ME and Metformin

[alex3619]

The answer is a plant based whole food vegan diet with no oil (fats from seeds and adocado only) no sugar and no salt

I used to do this to treat my ME. I got worse and worse and worse, though slowly over time. Its not a great idea for everyone. Several years after I started I had gone from mild ME to nearly severe, and one day was so sick I ate a meat pie or something. I was immediately much improved. That ended my vegan experiment. It took me a long time to tolerate the taste of meat again, and even to tolerate chocolate, though I never eat much of that.

I tried Metformin again last October. I had previously tolerated it. In three days my left foot, below a titanium implant and with vascular damage, went black. The skin on my ankle area and half way to my knee pealed off. A dozen ulcers formed. The last one healed late last month. Metformin can be very bad. Current biochemistry indicates it works by blocking Complex One and Pyruvate dehydrogenase ... in other words, its a lot like doubling down on ME chemistry.

I am currently on the diet very different to a vegan diet, a high protein diet (NOT ketogenic) and I am improving. Mostly protein, with some carbs, is how I would describe it. There seems to be a minimal amount of carbs needed to ensure gut function is not a problem. Most of my carbs are either higher protein carbs, such as chickpeas or kidney beans, or salad or low carb vegetables.

 

[brenda]

plant based whole food vegan diet with no oil (fats from seeds and adocado only) no sugar and no salt

Is this exactly what you were eating including no oil Alex? Whose protocol were you following? And another question, how is your diabetes? Is it being controlled by medications? Thanks.

 

[Murph]

I tried Metformin again last October. I had previously tolerated it. In three days my left foot, below a titanium implant and with vascular damage, went black. The skin on my ankle area and half way to my knee pealed off. A dozen ulcers formed. The last one healed late last month. Metformin can be very bad. Current biochemistry indicates it works by blocking Complex One and Pyruvate dehydrogenase ... in other words, its a lot like doubling down on ME chemistry.

I've just been reading about how metformin can turn on AMPK, in the attached reveiew paper on AMPK. I checked to see if anyone was reporting negative results from metformin and found your post. AMPK is turned on under a low ATP scenario, meaning it could be consistent with hyperactive purinergic signalling, where atp is leaking from cells. Low atp/high ampk also obviously results from exercise so there's a prima facie case to be suspicious of it.

AMPK is also implicated in red blood cell deformability. Whether the rbcs might be too spongy and release all their atp, causing vasodilation ; or are too stiff and release insufficient atp inhibiting vasodilation remains unclear. Although if your feet went black could that suggest the rbcs are too stiff to get through the capillaries? ( I gather much of the microvasculature is of a smaller calibre than the dimensions of an rbc, so deformability is crucial for getting blood to the ends of things- they have to squeeeeeeze through...)

I don't want to draw too many conclusions from one persons foot though!

 

[alex3619]

I don't want to draw too many conclusions from one persons foot though!

Hi, it was clearly a combination of things, including existing vascular damage and OI. My right foot was fine. Metformin has as its side effect increased lactic acid, including potential lactic acidosis. My comment was cautionary, but I used to tolerate Metformin and many PWME do.

 

[alex3619]

Is this exactly what you were eating including no oil Alex? Whose protocol were you following? And another question, how is your diabetes? Is it being controlled by medications? Thanks.

My diabetes went nuts after surgery five years ago, when I had a titanium implant to hold my left ankle together. It finally resolved back to almost its long term position just a month ago. However I went high protein when the Metformin did not work. This improvement was under a high protein diet, mostly chicken with some fish and some beef. Currently I am using tomato as my only fruit. I always eat some vegetables, and the most common is chick peas.

