliant, balanced system, in which other molecules (antioxidants) neutralize these ROS so that they can’t go off and cause trouble.
- You can limit the amount of ROS in your cells by eating high quality foods, full of antioxidants, and additionally by avoiding toxic foods that use these antioxidants up (2)
Saturated fat
- High levels of circulating fats are most damaging when that circulating fat is saturated. When we consume large amounts of certain saturated fats (within an insulin-stimulating diet), that saturated fat can get stored in reactive, stagnant pools, where it can interfere with the functioning of insulin receptors (3)
- But that saturated fat doesn’t have to come directly from fat we eat. When excess carbohydrates are consumed, they go through a process called de novo lipogenesis, which is simply the conversion of glucose to fat. When the body makes this conversion, the primary product is a palmitate, the very saturated fat that has been implemented in hundreds of studies as playing a causal role in insulin resistance.
Keep these mechanisms in mind while I continue on with my main model, with excess fat in the body causing insulin resistance.
How do macronutrients play a role in insulin resistance?
Now that we understand the mechanisms causing insulin resistance, we can ask the important questions of what causes these problems to occur. Two main questions need to be addressed:
First, how does the body end up in a situation with overstuffed fat cells, which in turn leads to high levels of fat circulating in the blood.
At the same time, we must ask why this excess fat is getting stored in the wrong places (i.e. non-adipose tissue), instead of getting burned up.
The answer, as previously discussed, is insulin, our fat storage hormone. When insulin gets stimulated the body goes into fat-storage mode, causing cells to store excess fat, while also preventing the burning of fat. When insulin levels are chronically high, fat will not get burned up. If there is sufficient space, the body tucks this fat safely away in adipose tissue. Once that tissue is filled up, that excess fat is forced to stay in circulation, or get unsafely tucked away in non-adipose tissue, such as muscle, liver, and pancreas cells, where it can cause insulin resistance.
Our key question is this: which types of foods irregularly raise insulin, causing fat to accumulate, and how can this accumulation be prevented?
One last thing before we get into macronutrients. Because we are discussing a topic involving excess fat accumulation, I have to make my usual plug for why I am going to (almost entirely) ignore the calorie balance hypothesis, the one that says that excess weight is a matter of simply eating too many calories and not burning enough of this. If you are unfamiliar with why I discredit this hypothesis, check out my series on calories and metabolism. Remember it is not how much you consciously consume and burn, but rather, the signals you send to the body that dictates your weight. Calories are important, but balancing calories is a result of the foods you choose, not a solution that should take all of our focus. Calorie balance is important for weight loss, but it is most often a dependent variable – not one that should always be intentionally manipulated.
Let’s start with the low-fat diet, the one that has gotten the most support over the years.
The low-fat diet operates off of the logic that fat causes insulin resistance. If you eat carbohydrates under your caloric threshold, then your body does not store fat, and therefore there is no way to induce insulin resistance. However, if you eat fat, then this dietary fat can interfere with the functioning of insulin receptors and cause insulin resistance (3).
Additionally, the low-fat supporters tend to criticize saturated fat, due to numerous studies showing the dangerous effects of high levels of saturated fat in the blood. The dangers of certain circulating saturated fats and their storage in muscle and liver cells include the production of dangerous compounds that cause inflammation and interfere with insulin receptors (3). Logically, this leads to the well-known advice to avoid saturated fat.
Does this diet work for preventing excess weight and insulin resistance? Well, given that it is the prevailing theory in the U.S., recommended across the board by government groups, I would assume that there is some credit to it.
And sure enough, there is. Researchers have looked at certain populations following an LFHC diet, including vegans and vegetarians, and have found superb health. There is no denying that vegetarians and vegans tend to be healthier than the general population, which is backed up by a number of studies comparing vegans/vegetarians to omnivores, often finding improved insulin sensitivity, among other improved health factors (4-7). In diabetic populations, this low-fat, plant-rich diet has been shown to reduce fat deposits, improve insulin sensitivity, and reduce the number of medications necessary for diabetics (7).
