The Case for Keto
On the latest book by Gary Taubes
In 48 hours I just finished re-reading the latest book by Gary Taubes, The Case for Keto, and this is my favorite of his books yet. I like this book because he explains the hormonal hypothesis of obesity, and makes a cogent argument against conventional “eat less, move more” and “everything in moderation” (except saturated fat) advice, and for a more physiologic approach to reversal of obesity and type 2 diabetes, or, more broadly, insulin resistance.
I liked it that Taubes is not writing this book for the lean and healthy of the world. He is writing this book for those who have a tendency toward obesity, or in his words those who “fatten too easily.”He acknowledges that the standard dietary recommendations for avoiding fat and exercising more have not helped stem the tide of metabolic illnesses. In fact quite the contrary has occurs: In the last 50 years obesity has increased by 250%, and diabetes by almost 700%. He makes a compelling argument in his book that obesity is not from eating too much, but because we eat carbohydrate-rich foods and drink carbohydrate-rich beverages, and the fat storage hormonal imbalance (elevated insulin levels) that this triggers. In the the latter half of his book he talks about the low carbohydrate, high fat (LCHF) ketogenic diet as a way through therapeutic nutrition to lower insulin levels, and thus help people who tend to fatten easily mobilize and burn fat.
So lets walk through some of the key points in the book:
- “Fat people are not lean people who eat too much.”
There are people who do not struggle with weight, and although as time has gone on this is a lower percentage of the population, they exist. And often lifelong lean people are able to eat in moderation, even a diet high in carbohydrates, and they do not struggle with weight. They don’t suffer from cravings to binge eat at the scent of fresh donuts, and they may not understand why an obese person may struggle. They believe that what they do, eating a balanced diet containing protein, healthy fat, and vegetables, fruits, and whole grains, and doing so in moderation, should be something that everyone should be able to do to obtain and maintain a healthy weight. Yet this advice, for “people who tend to fatten,” as Taubes puts it, does not work. He argues that the physiology of a person who tends to gain fat is not the same as that of a lean person, and thus we should not apply advice from one type of person to the other. In his book he turns around the tautological (circular) argument that we get fat because we overeat, and we know we are overeating because we are getting fatter by working through the math of traditional dietary advice for weight loss. He works through a chapter on the argument centered around a caloric approach to weight loss by starting with the argument that one pound of fat is equal to roughly 3500 calories. This is the measure that nutritionists will use to recommend eating 250 calories less per week, and you will lose 2 pounds of fat per month. He takes these numbers to describe the caloric differences people would have to take in, for example, to start putting on 2 pounds per year over the next 10 years, for a 20 pound weight gain over a decade. What it comes down to is 19.2 extra calories stored as fat every day. But people who diet will often decrease their caloric intake by at least this much and yet often do not see mobilization of those fat calories, so why is this?
2. Obesity is not a mere caloric excess problem, it is a hormonal imbalance problem. The role of insulin.
Fat cells are exquisitely sensitive to insulin, and this is a threshold effect. Our bodies are not a simple machine that runs on calories, no matter the source. And we have evolved over centuries to be able to maintain the energy needed inside our body to keep cells and organs going whether we are in feast of famine. In fact we utilize different energy stores every day (when we eat meals during the day and when we fast at night while sleeping). So in a few sentences, here is how this works. Glucose, while an important source of energy in our body, is toxic when it is elevated in our bloodstream. In fact, we have about 1 teaspoon of glucose in our bloodstream when we are in a healthy (“euglycemic”) state. Elevated blood glucose levels are toxic to the kidneys and blood vessels, as seen in diabetics who have increased prevalence of chronic kidney disease and heart and vascular diseases. When we take in a meal with many grams of carbohydrates, our cells will utilize what they can of this energy, and our blood sugar rises, so our pancreas secretes insulin to help lower the blood level of glucose rapidly. (In fact, when we smell freshly baked rolls or donuts, for example, the pancreas will often release insulin before we take a bike, called the cephalic phase of insulin release.) The role of insulin is to bring down the glucose levels, store the energy as glycogen in the skeletal muscles and liver, and when those stores are full, into fat cells. Then when we go through a fasting period, the insulin levels drop and we are able to mobilize fat to use for energy. When we eat carbohydrates and release insulin, it turns off our fat cells’ ability to burn fat, because insulin is an energy storage hormone. When we fast or avoid carbohydrates enough to create an insulin deficit, it allows for the mobilization of fat from fat cells. This is known and the Randle cycle. Unlike carbohydrate, dietary fat does not trigger the release of insulin. Protein will trigger some insulin release, but also the release of glucagon and growth hormone, so it is different from carbohydrate-stimulated insulin production.
Conventional thinking has perhaps drawn a faulty conclusion from this biochemistry by stating that carbohydrates (rather than free fatty acids or other energy sources) are the body’s preferred form of fuel. It is true that when we eat carbohydrates, the body will do what it can to burn and store glucose right away. But that does not mean that this is the preferred energy source over all others 24 hours per day. In fact the body has multiple ways to supply energy to the cells and maintain normal blood glucose levels even in the absence of sugar and carbohydrates (e.g., gluconeogenesis), so sugar and carbohydrates are far from an essential nutrient, per se.
