Mastering Nutrition

Question: Can you give any suggestions for increasing delta-6 desaturase activity? There's a bunch of nutrients involved in that, so many that you basically just need to do a comprehensive nutritional screening for whether something is missing there. You might just have low activity by genetics. It's probably not worth solving that problem. The big governor though is if you have if you have insulin resistance or you have low insulin levels from chronic carbohydrate restriction, that might increase it. But you also look at your inflammation because you might have some of the higher fatty acids being depleted from inflammation or oxidative stress. I mean, more nutrient-dense diet across the board, more carbohydrate, if that doesn't do it, then just maybe take a supplement or increase the liver and egg yolks to the point where the arachidonic acid is normal. Measure your CRP. If that's high, address inflammation. In the Testing Nutritional Status: The Ultimate Cheat Sheet, I have a big section on oxidative stress. I go through that testing. A starting point might be Genova's Oxidative Stress 2.0 blood panel. But if inflammation and oxidative stress are the things, work on those. If those aren't issues, then more nutrient density across the board, fix any nutrient deficiencies you find, increase carbohydrate if you're on low-carb. If none of those things work, then just increase your arachidonic acid level in your diet. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: What are the pros and cons of boosting sulforaphane? Sulforaphane, the nice thing is it promotes detoxification. The bad thing is it raises the need for iodine. I don't know what ratio to take, but you definitely want to make sure that you're getting some kind of iodine into your diet, whether it's through like 200 micrograms of iodine from a kelp powder supplement or you experiment with milligram amounts from a broken up Iodoral tab or whatever. Because I don't know the dose, I'm just going to say work slowly and work your way up. Certainly, if you have any signs of hypothyroidism or you have any brain fog, increase the iodine or decrease the sulforaphane would be my opinion. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: Is it true that we can’t absorb more than 1.5 grams of creatine at one time? I don't think that's true. From what I looked at, it looked like the absorption of creatine was really, really good. I don't know if someone was arguing maybe that we don't retain more than that. But I think the retention of your muscles is going to be best with creatine if you take it post-workout and if you take it with carbohydrate to stimulate insulin. But on the whole, I think that the absorption and retention is good enough that it's more a matter of how fast will you get to peak muscular creatine than it is about where you get in the long-term. Maybe if you follow all the best procedures to absorb and retain creatine, you'll get to the 30% increase in muscular creatine in two weeks taking 5 grams a day instead of four weeks. Maybe someone who doesn't follow any best practices takes six weeks. But ten weeks later, you're probably going to be at peak effect if you just take 5 grams of creatine at a time without paying attention to all the details around absorption. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: NMN vs. NR: What’s better? And is TMG necessary? Yeah. There are no human studies looking at NMN and how it's metabolized. There are studies of NR. No one has showed any positive benefits of supplementing NR in humans yet, but they haven't really done any long-term studies or looked at many things, and they really haven't looked at anything that I would really want to see for NR. They've looked at things like glucose and lipids and other metrics of metabolic health doesn't really do anything for that. This is what I would say. My strong suspicion is that NMN is not absorbed intact. It's broken down into NR and it's absorbed intact as NR, while NR is just absorbed intact in NR. I believe that both of those supplements are going to lead to NR getting into the liver. I mean, I would use NR because there's more data on NR, and I wouldn't use NMN because there isn't any data on it. But it probably makes no difference at all because they're probably both absorbed as NR. Maybe if your digestion is weaker, you're going to do better within NR than NMN because you probably almost certainly are not absorbing NMN intact. If you're not digesting it, then you're absorbing less of it. But probably for most people, it makes no difference. I believe that both of these are going to generate NAD levels in the liver much more effectively than nicotinic acid or niacinamide would, the two common niacin supplements that are available on the market now and have been taken for ages. I think it will be better at boosting NAD levels in the liver. I think that will allow the liver to nourish many other tissues in the body to get a better NAD response in those tissues. My suspicion is that this is going to have a positive effect for anti-aging, for cellular repair. I think it's probably going to have a lot of promise for mental effects in the brain where there's high NAD turnover for neurotransmitter release. I think it's going to have probably really good effects in the gut where there's high NAD