In episode 25, Insulin Resistance Isn't All About Carbs and Insulin, I explained why an individual cell would "decide" to stop taking up energy. Here in episode 26, I explain tissue-level energy overload, focusing on adipose tissue and liver.
At adipose tissue, the problem with fatness isn't the amount of fat. It's that we've reached the point where we can't get any fatter. Well, we can, but we can no longer do so while maintaining a healthy organizational structure within adipose tissue that allows blood, oxygen, and nutrients to get to where they need to go. Surprisingly, some of the things that enable proper expansion, and thus protect our metabolic health, are things that we usually think of as "bad," such as inflammation. In fact, the pro-inflammatory changes in the gut microbiome in response to an obesogenic diet provide information to adipose tissue that it needs to prepare for healthy expansion. And adipose expansion is most protective at the site of the "bad" body fat: visceral fat in the abdomen.
At liver, the problem is fat gets trapped in the liver, flattening out everything in the cell and hogging the space needed for glycogen storage, and this can happen even in a lean person.
I conclude with some practical recommendations about body composition and nutrient density.
In this episode, you will find all of the following and more:
In episode 23, I explained why ketogenesis isn't all about carbs and insulin. Here in episode 25, I explained why insulin resistance isn't all about carbs and insulin. If that doesn't sound crazy, let me put it this way: forget carbs; I'll even say insulin resistance isn't all about insulin.
We start with a riddle: what do obesity, exercise, cigarette smoking, and diets rich in fruits and vegetables all share in common? Hint: it's a centrally important physiological response to each of them that mediates their health effects.
In the course of answering this riddle, I explain the underlying physiology that I consider most important to "insulin resistance" and why I believe insulin resistance is best viewed as subset of something far more important. I conclude by outlining practical strategies to prevent and reverse it.
In this episode, you will find all of the following and more:
Why would an individual cell "decide" to stop responding to insulin?; the limitations of using blood insulin and glucose concentrations as a primary metric of insulin resistance are similar to the limitations of assessing your level of "boss resistance" by the number of phone calls you decline from your boss when you skip work; why your pancreas is sort of like your boss; reactive oxygen species (ROS) are central to the physiology; ROS inhibit aconitase and shunt internal energy toward fat storage; ROS inhibit further intake of energy; ROS inhibit fatty acid uptake into mitochondria; ROS inhibit glucose uptake; ROS increase the expression of the entire antioxidant system and xenobiotic defense system; Subbing players on the field in team sports provides a useful analogy to understand why ROS-mediated inhibition of cellular energy uptake is health-promoting when other cells can fill in; insulin resistance isn't all about insulin; some responses to cellular energy overload antagonize insulin; others mimic insulin; obesity vs. exercise; AMPK activation makes the net effects of ROS in exercise very different from obesity; micronutrient intake determines whether net effects of ROS support antioxidant defense; glutathione synthesis depends on both nutrients and insulin sensitivity and stimulation; insulin resistance isn't all about ROS. It's about the context in which ROS operate; the net hormetic pro-oxidant effects of fruits and vegetable polyphenol; the net toxic pro-oxidant effects of cigarette smoking; again, net effects of ROS aren't about ROS; their about the context in which ROS operate; nutrient density as a practical strategy in insulin resistance; body composition as a practical strategy in insulin resistance; low-carbohydrate diets as a useful practical strategy for body composition, with potential limitations in the long-term because of the importance of carbohydrates for antioxidant defense.
Whites have higher 25(OH)D than every other racial group, and the conventional explanation is that light skin evolved to allow sufficient vitamin D synthesis far away from the equator. In episode 24, I explain why these differences may relate to genetics of vitamin D metabolism that have nothing to do with skin color and may reflect a lower average need for 25(OH)D rather than a lower average ability to get enough. But "average" is the key word and when it comes to using this information on a practical level we need to look beyond racial categories and treat each person as an individual.