3. We are not obese because we eat too much. We eat too much because we are obese.
Often people cannot think about their life without [fill in a carbohydrate food or beverage here], and will crave these substances many times per day. Lean people will view obese people as lacking willpower or being weak. It is assumed that this is part of the gluttony that led them to this state. However, Taubes summarizes the work of researcher Hilda Bruch and others to argue to the contrary. Rather than thinking eating too much is the cause of obesity, “rather it’s the drive to accumulate fat, rather than use it for fuel, that leads to hunger and any seemingly excessive eating that occurs.”
4. Fat versus Obesity: An uncoupling of science and logic.
When we see processes that should go together function in an inconsistent manner, we call it an uncoupling (in pulmonary hypertension we talk about pulmonary artery and right ventricular uncoupling), and this is associated with worse outcomes. I invoke this phrase of science and logic uncoupling in the obesity epidemic, because it, too, has led to worse outcomes. We talk about fat biochemistry independent from the obesity epidemic, and this has likely led us down our pathway of failure to address the obesity epidemic. Scientists have known about the Randle cycle, and that insulin leads to fat storage. Physicians have seen diabetics gain weight when given exogenous insulin and have known for decades that this occurs. Yet when it comes down to why people are obese, the “move more, eat less” advice is so prevalent that often the same researchers and biochemistry textbooks that describe these metabolic pathways, do not get to the next step of ways to manipulate hormones to allow for fat mobilization and weight loss.
5. The key: Create an insulin deficit.
Physicist Rosalyn Yellow and physician researcher Solomon Bernson won the Nobel Prize in 1977 for the invention of radioimmunoassay, a technique to quantify small amounts of substances in the body, and they used it to study insulin. In the 1960s, they were able to show that people who were both obese and diabetic had elevated insulin levels, and described insulin as the “principle regulator of fat metabolism.” They then stated that to get fat out of fat cells “requires only the negative stimulus of insulin deficiency.” This is the essence of keto, as described by Taubes. In those who fatten easily, following a low carbohydrate, high fat ketogenic diet
7. The essence of keto: “For those who fatten easily, following an LCHF/ketogenic lifestyle may be ideal.”
If we can drive down the body’s insulin levels, it will then allow for the mobilization of fat from fat cells. Eating less but still eating carbohydrates will not get the insulin levels into a deficit, so for those who tend to store fat, it is important to avoid insulin-stimulating foods and get to that level. When we remove sugar and starchy carbohydrates from the diet, to be satiated, it must be replaced with something and that is where dietary fat comes in, and preferably natural fats. This helps induce satiety, which helps people maintain the diet. Because it takes a very small amount of insulin to decrease mobilization of fat from fat cells, a ketogenic diet (30 gm or less of carbohydrates per day) may be the easiest way to do this. Intermittent fasting is another technique that can help drive down insulin levels as well. One thing that is important to realize is that the insulin threshold to allow for mobilization of fat stores is different in different individuals. Because we do not routinely measure insulin levels, the biomarker we can see is weight loss/gain/stagnation. To get to a fat utilization mode, some people may be able to tolerate 50 grams of carbohydrates per day, others might need to go down to 20 grams per day. But the key is getting those insulin levels down.
8. What about saturated fat and what about a plant-based approach? Taubes has a nuanced discussion about the diet heart hypothesis, and whether we are shortening our lives should we choose to eat more fat in our diet. He is not heavy handed in this argument, but I think lays it out there nicely. We all have been taught to avoid fat, and follow a low fat, high carb diet, and while the experts are starting to embrace alternative approaches, this is so ingrained that many of us have to at least consider, will we be putting ourselves at risk for an earlier cardiovascular death? He cites the data from Virta Health where diabetic patients have successfully lowered their hemoglobin A1c, reduced the need for insulin, lost a significant amount of weight, and have improved their cardiovascular risk factors, summarized here (and we will go into these studies in more detail in future blogs). For those who believe that eating more plant-based is a more ethical choice, it is possible to be plant-based and even completely vegan keto, as Taubes discusses with one of his physician experts, Carrie Diulus, and orthopedic surgeon with Type 1 diabetes, who follows a vegan ketogenic lifestyle. (If you’re interested in vegan keto, you should follow her on instagram.)
There is a lot more to unpack from this book than I have touched on in this blog post. My goal is to whet your appetite (without causing your insulin level to bump) and encourage you to read his book. It is motivating to have a better understanding of the biochemistry of insulin signaling in obesity, which Taubes explains to a layperson reader quite well, as a better understanding of using the LCHF/ketogenic lifestyle a method through therapeutic nutrition to mobilize fat, lose weight, and feel good. As always, I think the more we can read to understand the why to do something will make the how easier to do, especially when making significant life adjustments.