When I was vegetarian I was eating vegetables and almost zero fat. No oils, butter, margerine etc. Fat was titrated using specific nuts, and the main one was Macadamia nut, which is almost pure monounsaturated fat. I cannot recall the exact amounts, but my saturated fat intake was about 2g per day, maybe 2.2g. Under that I got severe headaches. Polyunsaturated fat was several grams too, and the rest, a handful of grams, was monounsaturated. It was a controlled metabolic diet, in an attempt to regulate eicosanoid synthesis and hence the entire eicosanoid inflammatory response. I did improve in the short term, as in my ME improved and I could tolerate exercise more, it plateaued in the medium term, then I declined. I probably ate this way for about three years. Getting back into meat was a struggle, it tasted horrid. I started this in about 1993, and ended about 1996 or so. For a long time after this I also hated chocolate, it had too much fat in it.

 

[brenda]

@alex3619 Sounds like you had some deficiencies over time. You should watch iThrive. It is important to have a high nutrient dense diet.

 

[alex3619]

Everything was analysed, it was a metabolically controlled diet. Everything was weighed to the gram. Everything was computer analysed. I never discussed supplements, but they were there too. There might indeed have been a deficiency, but its not clear this kind of diet always works or is even desirable. Usually with extreme diets some do well, some don't and a few get worse.

In terms of research what I want to see is randomised controlled diets, with well characterised patients, good tests, and long term follow up. That is rare. Any links to those studies would be welcome.

In the first year it might have been said I was doing very well.

In one test of ketogenic versus high carb (low glycemic) there was no extra benefit to ketogenic. Ditto high protein. However the fastest way to induce the kinds of problems we see in diabetes is with carbs, and I don't just mean raising blood sugar. It induces saturated fat synthesis and storage too. I have not done any deep investigation on this though, at least not in the last decade.

Now I am a fan of a diet higher in monounsaturated fats such as the Mediterranean diet - for most people. How we respond individually is just that. However its not clear how much of that kind of diet is due to modifying macronutrients, and how much is due to increased phytonutrients.

Most of these claims about OTT results are from people who have a vested interest in it. They are not necessarily lying, they believe what they are saying. My answer is always the same ... show me the randomised controlled studies. Sometimes they are right, but when they are it can be proved.

 

[brenda]

@alex3619 I am in a Facebook group doing the high carb low fat diet and they are seeing improvements in a matter of weeks, regarding coming off meds and lowering BG. If they do not do the diet exactly, most of them have slower results. Fasting is a big thing in this diet - either intermittent or for days, of course supervised for those on meds as they have to cease them first.. I fast for 16 hours a day.

The high fat groups I was in previously, did not have the same fast results and then there was the problems that there are no long term studies done on a high fat/keto diet. They did not gain insulin sensitivity on that diet either,

 

[Eastman]

A recent paper:

Overweight and diabetes prevention: is a low-carbohydrate–high-fat diet recommendable?

Abstract
In the past, different types of diet with a generally low-carbohydrate content (< 50–< 20 g/day) have been promoted, for weight loss and diabetes, and the effectiveness of a very low dietary carbohydrate content has always been a matter of debate. A significant reduction in the amount of carbohydrates in the diet is usually accompanied by an increase in the amount of fat and to a lesser extent, also protein. Accordingly, using the term “low carb–high fat” (LCHF) diet is most appropriate. Low/very low intakes of carbohydrate food sources may impact on overall diet quality and long-term effects of such drastic diet changes remain at present unknown. This narrative review highlights recent metabolic and clinical outcomes of studies as well as practical feasibility of low LCHF diets. A few relevant observations are as follows: (1) any diet type resulting in reduced energy intake will result in weight loss and related favorable metabolic and functional changes; (2) short-term LCHF studies show both favorable and less desirable effects; (3) sustained adherence to a ketogenic LCHF diet appears to be difficult. A non-ketogenic diet supplying 100–150 g carbohydrate/day, under good control, may be more practical. (4) There is lack of data supporting long-term efficacy, safety and health benefits of LCHF diets. Any recommendation should be judged in this light. (5) Lifestyle intervention in people at high risk of developing type 2 diabetes, while maintaining a relative carbohydrate-rich diet, results in long-term prevention of progression to type 2 diabetes and is generally seen as safe.