In this episode, you'll find all of the following and more: should I offer online nutrition classes?; this will start of sounding like it's about racial groups, but it's really about individuals; blacks in America have lower 25 (OH)D than whites; the conventional hypothesis explains this as dark skin being poorly adapted to these latitudes; genetic evidence suggests light skin began evolving long after the migration from Africa; aggregate global 25(OH)D data do not support the conventional hypothesis; Caucasians have higher average 25 (OH)D than non-Caucasians at every latitude; Caucasians have higher average 25 (OH)D at temperate latitudes than non-Caucasians have at equatorial latitudes; blacks in America have higher bone mineral content than whites; calcitriol dominance favors getting calcium from our food, while PTH dominance favors getting calcium from our bones; genetic variation in the 1-hydoxylase can account for the difference in 25(OH)D between blacks and whites in America, but this has nothing to do with skin color or racial groups in the way we have socially defined them; calcium intake could influence how the genetic variation translates into 25(OH)D; this does not affect white 25 (OH)D, and it could be related to calcium intake; ancestral calcium intake could have mediated selective pressure on the relevant genes; blacks in the United States have higher average calcitriol and a higher average calcitriol-to-PTH ratio than whites; similar differences between Inuit and Danes: lower 25(OH)D, higher calcitriol, and lower PTH; a traditional diet raises 25(OH)D, raises calcitriol further, and suppresses PTH further; Asians have lower 25 (OH)D than whites in Hawaii; the references ranges may in effect be applying average white requirements to drive recommendations for everyone; the Maasai and Hadza have higher 25 (OH)D, but this may be due to higher calcium intakes, and/or higher ancestral calcium intakes that influenced their genetics; non-whites are probably adapted to lower 25 (OH)D than whites on average, but it is individual genetics rather than racial groups that are relevant; 25 (OH)D + calcitriol can be summed for a biological activity index; PTH should be in the lower half of the reference range; magnesium deficiency could confound the PTH measurement, but it probably has to be extreme.
This episode is part personal story, part practical how-to guide, and part insight. The insight I want to emphasize here is one that I think is far too often overlooked: sometimes we shouldn't be trying to lose weight because the time isn't right.
But if the time is wrong, how can we know? And once we know, what can we do to prepare our bodies for weight loss and allow the time to become right? The short answer is that if weight gain is due to stress, I strongly believe we should always destress first. For the detailed answer, listen in.
In this episode, you will find the following and more: why there is a time to lose weight and a time not to; why calories-in calories-out (CICO) is like gravity; the right approach to weight loss is likely to be the one that incorporates 2-3 intuitive principles that allow you to sustain a caloric deficit while feeling satiated and energetic; there are a lot of those principles, so the 2-3 that work best for you probably has less to do with their general efficacy and more to do with your own personal psychological and behavioral traits; my skinny teens, my powerlifting/bodybuilding musclehead body, my grad school-induced dad bod, getting my postdoc fatso on, putting 6-7" on my waist in my first semester as a professor; it all turned around when I read Tim Ferris's 4-Hour Workweek; running on a treadmill while sleeping 10 hours a day, traveling to destress, gaining with CrossFit, leaning out with CrossFit; using the greyhound formula recommended by Alan Aragon and Brad Schoenfeld in The Lean Muscle Diet; using MyFitnessPal to track calories as recommended by CrossFit South Brooklyn; R-Lipoic acid, D-biotin, acetyl-L carnitine, coenzyme Q10 (CoQ10), coenzyme B vitamins to smooth out energy between meals; Headspace app or other mindfulness meditation, yoga, dance, martial arts, could help self-awareness, the key to knowing when the time is right; destressing is the key to make the time right when it's wrong; resisting social pressure and self pressure to lose weight is, ironically, the key to making the time right to lose weight.
This episode is brought to you by US Wellness Meats. I use their livewurst as a convenient way to make a sustainable habit of eating a diversity of organ meats. They also have a milder braunschweiger and an even milder head cheese that gives you similar benefits, as well as a wide array of other meat products, all from animals raised on pasture. Head to grasslandbeef.com and enter promo code "Chris" at checkout to get a 15% discount on any order that is at least 7 pounds but under 40 pounds (it can be 39.99 lbs, but not 40). You can use this discount code not once, but twice!
Did you know that adding MCT oil to your pasta is more ketogenic than restricting your carbohydrates to ten percent of calories?
Many people think of carbohydrate and insulin as central to ketogenesis, but the direct biochemical event that initiate ketone formation is actually the oversupply of acetyl groups to the TCA cycle during conditions of oxaloacetate depletion.
While largely a biochemistry lesson, in this episode I also teach you the practical implications of this. There is more than one route to ketogenesis, and while they all produce ketones, they are fundamentally different in important ways.
Adding coconut, MCT oil, or exogenous ketones allows you to reap benefits of ketones without necessarily restricting carbohydrates and insulin, and that may be useful if you are also trying to reap some of the benefits of carbohydrate and insulin.
On the other hand, certain conditions that respond to ketogenic diets, for example refractory childhood epilepsy, need stronger degrees of ketogenesis than you can achieve simply by adding MCT oil to pasta.