So yes, a low-fat, plant-rich diet works well to prevent insulin resistance and diabetes. While the vegan community likes to stop here, I like to dig deeper. Yes, if you eat a lot of plants you will likely have great health! But does that mean it is the carb / fat ratio that is causing this?
We already know that the answer is no because an LCHF diet can also successfully prevent/reverse insulin resistance.
Patients put on an LCHF diet pretty consistently show extraordinary results in beneficial changes in their health markers, including HDL, triglycerides, weight, and insulin sensitivity (8-12). For example, a 2014 study (12) showed that level of carbohydrate consumption, experimentally varied in a step-wise function, resulted in a corresponding step-wise change in plasma palmitoleic acid, which is a strong marker of insulin resistance. By increasing carbohydrate consumption, the subjects’ blood responded with an increase in palmitoleic acid, a major marker of insulin resistance.*
As an interesting experimental twist, that step-wise increase in carbohydrate consumption went hand-in-hand with an experimental step-wise decrease in saturated fat consumption. While the experimenters increased carbohydrate in the diet, they decreased saturated fat, and they found that the amount of saturated fat consumed did NOT result in any change in plasma saturated fat. This finding, that plasma saturated fat levels do not reflect levels of saturated fat consumed, has been replicated (13).
Therefore, this leads to the conclusion that levels of circulating (saturated) fat, arguably the dominant cause of insulin resistance, is dependent on the amount of carbohydrate consumed, not the amount of fat consumed.
If none of that convinces you, here’s the latest from the LCHF world: a clinical trial, published in 2018, which followed over 200 participants from start to finish (11). Here’s what they found:
“After 1 year, patients in the (LCHF group), on average, lowered HbA1c from 7.6 to 6.3%, lost 12% of their body weight, and reduced diabetes medicine use. 94% of patients who were prescribed insulin reduced or stopped their insulin use, and sulfonylureas were eliminated in all patients. Participants in the (control) group had no changes to HbA1c, weight or diabetes medicine use over the year. These changes in (LCHF) participants happened safely while dyslipidemia and markers of inflammation and liver function improved.”
Yes, diets that take the carbohydrate (and therefore the glucose and insulin) out of the picture works wonders to reverse diabetes and insulin-resistance. This isn’t rocket science. Insulin resistance is a problem of excess fat storage. Excess fat storage is a problem of excess insulin stimulation, which both causes fat storage AND halted fat oxidation. No insulin = no excess fat.
But we can’t just stop here, because again, an HCLF diet works too! There are millions (billions throughout history) of people who eat plant-rich, high-carb diets and have no fat storage problems and no insulin resistance. So why is this?
Here’s my answer: all this talk of high-carb vs. high-fat diets may be the wrong direction to go in. If insulin resistance is a problem of excess fat storage and halted fat oxidation, and BOTH an HCLF and LCHF diet work to reverse it, maybe we shouldn’t be putting so much emphasis on macronutrients. Maybe instead we should put the focus elsewhere on the thing that causes fat storage and halted fat oxidation – yes, that is insulin.
This sort of discussion would include macronutrients, as they are a component of insulin stimulation. But it turns out they aren’t everything – if they were, one of these diets wouldn’t work. Instead, there has to be something else more worthy of our main focus.
I have one more article for you, one in which I will jump straight to my thoughts on insulin resistance and dietary decisions.
As always I won’t keep you waiting, because the answer is simple and can be employed right now. Anyway, if you know anything about my work you probably already know the answer: just eat real food. With some variability, consuming real foods, consisting of whole fruits, vegetables, and other plant foods, along with high-quality fat and moderate intake of protein, keeps insulin levels low and prevents fat accumulation and insulin resistance.
For the full discussion of this, head over here.
