A very helpful synthesis of the research on the response to different carbs. I am a fairly lean woman in my 40's who is active and eats a diet relatively low in saturated fats, but very high monounsaturated whole food diet (I estimate I get at least half my caloric needs from nuts and seeds - followed by yogurt, some cheese, eggs, fruits and veggies, and periodic fish). My doctor, who didn't feel I needed it tested, recently okayed my query to get my lipids tested. I had come across a phenotype called "lean mass hyper-responder" - and I wondered if I would fall under this category given my relatively low carb (I didn't think I was anywhere near being ketogenic) and high fat diet. Sure enough - my LDL-C and HDL-C were high, and my triglycerides low. I am now exploring increasing my "healthy" starchy foods - I love winter squash (in the winter) and other nutrient dense foods that goes beyond just insulin/glucose - but is based on optimizing nutrients and antioxidant capacity. The rest should follow - hopefully.
I would see my conversation with Dominic D’Agostino for more details on the LMHR phenotype. It’s apparently more common than first thought. According to the Lipid Energy model, the high LDL is okay, a way for your body to transport fat around in a low carb state. I would get vLDL tested if possible. You always want that low. My personal opinion is that low vLDL with “high” LDL is not something to worry about, unless is VERY high.
Thank you! I should have figured you would have already covered this topic. I look forward to listening to it. I have thus far only scanned the abstract and also look forward to reading in detail the epidemiology paper you linked to in Scientific Reports. It is reassuring that my total cholesterol values (214 mg/dL) was found to be linked to the "lowest mortality" group. Even though I am aware of the LMHR phenotype, it was a bit stunning to have TC flagged as 'out of range' high for someone who munches raw walnuts and pistachios for the sheer joy of it.
Your cholesterol is out of range based on the simplistic thresholds most physicians memorize. However, as you can see, cholesterol levels a bit above 200 for your demographic are actually associated with power mortality. Most physicians don’t even know this, and will reflexively want to put you on a statin because your result is above a single, magic, one-size-fits-all threshold.
For better or for worse, my doctor knows I'm stubborn one when it comes to such. She didn't even try to suggest I follow orders to get vaccinated after recovering from CoVID (early circulating strain) given I'm an immunologist and would point out the irrationality of such a recommendation. Given my clean bill of health, I suspect she knows how I would receive the recommendation for statins - and I feel well prepared now with info for my scheduled follow-up to discuss my results. Thank you for the recommendation to listen to your discussion with Dr. Dominic D’Agostino - super interesting!
Eating fiber together with sugar will certainly be better than eating sugars in isolation. However, I also *suspect* that whole foods with fiber + sugar will be different than processed foods composed on comparable amounts of fiber + sugar (e.g. in the form of HFCS). Imagine two foods, Food A and Food B. Food A is a natural whole food with some amount of fiber, glucose, and fructose. Food B is a processed food engineered to contain the same exact amounts of fiber, glucose, and fructose. These two foods, even if they contained nothing else, would *not* necessarily be metabolized in the same way. The sugars may be embedded within the physical substrate of the fiber-containing foods in different ways. The would mean different rates of of absorption, etc.
Yes, insulin resistance is a reduction in cells' sensitivity to insulin due to too much insulin signaling. However, this does not mean insulin is the only factor. First, keep in mind that insulin resistance can develop in specific cells and tissues at different times, and also that the liver is arguably the most important tissue in this context because it's the organ that responds to insulin secretion to regulate glucose storage (which is the process that breaks in diabetes).
The cultures that eat very high-carb diets (>90% calories from carbs) are also *not* eating other things concurrently. For example, they are not eating high levels of fats together with their high-carb diet, nor are they consuming processed foods and large amounts of concentrated sugars. Among other things, they're not eating liquid fructose (no fiber) together with their crab-rich, insulin-spiking potato diet.