Understanding the difference allows you to better make practical decisions about your diet that are most consistent with your priorities.
In this episode, you will find all of the following, and more:
An overview of the TCA cycle and burning carbohydrate for energy; the critical importance of oxaloacetate (OAA) to allow acetyl groups to enter the TCA cycle; how we burn fat on a mixed diet; the meaning of the phrase, "fat burns in the flame of carbohydrate" or “fat burns in a carbohydrate flame"; loss of lean muscle mass can occur if dietary carbohydrate and protein are too low to maintain OAA levels, and fat cannot spare this loss; under carbohydrate restriction, OAA is not repleted by carbohydrate and is used for gluconeogenesis, while more fatty acids reach the liver to make acteyl CoA; the oversupply of acetyl groups in excess of OAA initiates ketogenesis; insulin shifts fat to adipose tissue, but this doesn't cause obesity; MCTs go straight to the liver via the portal vein rather than going to the blood via the lymph in chylomicrons, and they thereby avoid that effect of insulin; insulin suppresses the carnitine shuttle; MCTs do not require the carnitine shuttle and are therefore immune to this effect of insulin; MCTs at breakfast suppress food intake at lunch; MCTs added to pasta increase beta-hydroxybutyrate; two ways of getting ketones: selective deprivation vs. abundance; if you are trying to get ketones but having negative effects of carbohydrate restriction (e.g. declining exercise performance in sports requiring anaerobic glycolysis, declining thyroid hormone and sex hormones, elevated cortisol and LDL-C) you can add MCTs to get the ketones; comparison of beta-hydroxybutyrate concentrations from MCT vs. 10% carb vs. classical ketogenic diet.
In this episode, I give my take on a recent masters thesis paper by Rachel Gregory from James Madison University, which reports a study where just under 30 members of Rocktown CrossFit and Sports Performance were randomized to do CrossFit for six weeks with a normal diet or a low-carbohydrate ketogenic diet.
The ketogenic diet led to weight loss and loss of bodyfat without hurting the performance on a 6-7-minute for-time workout-of-the-day (WOD)-style test involving a 500-meter row, 40 bodyweight squats, 30 ab mat situps, 20 hand-release pushups, and 10 pullups.
Herein, I explain why I think this study does show that the average person can lose weight and get fit with this method, but why it doesn't really get to the heart of the questions I would be interested in, which are these: how would a ketogenic diet impact maximal performance on weight-lifting sets of 5-12 reps, or in sports involving short bursts of energy such as football, basketball, baseball, soccer, and tennis, and do the hormonal adaptations to the diet ultimately have the potential for negative impacts on thyroid hormone, cortisol, LDL-cholesterol, and sex hormones?
In this episode you will find all of the following and more:
The protocol of the study; changes in caloric intake, body weight and body composition; why the ketogenic diet's spontaneous decrease in calories can easily be explained by the effect of variety restriction on food reward, as Stephan Guyenet has explained well over at Whole Health Source; the changes in performance that occurred; how carbs, fat, and creatine impact the three energy systems of phosphagen or creatine phosphate, anaerobic glycolysis, and oxidative phosphorylation; why carbohydrate intake would primarily impact maximal performance at tasks requiring 15-90 seconds of intense work rather than a 6-7 minute WOD; why the ability to raise a 5RM to a new PR in trained subjects would have been a better question to address these concerns; why most team sports would also fall into this category; why free T3 (fT3), cortisol, LDL-C, and sex hormones (testosterone, estrogen, progesterone, etc) should be examined; and why how full your "stress bucket" (allostatic load) is will most likely be the ultimate determinant of whether these hormonal systems are negatively affected.
In this episode, I tell the story of my own battle with eczema. I begin by describing my extraordinary recovery from extreme eczema using the right probiotic. I then describe how a more recent relapse led me to discover the incredible importance of mitigating soap exposure when gut-related approaches don't seem to work.
In this episode, you'll find the following, and more:
Chris Kresser’s interview with Glenn Taylor on fecal microbiota transplants inspired this episode.
My own story with eczema.
Recovery with Garden of Life's Primal Defense (now Primal Defense Ultra).
Mild re-occurrence tied to poor gut, poor sleep, high work stress.
Key feature of an effective probiotic for me is S. boullardii plus bacteria.
Prostaglandin E2, derived from arachidonic acid, plays a central role in preventing eczema by water-proofing the skin.
Humidity can "hide" eczema by preventing water loss through a dysfunctional skin barrier.
