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.
Why I drink coffee and won't apologize for it, but why I'm skeptical of the large body of literature associating coffee consumption with reduced disease risk. Do we drink coffee by choice? Sort of. I discuss why our genes may play a role in our coffee consumption and may be the ultimate influence on the risk of diseases that ultimately cannot be changed by coffee consumption.