Fructose is problematic because it is only metabolized in the liver, unlike glucose. When you consume high-fructose corn syrup, for example, it's liquid sugar with no fiber--a roughly 50/50 mix of glucose + fructose. The glucose causes insulin release, while the liver has to simultaneously process the fructose. At a very basic level, I think of it this way: when the liver is "distracted" or "overloaded" because it's processing too much at once, things start to break more easily. Fructose in the liver can also stimulates lipid production. The insulin signal from the glucose tells cells to store that fat... and eventually that results in fatty liver disease. That's one reason why combinations of nutrients are important to consider, and why the prevalence of HFCS in modern processed foods is so good at helping drive fatty liver disease.
One of the important ways HFCS is different from the sugars found in whole foods like fruit is that HFCS is liquid glucose + fructose, often inside of processed foods containing little to no fiber. The fiber found in fruits blocks or at least slows down the fruit sugar from going directly into the liver via the portal vein. In the absence of fiber, concentrated amounts of sugar in HFCS can directly go to the liver, quickly. As a result the organ is more "overloaded."
Sucrose is only metabolized by the liver. In that respect it's like alcohol. It used to be that only alcoholics got fatty liver disease. Now all sorts of people do, including children who have never consumed alcoholic beverages. A major reason for this is overconsumption of sugary foods containing fructose. Again, the dual-combination of glucose + fructose is a major issue here, especially in the absence of fiber. Glucose means insulin which means, "store excess energy as fat." The fructose stimulates fat synthesis in the liver, which is then stored as fat due to the insulin. Fatty liver.
Well written, enjoyed reading this. Thanks for sharing this with us.
A very helpful synthesis of the research on the response to different carbs. I am a fairly lean woman in my 40's who is active and eats a diet relatively low in saturated fats, but very high monounsaturated whole food diet (I estimate I get at least half my caloric needs from nuts and seeds - followed by yogurt, some cheese, eggs, fruits and veggies, and periodic fish). My doctor, who didn't feel I needed it tested, recently okayed my query to get my lipids tested. I had come across a phenotype called "lean mass hyper-responder" - and I wondered if I would fall under this category given my relatively low carb (I didn't think I was anywhere near being ketogenic) and high fat diet. Sure enough - my LDL-C and HDL-C were high, and my triglycerides low. I am now exploring increasing my "healthy" starchy foods - I love winter squash (in the winter) and other nutrient dense foods that goes beyond just insulin/glucose - but is based on optimizing nutrients and antioxidant capacity. The rest should follow - hopefully.
I would see my conversation with Dominic D’Agostino for more details on the LMHR phenotype. It’s apparently more common than first thought. According to the Lipid Energy model, the high LDL is okay, a way for your body to transport fat around in a low carb state. I would get vLDL tested if possible. You always want that low. My personal opinion is that low vLDL with “high” LDL is not something to worry about, unless is VERY high.
https://mindandmatter.substack.com/p/ketosis-and-ketogenic-diet-brain
See also the data on LDL levels and mortality rates for women who in your age group: https://www.nature.com/articles/s41598-018-38461-y
Thank you! I should have figured you would have already covered this topic. I look forward to listening to it. I have thus far only scanned the abstract and also look forward to reading in detail the epidemiology paper you linked to in Scientific Reports. It is reassuring that my total cholesterol values (214 mg/dL) was found to be linked to the "lowest mortality" group. Even though I am aware of the LMHR phenotype, it was a bit stunning to have TC flagged as 'out of range' high for someone who munches raw walnuts and pistachios for the sheer joy of it.
Your cholesterol is out of range based on the simplistic thresholds most physicians memorize. However, as you can see, cholesterol levels a bit above 200 for your demographic are actually associated with power mortality. Most physicians don’t even know this, and will reflexively want to put you on a statin because your result is above a single, magic, one-size-fits-all threshold.
For better or for worse, my doctor knows I'm stubborn one when it comes to such. She didn't even try to suggest I follow orders to get vaccinated after recovering from CoVID (early circulating strain) given I'm an immunologist and would point out the irrationality of such a recommendation. Given my clean bill of health, I suspect she knows how I would receive the recommendation for statins - and I feel well prepared now with info for my scheduled follow-up to discuss my results. Thank you for the recommendation to listen to your discussion with Dr. Dominic D’Agostino - super interesting!
Ahh okok.
So if I eat a crap ton of fiber while I eat HFCS most of the effects would be mitigated?