Minimizing exposure to soap with kitchen gloves and by avoiding unnecessary hand washing are central to preventing topical aggravation of eczema.
Topical application of a fat -- such as shea butter -- after soap exposure can mitigate the damage caused by the soap.
It's important to pay attention to both the internal, systemic causes of eczema and the external, topical factors that will aggravate eczema once it has started.
This episode is a recording of the Facebook Live event, "Ask Chris Masterjohn, PhD, Anything About Health, Fitness, and Nutrition" that originally aired on Tuesday, July 12, at 5:00 PM eastern time.
In this episode you will find all of the following and more:
This episode is a recording of the Facebook Live event, "Ask Chris Masterjohn, PhD, Anything About Fat-Soluble Vitamins" that originally aired on Wednesday, June 29, at 5:00 PM eastern time.
In this episode you will find all of the following and more:
Fat-soluble vitamin nutrition during warfarin therapy, and the critical importance of working with the supervising cardiologist or whoever prescribed the warfarin.
Overuse of vitamin D supplements, and the use of parathyroid hormone (PTH), diet, and lifestyle analysis for a more prudent approach.
My opinion on Life Extension's vitamin K supplement.
Too many fat-soluble vitamins versus nutrient imbalances.
Accidental poisoning of pets with warfarin analogues designed to kill rodents, and treating the pet.
Does it matter what time of day you take vitamin D?
Are nutritional databases reliable?
I predict technology that could help nutritional databases become more reliable and usable.
Is Bulletproof coffee sufficient to help fat-soluble vitamins get absorbed?
How I manage my own vitamin D intake and sun exposure to balance the priorities of getting sufficient vitamin D and circadian rhythm stimulation while avoiding sun-induced skin damage.
Resveratrol: even the hormetic dose requires many nutrients found in foods to have its effect.
Balancing vitamins A and D in pregnancy.
Use of low-dose aspirin in pregnancy.
How to get a day’s intake of calcium.
Fermented cod liver oil: amines and self-experimentation.
Is it ok to take vitamin D in large doses once per week instead of small doses daily?
Do babies need to take vitamin D supplements?
What can be done to help fat-soluble vitamin absorption?
This episode is a recording of the 06/25/2016 Facebook Live event, "Ask Chris Masterjohn, PhD, Anything About Methylation."
Among the questions answered and topics discussed in this episode are the following:
An MTHFR mutation (e.g. C677T) even with normal homocysteine could mean that you are taxing your choline supply and wasting glycine into your urine. Boosting choline and glycine intake could help. What may surprise you is that so could supplementing with creatine!
How to implement the above strategies with natural foods?
Can targeted SAMe supplementation be useful for diagnosing methylation problems?
Choline and fatty liver disease.
Why is my serum B12 soaring through the roof when I haven't even been supplementing?
COMT mutations regulating the balance between mental stability and mental flexibility via dopamine, and whether supplementing with 5-methylfolate could worsen mental problems in people with high COMT activity. Potential relations to obssessive compulsive disorder (OCD) and to post-traumatic stress disorder (PTSD).
How should you get choline if you're allergic to eggs?
With an MTHFR mutation and high liver enzymes, choline would seem to be in order, but should you also rethink your high-fat diet?
All this and more!
In this episode, I discuss dietary management of familial hypercholesterolemia (HeFH). This question was asked on the Facebook Live episode from 06/16/2016, "Ask Chris Masterjohn, PhD Anything About Heart Disease," but I was unable to get to the question within Facebook's time limit.
Please note that HeFH is a medical issue and the purpose of this episode is not to diagnose or treat anyone with HeFH. This is educational in nature and the information should only be used to manage HeFH under supervision of a qualified health professional.
Herein, I discuss why I believe the Kitavan diet should serve as an ancestral diet on which to model dietary management of HeFH. It is a low-fat, low-cholesterol, high-carbohydrate diet where most of the fat is highly saturated because it comes from coconut, some of it is is from fish, and where the carbohydrate mostly comes from starchy tubers but some comes from fruit.
The best way to get to the root of the problem in heterozygous FH is to take the one working gene for the LDL receptor and try to bring it up to the expression level that would be found in someone without FH. This can be done by maximizing the biological activity of thyroid hormone (within the range considered euthyroid) and by maximally suppressing PCSK9 activity with the help of strong insulin signaling. These come down to managing good body composition and eating a low-fat, protein-adequate, micronutrient-adequate, high-carbohydrate diet.