*Palmitoleic acid is used as a marker of de novo lipogenesis (DNL), the process in which the body converts glucose to fat for storage. When carbohydrates are consumed in excess, or if carbohydrate is consumed in high, easily broken down doses (e.g. processed foods), then the body converts this glucose load to fat. Palmitoleic acid is a product of this reaction but is rarely found in nature, and therefore is used as a mark that one’s body is undergoing DNL.
References
- Perry, R. J., Camporez, J. P. G., Kursawe, R., Titchenell, P. M., Zhang, D., Perry, C. J., … Shulman, G. I. (2015). Hepatic acetyl CoA links adipose tissue inflammation to hepatic insulin resistance and type 2 diabetes. Cell, 160(4), 745–758. http://doi.org/10.1016/j.cell.2015.01.012
- Perumalla Venkata, R., & Subramanyam, R. (2016). Evaluation of the deleterious health effects of consumption of repeatedly heated vegetable oil. Toxicology Reports, 3, 636–643. http://doi.org/10.1016/j.toxrep.2016.08.003
- Estadella, D., Da Penha Oller Do Nascimento, C. M., Oyama, L. M., Ribeiro, E. B., Dâmaso, A. R., & De Piano, A. (2013). Lipotoxicity: Effects of dietary saturated and transfatty acids. Mediators of Inflammation, 2013. http://doi.org/10.1155/2013/137579
- McMacken, M., & Shah, S. (2017). A plant-based diet for the prevention and treatment of type 2 diabetes. Journal of Geriatric Cardiology, 14(5), 342–354. http://doi.org/10.11909/j.issn.1671-5411.2017.05.009
- Goff, L. M., Bell, J. D., So, P. W., Dornhorst, A., & Frost, G. S. (2005). Veganism and its relationship with insulin resistance and intramyocellular lipid. European Journal of Clinical Nutrition, 59(2), 291–298. http://doi.org/10.1038/sj.ejcn.1602076
- Barnard, N. D., Cohen, J., Jenkins, D. J. A., Turner-McGrievy, G., Gloede, L., Jaster, B., … Talpers, S. (2006). A low-fat vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes. Diabetes Care, 29(8), 1777–83. http://doi.org/10.2337/dc06-0606.
- Kahleova, H., Matoulek, M., Malinska, H., Oliyarnik, O., Kazdova, L., Neskudla, T., … Pelikanova, T. (2011). Vegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with Type2 diabetes. Diabetic Medicine, 28(5), 549–559. http://doi.org/10.1111/j.1464-5491.2010.03209.x
- Feinman, R. D., Pogozelski, W. K., Astrup, A., Bernstein, R. K., Fine, E. J., Westman, E. C., … Worm, N. (2015). Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition, 31(1), 1–13. http://doi.org/10.1016/j.nut.2014.06.011
- Volek, J. S., & Feinman, R. D. (2005). Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutrition and Metabolism, 2, 1–17. http://doi.org/10.1186/1743-7075-2-31
- Gannon, M. C., & Nuttall, F. Q. (2004). Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes. Diabetes, 53, 2375–2382.
- Hallberg, S. J., McKenzie, A. L., Williams, P. T., Bhanpuri, N. H., Peters, A. L., Campbell, W. W., … Volek, J. S. (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. Diabetes Therapy. http://doi.org/10.1007/s13300-018-0373-9
- Volk, B. M., Kunces, L. J., Freidenreich, D. J., Kupchak, B. R., Saenz, C., Artistizabal, J. C., … Volek, J. S. (2014). Effects of step-wise increases in dietary carbohydrate on circulating saturated fatty acids and palmitoleic acid in adults with metabolic syndrome. PLoS ONE, 9(11), 1–16. http://doi.org/10.1371/journal.pone.0113605
- Forsythe, C. E., Phinney, S. D., Feinman, R. D., Volk, B. M., Freidenreich, D., Quann, E., … Volek, J. S. (2010). Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet. Lipids, 45(10), 947–962. http://doi.org/10.1007/s11745-010-3467-3