Monday, May 15, 2017

VLCHF Diet for Psoriasis Experiment Week 2 Report

I have been eating very low carbohydrate, high fat for two weeks now.  My digestible (net) carbohydrate intake has been below 50 g on most days, provided by oranges, berries, onions, beets, carrots, winter squash, and greens (mostly spinach, lettuce, kale).

I've continued to eat 300-400 g of meat daily, mostly beef (roast, brisket, sirloin steak, ground), with some pork, chicken, and sardines.  I had at least half a dozen eggs over the week.  My protein intake has been in the range of 120-140 g per day.  I have found my desire for protein is less than my desire for fat.

I have gotten roughly 65-70% of my calories from fats, mostly clarified butter, bacon drippings, fat naturally occurring on meats (all saved), heavy cream, coconut cream, and nuts, with some tallow, olive oil, high-oleic sunflower oil, and liquid fish oil (~1-1.5 tsp. daily).  I've been getting around 150 g total fat in a day, with about 55 g of that from saturated fatty acids.  My cholesterol intake has ranged from about 350 to 1000 mg per day, mostly depending on egg yolk intake.

So, what has happened to my skin?  Take a look.
I find this photo of my eye remarkable.  The skin above the eye is much healthier, but the eye itself has changed.  The sclera is whiter with less blood vessels visible.  The iris is a bluer green and more clearly defined around the edges. I can't recall my iris ever being this blue-green.  In the April 30 and May 8 photos, there is a brown area around and especially above the pupil, which has greatly reduced in area.  Iridology identifies that area around the pupil as indicative of the condition of the intestine, with the yellow-brown discoloration indicating inflammation. 

The left ear has always been had the most severe visible lesion.  In the past week it has reduced by more than half, perhaps 75%, from May 8, and its reduced by at least 90% since April 30.

On the right ear, the visible lesion looks to me to have changed very little in the past week.  However, not visible in this photo is the improved condition inside the ear, particularly on the inside of the tragus (the flap over the ear canal). 

On the scalp, the size of the area with thickened, flaking skin has reduced by an estimated 50%.  The skin is not as thick, and there are no large flakes coming off anymore, only fine dust.  It still itches some, but not as much as two weeks ago, I'll estimate about a 75% reduction in itching, which is now primarily confined to an area about 2.5" in diameter encompassing but offset to the left of the occipital protuberance. 

The lesion on my tailbone has also improved.  The surface area affected has reduced by about 40-50%.  

My digestion and elimination have been functioning very smoothly.  My sleep has been sounder than before starting VLCHF.   I have had an abundance of physical and mental energy, more than when I was eating a high carbohydrate diet.  I am less irritable and more energetic and capable of mental focus toward the end of my daily ~16 hour fasts. 

Food preparation is quick and easy.   Food costs have decreased somewhat because we aren't spending on large hauls of low calorie fruits and vegetables.  As I will show in an upcoming post, on a cost per calorie basis, animal fats are far more economical than fruits and vegetables.

I've been making progress in both strength and mobility training.  The residual swelling and stiffness in my left knee (injured in September 2015, when I was eating a vegan high carbohydrate low fat whole foods plant based diet) has reduced and I can now sit in a full squat position for 14 minutes straight and sit on my heels for 5 minutes straight with tolerable discomfort in that knee (sitting on my heels was impossible for 17 months while still eating the plant-based diet).

One other tentative observation:  It seems that I may have less underarm odor.  During the past 5 years I have had a problem with strong underarm odor and staining of white shirts.  When I would eat a lot of brown rice, my underarms would emit the odor of rice, then turn sour.  Underarm odor is caused by bacterial growth, and bacteria thrive in sugar-laden mediums.  I have the hypothesis that this diet has reduced my blood sugar level, which has reduced the amount of sugar in my skin, which in turn has reduced the growth of bacteria that produce odorous compounds.  This needs further observation for confirmation. 

I am very pleased with these results so far, and most impressed with the change in the whites and irises of my eyes, and the apparent improvement in my body odor.  I look forward to seeing what occurs over the next week. 


Shameer Mulji said...

Very impressive. I recently received a link in my twitter feed related to meat / saturated fat causing Diabetes.

What are thoughts on this? Personally, I'm not buying it. I've noticed a lot of people getting healthier on Paleo / LC diets.

Don Matesz said...

Correlation is not causation. In conventional diets, meat travels with very high carbohydrate, high glycemic foods. Hence it is generally found at the scene of the crime.

If meat was a cause for diabetes, not just a "risk factor," it would be impossible to reverse diabetes on a meat-based diet high in saturated fats. This study showed reversal of diabetes on low-carbohydrate diet high in saturated fats and meat-based:

Therefore, meat does not cause diabetes. Saturated fat does not cause diabetes. Diets high in carbohydrate (sugar) cause diabetes, especially when the sugar is eaten in conjunction with saturated fats.

Charles Grashow said...

So - what is your diet now? What do you eat on a regular basis? Have you gone back to a LCHF paleo type diet or are you still a LFHC vegan?

Charles Grashow said...