Restricting cholesterol may be helpful, but it also comes at the cost of cutting nutrient density, since some of the most nutrient-dense foods -- liver and egg yolks -- are also rich in cholesterol. Therefore, it should be #2 in the line of defense rather than #1.
Replacing saturated fat with polyunsaturated fat and using statins should both be tools in the kit, but they should be tools much further down the line of resort because they are less related to the root of the problem and they may come at costs that compromise health and longevity.
This episode is a recording of the 06/16/2016 Facebook Live event, "Ask Chris Masterjohn, PhD Anything About Heart Disease."
Among the questions answered in this episode are the following:
Should we be micromanaging specific saturated fatty acids to prevent heart disease?
Should we use our knowledge of our ApoE genotype to help decide what to eat (and specifically, should the E4 allele causes us to avoid saturated fat)?
The persistent importance of the total-to-HDL-cholesterol ratio.
Why the vitamin E content of HDL particles could be determining its protective functions.
Can established heart disease be reversed?
Does moderately high blood pressure directly contribute to heart disease, or is the association between moderately high blood pressure and heart disease reflect some underlying factor that contributes to both?
Do Americans consume too much calcium?
Using essential oils to combat heart disease.
How do we approach the question of using diet and lifestyle versus medication?
This is a recording of the Facebook Live episode from Saturday, June 11, 2016, where I offered you the chance to ask me anything and did my best to answer your questions. In this episode you can find the following:
2:11 Is it the saturated fat that causes inflammation in animal models of obesity?
9:37 What do I think about Ray Peat’s and Andrew Kim’s views on sugar?
19:01 How essential are antioxidants in the diet? How much is too much?
29:38 What do I think about Brian Peskin’s work on “parent” essential oils?
31:16 What do I recommend as tests for folate status?
35:58 What would I recommend to recover from an accidental exposure to gluten?
44:33 What would I recommend telling a group of doctor’s interested in nutritional therapy about fats and cholesterol? (this includes a bit about choline)
54:49 How much protein should we eat to balance the priorities of muscle mass and longevity?
1:05:36 Is nutritional ketosis desirable for a healthy person, and is 100 grams of carbs per day enough?
1:19:51 What do I think about the potential for gluten withdrawal to help with neuromuscular issues and gross motor delays in children despite negative IgA tests?
1:24:22 Can someone’s triglyceride-to-HDL-cholesterol ratio be too low?
In this episode, I wrap up glycation week by discussing why glycation may play essential physiological roles in the body. In the early days of methylglyoxal research, Albert Szent-Gyorgyi, who won the 1937 Nobel prize in Physiology or Medicine for his discovery of vitamin C and critical steps in energy metabolism, saw the molecule as part of a regulatory system. In the early research into glycolysis, the system that converts methylglyoxal to pyruvate was seen as part of energy metabolism. Only later did glycation become synonymous with toxicity. Current science can be used to make a compelling case that methylglyoxal is normally produced as part of glycolysis to prevent a dangerous buildup of glyceraldehyde and that it rises during carbohydrate restriction to help preserve much-needed glucose and to enable the conversion of fat to additional glucose. This could be seen as an elegant system of regulation and a key part of energy metabolism. Nevertheless, it is unclear where the dividing line between physiology and pathology lies, and I see the apparent rise of methylglyoxal during carbohydrate restriction as part of a stress response that should not be chronically activated.
In response to popular demand, this week is glycation week. In this episode, I discuss the strengths and limitations of using Hba1c to measure our cumulative recent exposure to blood glucose and diabetes risk. Many people will be familiar with the fact that variation in red blood cell turnover confounds this measurement. Less well known is that variations in the deglycating enzyme fructosamine 3-kinase (FN3K) also confound the measurement. Counter-intuitively, if you have a higher rate of this deglycating enzyme but a lower rate of downstream metabolism of 3-deoxyglucosone, your lower Hba1c could actually mean MORE glycation. I conclude that Hba1c is a useful test, but only in the context of a bigger picture put together with more information.
In this episode, I discuss some important insights from my Paleo f(x) talk and audience responses to it, including the potential dangers of treating type 1 diabetes with a low-carb diet, the importance of carbs and bodyfat for fertility and sex hormones, and why some people might have a great sex hormone profile on a long-term ketogenic diet despite the importance of insulin's contribution to fertility. I also discuss Headspace meditation, contrast showers, Snapchat, U.S. Wellness Meats liverwurst, Kettle and Fire's upcoming chicken broth and chicken mushroom broth, and my interview with Ben Greenfield.