turnover because the gut faces so much damage by just being forced to deal with everything that you put into your body, unlike everything after the gut, after absorption, which has really high quality control. I think it's going to be great for skin issues. I think that in order to get the best NAD response and to tax the methylation system the least, you want to take a smaller dose with every meal rather than taking a higher dose once. I would take like 150 milligrams max at a meal. If you're going to take 450 milligrams, I'd take 150 at each of three meals. If you want to take less than that, you either use the powder or empty half of it out in a capsule. Like take half the capsule, empty it out into your mouth with a meal, 150-milligram capsule to do that. It will give you 75 milligrams. Take that three times a day. Then there's no good test to really see whether it's doing anything for you. You really have to judge it by your response. Are you getting tangible benefits from it? If so, then I think it's fine to keep it up. But yeah, I would take 100 milligrams of TMG for every 200 milligrams of nicotinamide riboside or nicotinamide mononucleotide. Personally, I wouldn't use the NMN and use the NR because there's more data on it.  This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: What to do about cataracts. Carl Rayner says, "Cataract in one eye becoming noticeable. This eye had a posterior detachment about 11 years ago, which is basically healed. I've been on a low-carb diet for over 40 years. Eat raw cream cheese, eggs, meat and liver. In the past few years, adding fasting and more keto diet. Saw your thoughts about glutathione on the cheat sheet and interview with Wendy Myers. Am I on the right track and what else could I do? Grain intolerant. What testing beyond normal tests might be helpful?" I believe that cataracts in the eye are largely driven by the glycation of lens proteins. The glycation of lens proteins is largely driven by methylglyoxal, which I did my doctoral dissertation on. In direct contradiction to much of the low-carbohydrate literature, glycation is not all driven by carbs. Methylglyoxal is quantitatively the most important source of advanced glycation end products in the body. Methylglyoxal can be derived from glucose, or it can be derived from ketones, or it can be derived from protein. No one has ever done a very good study to determine whether you have more methylglyoxal on a ketogenic diet versus a high-carb diet. But there was one poorly designed study where they took a small handful of people. They said, "Here's the Atkins diet, new diet," Or what is it called? Atkins New Diet Revolution or whatever that book was called. They said, "Here, read this, go forth and do it." They went home, presumably they read the book or part of it, and they tried to do it. They came back, they lost weight, they had elevated ketones and guess what? They also had significantly higher methylglyoxal. Also, everything in the pathway that leads from ketones to methylglyoxal was elevated. I would say the data were very strong that in those people, they had higher levels of methylglyoxal because they had higher ketone levels that were generating it. They went on the Atkins diet, and they worsened their glycation risk by making a lot more of the thing that causes most advanced glycation end products and the thing that is probably overwhelmingly driving cataracts. But they didn't show any health consequences, and they certainly didn't measure cataracts in that study because that wasn't the point of it. They left more questions than answers. For example, what if they had a control group that lost the same amount of weight on a high-carb diet? My suspicion is that methylglyoxal would have gone up during weight loss but just not as much. I also think that if those people stabilized their new weight and then they worked carbs back into their diet, their methylglyoxal would go back down. In fact, I have a consulting client who developed cataracts that corresponded very well with when he started intermittent fasting. He did have poor glutathione status. We were able to improve his glutathione status, but the cataracts didn't go away. Todd Becker asks, "How do you test methylglyoxal levels?" You don't. You become a guinea pig in a lab because doing a study on it. That's about it. Look, I'm not against keto and I'm not against intermittent fasting. But if you're specifically talking about dealing with cataracts, you're probably not going to get the cataract to go away, but you probably can stop them from getting worse and stop them from forming. I think intermittent fasting and keto is probably going in the wrong direction. One thing that I do think, I don't think you're going to measure your methylglyoxal levels, but I think you should test your glutathione levels because glutathione is what detoxifies methylglyoxal. If you listen to my riboflavin podcast, we talked about cataracts being a sign of riboflavin deficiency and also being one of the things that's being investigated for whether riboflavin supplementation can help it. Why does riboflavin supplementation help that? For the exact same reason as when I went on that big, longwinded answer about glucose-6-phosphate dehydrogenase deficiency at the beginning, the riboflavin is there to boost glutathione recycling. I think