Have you seen these studies?
Ma-Pi 2 Macrobiotic Diet Intervention in Adults with Type 2 Diabetes Mellitus

At 6 months, anthropometric variables were significantly lower, lean body mass was preserved, and glucide and lipid metabolism was controlled. All participants were able to eliminate insulin treatment, and 25% continued treatment with glibenclamide only. Mean total cholesterol, LDL cholesterol and triglyceride values dropped 16.4%, 22.7% and 37.0%,
respectively, while mean HDL cholesterol rose 97.8%. Mean glycemia and HbA1 values also decreased 63.8% and 54.5%, respectively. According to lipid levels and ratios, cardiovascular risk was also considerably reduced. Hemoglobin, total protein, albumin and creatinin levels indicated that nutritional safety was maintained. There were no adverse events.
Ma-Pi 2 macrobiotic diet intervention during 21 days in adults with type 2 diabetes mellitus, Ghana 2011
Ma-Pi 2 macrobiotic diet and type 2 diabetes mellitus: pooled analysis of short-term intervention studies
A 6-month follow-up study of the randomized controlled Ma-Pi macrobiotic dietary intervention (MADIAB trial) in type 2 diabetes
Medium- and Short-Term Interventions with Ma-Pi 2 Macrobiotic Diet in Type 2 Diabetic Adults of Bauta, Havana
Treatment of reactive hypoglycaemia with macrobiotic Ma-Pi 2 diet for prevention of type 2 diabetes: the MAHYP randomised crossover trial

And these

Don Matesz said...


I described my diet very clearly in the first three paragraphs of this post.

Yes, I have seen some of the studies on the Ma-Pi macrobiotic diet. All are relatively short term (e.g. 12 weeks) and in most the subjects are losing weight due to caloric deficit, which means their actual fuel mix is not as low in fat and high (% wise) as the food they were eating. They were burning some body fat up daily as part of their fuel mix.

For example a 300 calorie deficit translates to 33 g of fat being burned daily. If a diet is 2000 kcal and 15% fat, that's 300 kcal from dietary fat, plus 300 kcal from body fat = 600 kcal total from fat, while 2300 kcal total is being metabolized, which makes the actual fuel mix 26% fat.

Another observation is that they authors count all the calories of grains, beans and vegetables as if all were equally absorbed. This is not likely the case. Although broccoli e.g. produces X calories per 100 g in a lab burner, or by calculation from the composition of the vegetable (P, F, C), known as Atwater factors, it has been shown that in real life digestion, these numbers overestimate that calories absorbed from whole plant foods.

And, eating whole foods as opposed to processed foods increases post meal energy expenditure.

So the caloric deficit may be greater than suggested by the Atwater caloric values of the diet cited in the tables.

It is my experience that any specific mix of foods (e.g. the Ma-Pi diet) can have very different effects over short term compared to long term, and also in caloric deficit versus caloric balance.

Caloric deficit induces a catabolic metabolism which of course reduces blood sugar, lipids, etc. Hence caloric deficit is going to benefit T2 diabetics over a short term, no matter how it is achieved.

In some of these studies dramatic improvements were seen over 4-6 weeks, then the values (FBG, triglycerides, LDL) started to creep back up. This may occur because initially people are unfamiliar with the diet and eat less, then as time goes on they learn to eat more (perhaps cheat more), which reduces the rate of catabolism and leads to rebound of the values.

People get on me for having tried ways of eating for years before giving them up. But I learned how each way affected me over a long term, not just a few months. Scientific studies are almost always short-term, up to 6 months is the general maximum. I think these can give clues but not enough data to make conclusions about the long-term benefits (or problems).

Charles Grashow said...

Don said...
A general comment,

Could one of you who defend egg yolks and attack this study please provide me with the evidence that dietary cholesterol is either beneficial to atherosclerosis (not only blood lipids) or even essential to human health?

In other words:

1) Provide me with a set of references to experiments showing that eating eggs reduces the build up of atherosclerotic plaque, i.e. that eating eggs and cholesterol helps heal arteries damaged by atherosclerosis.

The studies would look like this: A group of people with established atherosclerosis are randomized to be put on one of two diets, the control having no dietary cholesterol (i.e. vegan), and the other identical in all respects except that a portion of plant foods is replaced with an equicaloric portion of whole eggs. To be favorable to your defense of eggs, the study outcome would be that the people eating the eggs have a more rapid reduction of atherosclerosis than those eating no cholesterol.

2) Provide me with some evidence that dietary cholesterol is essential for human cardiovascular and general health.

Good luck!

Charles Grashow said...

Don said...

I am not going to take any statins, except those that naturally occur in plants.
I am not going to eat animals.
Even if I would benefit from more fat, it is not necessary to eat animals to eat more fat.

Charles Grashow said...
Don Said - " It is not necessary to eat animals to obtain health. Even if it was, I wouldn't do it."

That says it all.

François Létourneau said...

Charles, thanks for this.

Don, I don't know, but it just appears to me you lost all sense of objectivity. Don't know what is motivating you right now, but it looks like its not logic.

Reading your past posts really had me confused.

Here, you claimed

''If meat was a cause for diabetes, not just a "risk factor," it would be impossible to reverse diabetes on a meat-based diet high in saturated fats. This study showed reversal of diabetes on low-carbohydrate diet high in saturated fats and meat-based:

Therefore, meat does not cause diabetes.''

Well, as Charles as just shown, and as I know that you know, there are plenty of studies showing improvement of glycemic control and diabetic complication using a high-carb, high-fiber diet. I can even show you studies showing improvement of glycemic control using a high sugar diet.

Hence, following your own logic, carbohydrate do not cause diabetes.

Also, your reference was also confounded by weight loss, it was only 10 weeks long, there was no control group, and I find it interesting that although the high-fat intervention lead to weight lost (mean 9kg ), c-reactive protein and LDL-C still went up. High LDL-C and inflammation are both two strong risk factors for CHD, althought it now looks like you don't believe in the lipid hypothesis anymore.

Your claims are very weird to me. The WFPB Don would have called out someone using that study easily.

I could understand if you just wanted to try something else. But instead you seem rather motivated to ''prove'' that carbohydrate are now unhealthy and that animal product are optimal, even if that means using low quality evidences or making claims that can easily be refuted.

Sorry if I come across rude, I used to enjoy your blog, now I read your article and i'm like... eh?