In this episode, I show you how you can determine whether your genetics are contributing to your sensitivity to blue light, poor sleep, and poor daytime alertness, and what you can do about it. Specifically, I look at the research showing that variations in the gene for the vitamin A-dependent protein melanopsin underlie sensitivity to blue light and teach you how to figure out your own genetics for this protein using a 23andMe account (they don't have a health report for it, but the hack around that is easy).
In this episode, I answer a listener's question about whether I am worried about my phosphorus intake and whether a high phosphorus intake is ok as long as it is balanced by calcium. I describe the biochemistry and physiology of the system that regulates calcium and phosphorus, their distribution in foods, how to determine the right balance in the diet, and how to use parathyroid hormone (PTH) as a blood measurement to assess whether the dietary balance is working for an individual.
In this short episode, I describe how voodoo flossing my computer-damaged wrists has made a tremendous difference in my ability to tolerate weight lifting (especially Olympic lifting) without wrist pain. I use a protocol from Kinetics Sports Rehab that I modify slightly to make my own, which builds on a concept developed by Kelly Starrett of San Francisco CrossFit and MobilityWOD. I don't think you need to lift weights to benefit from this (though I think you should lift weights). I think this is something that has the potential to provide great benefit to anyone who uses a computer a lot. Since it only takes 1-2 minutes per day per wrist, it's worth a shot!
In this episode I describe why a set of two yoga blocks has beenone of my best low-cost investments in the last year, playing avariety of unexpected roles around my apartment, and allowing me tomake major strides in increasing the diversity of positions I canwork in to get a healthier level of hip mobility. A standing deskis not enough, and yoga blocks allow me to rest in a squattingposition or sit with greater external rotation in my hips, therebygently challenging the range of motion that sitting so much hastaken its toll on over the years.
In this episode, I respond to a listener's question aboutwhether glycation is a good argument against a high-carbohydratediet. I agree that we should avoid refined carbs and emptycalories, but in this episode I describe why "glycation" is reallya misnomer and why carbohydrate is actually likely to protectagainst glycation. Glycation can be driven by the metabolism ofprotein, carbohydrate, and fat. Insulin protects against glycationfrom all three sources, and insulin signaling is strongest aftereating carbohydrate. In fact, glycation may actually serveimportant physiological roles under conditions of low insulinsignaling, so it is important not to view it as an intrinsically"bad" process. Although there are many unknowns, the evidence, evenif relatively weak, suggests that restricting carbohydrate is morelikely to increase glycation rather than decrease it.
In this episode I describe how I have designed my evening and morning routines to maximize my quality sleep and productivity. I include the roles of blue-light deprivation using f.lux, iOS 9.3 Nightshift, blue-blocking amber fits-over glasses and lights from lowbluelights.com. I also include the roles of list-making, television, movies, video games, paperback fiction, making the bed, morning walks, and low-decision, high-nutrition, time-saving breakfasts.
I am often asked what I eat, so here is my answer. To simultaneously meet the goals of productivity, fat loss, and good nutrition over the last few months, I get most of my food through Thrive Market and Whole Foods via Instacart, use Epic Liver Bites, Kettle and Fire broth, fresh meats, eggs, cheese, starches cooked in big batches, and supplemental fruits and vegetables. I also discuss how I have been maintaining protein and calories for fat loss and use MyFitnessPal to track my calories, and how that has helped me sleep.
In his April 7, 2016 piece in The Guardian, "The Sugar Conspiracy" Ian Leslie argues that the politics of nutrition has blinded us to the fact that sugar is more deserving than saturated fat of the status of dietary arch-villain and that the politics continue but the status of sugar and saturated fat are starting to switch. But we need to move beyond nutritional boogeymen, not switch one for another. Our sense of history and physiology -- key concepts about the historical role of Ancel Keys, the rate at which sugar is converted to fat in a process called de novo lipogenesis, and whether insulin's stimulation of fat storage can offer a plausible explanation of obesity -- get distorted when we try to make a public enemy out of sugar, just as they do when we make a public enemy out of saturated fat. It's time for a more nuanced view.
Is it really true that saturated fatty acids (SFAs) are the "bad fats" and polyunsaturated fatty acids (PUFAs) are the "good fats"? Christopher Ramsden uncovered previously unpublished data undermining the conventional wisdom that we should replace saturated fats with polyunsaturated vegetable oils to lower cholesterol and prevent heart disease. The public health establishment dismissed the findings. Here's my take.