the whole story, all these pieces knit together to a very, very, very nice story, clean story saying what you want in your eye to avoid cataracts from forming and getting worse, forming in the first place and getting worse, is you want low levels of methylglyoxal in your lenses. How do you get that? You have very good glutathione status. The keto thing is a maybe. There's no maybe that maybe keto makes that better, but there's a maybe that maybe keto makes that worse. You can't test the glutathione levels in your lens proteins, but you can test the glutathione levels in your blood. I would use the cheat sheet in a very targeted way for everything that's relevant to your glutathione status. I would follow the recommendations in there about how to boost your glutathione status. I would use your blood levels of glutathione as a metric. Rather than getting them in the normal range, I would try to get them as high within the normal range as you can, and titrate your approaches according to what works. Test it every couple of months, make one very important change. Well, actually, follow all the steps in optimizing glutathione status right now or all the ones you're willing to do. Follow them for eight weeks, test glutathione status, get a baseline glutathione if you can, but eight weeks of all my suggestions or whatever you're willing to do with them. Retest the glutathione, see if it helped. If it helped, then tweak one thing at a time after that. Do that one thing very consistently and stably for four to eight weeks. Retest glutathione. Whatever I said for glutathione, also consider maybe supplementing with high-dose riboflavin in there. Maybe 100 milligrams of riboflavin at each meal, I would probably revise my glutathione recommendations in the cheat sheet to include that as a possibility. Yeah, optimize against glutathione and consider riboflavin supplementation. Be very open-minded about the carbs, the keto and the fasting because those might be great for many things, but they're definitely not optimal for glutathione and methylglyoxal. Thanks, Carl. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: If free T3 looks good, why is TSH still a little high? Why hasn't the T3 brought it down enough? Your thyroid gland makes thyroid hormone. Thyroid hormone increases your metabolic rate and does a lot of related things. Your hypothalamus is governing that by controlling your pituitary, the master endocrine gland, and its secretion of TSH, which is what controls the thyroid gland and makes it make more thyroid hormone. The way that the feedback occurs is that the circulating T4 is converted to T3 inside the cells of the pituitary. That is what suppresses the production of TSH, which is basically the pituitary monitoring the thyroid hormone levels to know whether the thyroid has done its job. If the pituitary, the master endocrine gland, decides that the thyroid has done its job, it takes down TSH, the signal to make more thyroid hormone. You really are not looking at whether the free T3 is suppressing the TSH. Ninety percent of that suppression comes from circulating T4 that's converted to T3 inside the pituitary gland. You really are looking at whether the T4 is on the high end of normal or not.  If your reverse T3 is on the higher end of normal, then that explains it. You basically have your brain telling your thyroid gland that it needs more thyroid hormone, but you have much of the rest of your body deciding that it's not in the position to carry out the effects on the metabolic rate that the thyroid hormone is demanding. It's converting the thyroid hormone into reverse T3, which is basically a thyroid antagonist. If your reverse T3 is high, then I think you want to look at things like calorie intake, carb intake, and stress levels because I think those are the main things that might make your body want to resist the signal of thyroid hormone by making the reverse T3. If the reverse T3 is good, meaning it's pretty low, then I think that means that there is something either in your brain, specifically in the hypothalamus or in the pituitary or somewhere in the combination where they're just deciding that your body needs more thyroid hormone than you have. My suspicion is that that's going to relate to how sensitive your cells are to the thyroid hormone, if your cells are somewhat resistant. Remember in the last AMA, this got brought up, and I talked about zinc deficiency and high free fatty acids being the primary things that are going to reduce sensitivity to thyroid hormone or cellular uptake. There are some indications that high free fatty acids might also decrease cellular uptake, but not much is known about what governs cellular uptake. In fact, there are some genetic variations in cellular uptake. If the thyroid hormone levels are high in your blood because they're not getting into the cells, then that could easily explain everything. It's just that your problem seems pretty moderate because you're not saying that your thyroid hormones are sky high and your TSH is sky high. You're just saying everything is a little on the high side of normal. It sounds like there's not a big problem, but that something somewhere your body is determining that you need a little bit more thyroid hormone. If you can address zinc, free fatty acids, and I would address zinc and free fatty acids as the top things, unless the reverse T3 is high, target carbs, calories, and stress. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: What food supplements and training programs are good for developing muscle mass? Overwhelmingly, what matters for muscle mass is working out, eating enough protein, and eating enough calories.  You want to try and hit 10-20 sets per muscle group per week with eat set hitting within 80% of failure. So, if your doing a set of 8 reps but you could have done 20 reps with your chosen weight, that doesn’t count. You would want to pick a weight that you can lift no more than 10 times. Ideally, you’ll do some sets in the 5-rep range, 10-rep range, and 15-rep range.   For protein, you probably want to be up around 1 gram per pound of body weight or per pound of target body weight.  Then calories, you do need a caloric excess, but you don't want to get fat. If you know how many calories you need to be weight-stable, I recommend titrating the calories up 100 calories a day and then track your progress if you are gaining waist circumference. I know this is a little bit harder when you're a woman because you're going to have more fluctuations in water weight, but in terms of simple things to do to track your progress, waist circumference is valuable, and looking in the mirror is valuable.  If you can get an actual Bod Pod or DEXA scan, then that would give you more reliable information. There's a device called Skulpt. It's bioimpedance, I believe, but it's taking it at many different points where you take so much data that it actually becomes pretty accurate, but it's very time-consuming. Anyway, take your choice of what you're going to use to track your progress. If you're not gaining any fat, you can very slowly add your total calories. If you are gaining fat, you need to cut back on the calories. But you need to have a caloric excess to maximize your muscle gains. That right there is probably 90% of it and anything else is probably completely pointless unless you are a very good athlete, in which case you're going to be looking for what's the next. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: Should I manage my total cholesterol of 305 just for my doctor or should I be doing it for my own sake? If so, how should I do it? You should want to improve your lipid profile for a lot more than to please your doctor. Let's revisit this from a cholesterol skeptic point of view. Uffe Ravnskov, he wrote a book called The Cholesterol Myths. In that book, he shows a graph from the Framingham study where he maps out the people who have heart disease and the people who don't. If you look at that graph, one thing that you see is that everyone who had total cholesterol over 300 had heart disease and no one who didn't have heart disease had cholesterol that high. Look, the only way to have a total cholesterol of 300 or more in most cases is to either have a thyroid disorder or to have a familial hyperlipidemia. We're talking about fasting levels here. You should want to manage your blood lipids for your own sake because people with familial hypercholesterolemia have a dramatically increased risk of having heart disease decades earlier than it becomes normal for the general population.  I'm not saying it's 100% certain that if you have a cholesterol of 300 you will have heart disease, but you are way disproportionate in risk for that reason. You definitely want to address this for the sake of your health. I think that if you have weight to lose, that losing weight should be one of the first things that you do to normalize your blood lipids and your inflammation. Being overweight also contributes to elevated free fatty acids, and elevated free fatty acids do raise your blood lipids. That's, in fact, the entire rationale of using high-dose niacin to lower LDL-C is by suppressing free fatty acid release. It’s also important to address any inflammation in your gut. You might have microbiome issues, and working more high-fiber vegetables into your diet and diversifying across the different plant fibers is a great way to nourish your microbiome, reduce inflammation that comes from the intestines that would negatively affect your blood lipids. If these things that we just talked about aren't enough to get the blood lipids into the normal range, then I think you want to experiment with eating more carbohydrate and a low-fat diet, but selecting those foods to maintain nutrient density. You could add something like psyllium husk fiber , which might be both good for your gut and the inflammation coming from your gut. It will also help reduce your cholesterol by making bile acids go into your feces and making your liver draw cholesterol from the blood. If those natural things don't get your blood lipids into the normal range, then I think that you should consider being open to pharmacological methods. I've gone through all the cholesterol-skeptic literature and I'm against demonizing cholesterol. I do not believe that high cholesterol is the cause of heart disease. But if your lipids are that high, it's overwhelmingly because you are not clearing them from the blood, and not clearing them from the blood is the single most important risk factor for them oxidizing, and them oxidizing does cause heart disease.  This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.