Or it being a liquid concentration of glucose + fructose especially bad.
Not planning on eating HCFS, just curious.
Eating fiber together with sugar will certainly be better than eating sugars in isolation. However, I also *suspect* that whole foods with fiber + sugar will be different than processed foods composed on comparable amounts of fiber + sugar (e.g. in the form of HFCS). Imagine two foods, Food A and Food B. Food A is a natural whole food with some amount of fiber, glucose, and fructose. Food B is a processed food engineered to contain the same exact amounts of fiber, glucose, and fructose. These two foods, even if they contained nothing else, would *not* necessarily be metabolized in the same way. The sugars may be embedded within the physical substrate of the fiber-containing foods in different ways. The would mean different rates of of absorption, etc.
That makes a ton of sense.
The tricky part would be to determine if Food B was bad for your health.
There is a big difference between a cookie, a cereal, veggie burger, or minced meat; for example. Technically all processed.
Maybe we could categorize them by having HFCS or not. That may be more actionable in the path to healthy eating.
Great post!
I didn't get why we want to reduce insulin uptake.
I mean yes, insulin resistance is bad. Of course.
But is it caused by insulin spikes?
Eating potatoes and beans give you huge insulin spikes. But there are cultures that eat 95%+ tubers.
Also you said so yourself. Fructose does weird things without spiking insulin.
That's why I wonder why it's it relevant that some foods produce a huge insulin spike. If it is done by potatoes or seems fine.
Yes, insulin resistance is a reduction in cells' sensitivity to insulin due to too much insulin signaling. However, this does not mean insulin is the only factor. First, keep in mind that insulin resistance can develop in specific cells and tissues at different times, and also that the liver is arguably the most important tissue in this context because it's the organ that responds to insulin secretion to regulate glucose storage (which is the process that breaks in diabetes).
The cultures that eat very high-carb diets (>90% calories from carbs) are also *not* eating other things concurrently. For example, they are not eating high levels of fats together with their high-carb diet, nor are they consuming processed foods and large amounts of concentrated sugars. Among other things, they're not eating liquid fructose (no fiber) together with their crab-rich, insulin-spiking potato diet.
Fructose is problematic because it is only metabolized in the liver, unlike glucose. When you consume high-fructose corn syrup, for example, it's liquid sugar with no fiber--a roughly 50/50 mix of glucose + fructose. The glucose causes insulin release, while the liver has to simultaneously process the fructose. At a very basic level, I think of it this way: when the liver is "distracted" or "overloaded" because it's processing too much at once, things start to break more easily. Fructose in the liver can also stimulates lipid production. The insulin signal from the glucose tells cells to store that fat... and eventually that results in fatty liver disease. That's one reason why combinations of nutrients are important to consider, and why the prevalence of HFCS in modern processed foods is so good at helping drive fatty liver disease.
My conversation with Robert Lustig got into some of this: https://mindandmatter.substack.com/p/obesogens-oxidative-stress-dietary
Ahhh! Gotcha.
You are right; most cultures eat carbs or fat, but most don't at the same time.
And do you think HFCS is the main culprit or fructose as a whole?
Like if I eat strawberries and potatoes at the same time, would it be bad?
Also sucrose doesn't seem too bad.
And I'll give the conversation with Robert a listen! Haven't listened to that one.
One of the important ways HFCS is different from the sugars found in whole foods like fruit is that HFCS is liquid glucose + fructose, often inside of processed foods containing little to no fiber. The fiber found in fruits blocks or at least slows down the fruit sugar from going directly into the liver via the portal vein. In the absence of fiber, concentrated amounts of sugar in HFCS can directly go to the liver, quickly. As a result the organ is more "overloaded."
Sucrose is only metabolized by the liver. In that respect it's like alcohol. It used to be that only alcoholics got fatty liver disease. Now all sorts of people do, including children who have never consumed alcoholic beverages. A major reason for this is overconsumption of sugary foods containing fructose. Again, the dual-combination of glucose + fructose is a major issue here, especially in the absence of fiber. Glucose means insulin which means, "store excess energy as fat." The fructose stimulates fat synthesis in the liver, which is then stored as fat due to the insulin. Fatty liver.