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.