Question: "Do you have any recommendations on how to get enough calcium on a low-carb, no-dairy diet? I've read that vegetables provide calcium, but bioavailability is poor." The bioavailability of calcium from different vegetables is highly dependent on the specific vegetables.  Cruciferous vegetables have very good bioavailability. It's better than from milk. Spinach has like close to zero bioavailability. It's terrible and you shouldn't even count it. Nuts and seeds have about 20% of the calcium being absorbed. If you compare that to milk --- milk is probably going to be like 30% or 40%. Cruciferous vegetables are going to be like 50% or 55%. The real problem is the volume. If you look at broccoli or kale and you look at how much volume of those foods do you need to eat in order to get 1000 to 1500 milligrams of calcium a day, which is the target, it's a ridiculously high volume.  I'm a bit skeptical that you want to eat more than say 200 or 300 grams measured cooked of those foods a day because they're increasing your iodine requirement. At some point, they become a liability for your thyroid gland. I think it's best to eat two or three servings of those cruciferous vegetables a day, and that's basically maxing out the calcium that you can get from them. You're just not going to get anywhere near the 1000- to 1500-milligram target. A low carbohydrate, non dairy containing diet is emulating the traditional diets of the Arctic where plant foods were very limited. How did they get their calcium? They crushed up fish bones. They freeze-dried fish bones, they pulverized them, and they ate the bone powder. Bone meal is a traditional food. Some consider it as a supplement but it is the historic source of calcium in traditional diets that were low-carb. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a. Access the show notes, transcript, and comments here.

Question: What should people with glucose-6-phosphate dehydrogenase deficiency be doing not just about glutathione, but about folate, vitamin K, fatty acids, and neurotransmitters?  G6PD, glucose-6-phosphate dehydrogenase deficiency, is an inborn error of metabolism. It's the most common one in the world. About 8% globally have some impairment in this enzyme. The reason that it's important is because glucose-6-phosphate dehydrogenase is the enzyme that allows you to make NADPH, which is a specific derivative of niacin that's involved in antioxidant defense, detoxification, synthesis of neurotransmitters, and synthesis of nucleotides, which are needed for cell division because they're parts of DNA. Someone with G6PD deficiency is vulnerable to hemolysis, or the destruction of red blood cells, because of glutathione deficiency. Glutathione reductase uses energy and NADPH, the thing that you can't make, to recycle glutathione. But it also uses riboflavin. So, one of the adaptations that someone with this impairment has to try to protect themselves is for the glutathione reductase enzyme to hog all the riboflavin so that it says, "I don't have enough of the raw material I need to make this happen, so I'm just going to make myself get way better at using what I do have." That's an adaptation to compensate for not being able to make NADPH is just to get way better at using NADPH to recycle glutathione. Supplementing glutathione is not necessarily a bad idea. You just have to be aware that at a certain point you just can't solve every one of the dozens of problems that are happening. I think that you should measure your glutathione status. Probably the best test available, not because it's the best we could have available but because there's nothing better right now, is LabCorp's test for glutathione. If that looks low, then I would supplement with glutathione to try to bring that up to normal.  For the folate recycling, you have to consider this basically as if you had a really bad MTHFR polymorphism because G6PD is needed to make the NADPH that MTHFR uses, again, with the help of riboflavin to make the methyl group on methylfolate. You can take some methylfolate, but as I've made the point in my MTHFR protocol at chrismasterjohnphd.com/methylation, you have to take 18,000 times the RDA to compensate for the 18,000 times a day that you add a methyl group to the folate molecule using that enzyme. It's not safe to take anywhere near that much folate. What I would do is just very strictly follow the MTHFR protocol that I have at chrismasterjohnphd.com/methylation, and that involves doubling your choline intake because you don't need NADPH to use choline to support methylation. Just as if MTHFR didn't work because of genetics and not enzyme, what you would do is you double your choline utilization for methylation because you're not good at using folate.  On recycling vitamin K, it probably just means that you need a high amount of vitamin K in your diet. I think it's probably similar as if you had a bad VKOR polymorphism. VKOR is the enzyme that recycles vitamin K using NADPH that you got from this pathway that's not working right when you have G6PD deficiency. In terms of all this stuff that you are not good at synthesizing, like cholesterol, fatty acids, nucleotides, and neurotransmitters, I think the only thing that you can do for that is to try to eat a lot of these things preformed. That means eating a diet rich in relatively lean animal foods because they have a lot of preformed stuff, like cholesterol, in them and mainly in the flesh, not the fat. With plants, you want to eat mostly fibrous vegetables because they are highly cellular and rich in nutrients that you can’t make.  You don't want to go extremely low-fat, but if you eat a diet fairly rich in animal foods, you're going to get a lot of the specific fatty acids that you can't make. A high-fat diet is mostly giving you just a bunch of fat that you could have made yourself. This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019 If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a Access the show notes, transcript, and comments here.