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A Few More Thoughts on Diabetes

After reading some more hyperlipid I have begun to question whether it is the adipose tissue or the liver that goes first in the pathogenesis of diabetes. One way to imagine the progression of diabetes is that through heavy fructose consumption, the liver becomes damaged and stops being able to manage glucose in the blood thus leading to elevated blood glucose levels. The pancreas thus overproduces insulin in an attempt to compensate for this and this process, which is simultaneous with hyperphagia due to disruption to leptin by excess fructose and toxin exposure, leads to the insulin resistance of fat cells and thus elevated NEFAs in the blood.

I have heard that elevated NEFAs appear before elevated BG so I would guess that these processes happen simultaneously but that the adipose tissue fails first as a result of hyperphagia and that this causes the pancreas to overcompensate with insulin hastening the arrival of hepatic insulin resistance soon thereafter. In any case, the factors that cause this remain the same, fructose and other dietary toxins that promote hyperphagia. The question is whether fructose or the hyperphagia that high fructose consumption can induce is the primary factor in this process. If it is the former then hepatic insulin resistance should happen first, if it is the latter then adipose insulin resistance should happen first. These are likely simultaneous processes where one has more susceptibility to what is happening and becomes insulin resistant first.

EDIT: I think that perhaps the way it works is something like this. Fructose damages leptin and this causes hyperphagia. Hyperphagia forces the body to fatten to avoid lipotxicity. At some point, the body refuses to fatten any longer and so the fat cells become insulin resistant and elevated NEFAs is the consequence. The pancreas secretes more insulin in response to the elevated NEFAs. The liver, simultaneous with this, is getting damaged by fructose leading to non-alcoholic fatty liver disease and once the pancreas goes into overdrive to control the elevated NEFAs, hepatic insulin resistance occurs and the liver stops being able to ration out glucose and process fructose well. Now you also have elevated blood sugar levels and the pancreas is going nuts with insulin production. Now you have diabetes. So far this is what makes the most sense to me.

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Filed under: Diabetes, Hormones, Insulin, NEFAs, Obesity, Pathogenesis

Some Thoughts on the Pathogenesis of Diabetes

Let me preface this by saying that I am not a scientist at all. I was trained in semiotics and film/video production.

One of the things that I’ve been wondering about ever since I started looking at CarbSane‘s blog is where elevated non-esterified fatty acids (NEFAs) fit in in the grand scheme of things. Let me elaborate a little first so that this makes sense. The theory of fattening and insulin resistance that is usually given goes something like this: carbohydrates are the most insulinogenic macronutrient and the SAD (Standard American Diet) is a high carb diet and over time this leads to chronically elevated insulin levels, especially if you are snacking all the time which you are more likely to do on the SAD since you’re running on glucose (instead of fat) which your body has limited storage for. Additionally, insulin is the master hormone for fattening and if it’s always high then you are always accumulating fat rather than burning it. Of course, this has some truth to it but the picture is a bit more complicated than this and I’ve been looking for a way to reconcile this with some more nuanced descriptions of how fattening actually works.

Insulin is not the only hormone implicated in this process. There are, at the very least, two others: leptin and ASP. But anyway, that isn’t exactly my point. CarbSane mentions often how the one thing that bothers her the most about low carb is that it is necessarily a high fat diet and that elevated NEFAs in the blood appear connected to sudden cardiac death (SCD) as well as diabetes (that is, elevated NEFAs are supposed to happen before the elevated blood sugar happens). But looking more at her posts, it seems that the likely mechanism of fattening and eventually diabetes works something like this:

-One goes into caloric surplus in some way (for now, it is my belief that nutrient poor foods like most grain carbs combined with liquid calories and food toxins like fructose or those found in grain carbs induce hyperphagia over time either as a function of form (such as the difficulty of the body recognizing liquid calories) or damage to the leptin receptor (the possibility of wheat lectin binding leptin has been hypothesized by Stephan)).

-Now that you are in caloric surplus, you begin to store more and more fat. You begin to have chronically high levels of insulin to inhibit lipolysis of all that fat which is necessary to avoid elevated NEFAs and lipotoxicity in the body.

-Eventually, however, fat cells become insulin resistant and this leads to elevated NEFAs which continues to exasperate production of insulin in the body. Over time, the rest of you becomes insulin resistant and now you are diabetic.

-To summarize, it appears the problem is pathological overeating caused by some damage to leptin which eventually leads to fattening and chronically elevated insulin through insulin’s attempt to inhibit the lipolysis of all that fat tissue and this eventually leads to insulin resistance in fat cells, elevated NEFAs and, eventually, elevated blood sugar and diabetes.

The reason Paleo diets work, I believe, is because calorie intake is spontaneously reduced through the consumption of nutrient dense foods. This caloric deficit combined with the removal of the bulk of food toxins and the change from glucose to fat as the main fuel source makes it so that now those fats can actually be burned and used for energy and the hormonal system has a chance to heal. Hence, no macronutrient in particular is the culprit but food toxins and low-grade macronutrients (which are usually grain carbs) that lead to the initial caloric excess that changes the body’s fat setpoint. This is why this sort of thing doesn’t happen to the Kitavans. For someone who is metabolically healthy, it would seem that as long as the foods you eat are whole foods, macronutrient ratios don’t really matter that much.

In relation to NEFAs there is another issue of interest. CarbSane is worried about the elevated NEFAs that seem to be produced in those on very low carb (VLC) diets, however, I believe this worry may be misplaced. The reason I believe it may be misplaced is because the phenomena of elevated NEFAs seems to be caused by very different things in diabetes than in a VLC diet and I do not believe elevated NEFAs are sufficient to produce diabetes in an individual outside of the context of elevated NEFAs in the pathogenesis of diabetes described above. On a VLC diet, insulin is being minimized and so lipolysis is encouraged and since virtually no carbs are being eaten this makes sense as lipids are the main fuel source. A normal person on the SAD would have a lower level of NEFAs but they are also running on a combination of lipids and glucose so this makes sense. On a VLC diet, the elevated NEFAs are also not occurring in defiance of insulin but because the diet is designed to produce little insulin in the body. Hormones are thus not being disturbed in the same way. Also, I wonder how rigorously “elevated” is being applied which is to say that if people on a VLC diet have elevated NEFAs relative to those on the SAD, I’m not sure if that really means anything. In the pathogenesis of diabetes it does since a diabetic on the SAD versus a “normal” person on the SAD can be compared to one another to see what difference the pathological state is having on that person. VLC is designed to elevate NEFAs so unless your body is trying to kill you, I find it hard to believe that elevated NEFAs in the context of normal functioning are a problem or that we would be designed in such a way that would put our lives in mortal danger if we were forced to survive on a VLC diet. Once again, I must say that I believe that any macronutrient ratio is perfectly fine so long as food toxins are not consumed and whole foods are consumed.

Looking through some posts at hyperlipid (this one in particular) it would seem that VLC produces a temporary physiological insulin resistance since the body is getting adapted to low carb intake but that this is not pathological and if one were to change to high carb the next day, the body would adapt to it and become insulin sensitive within a week. Thus, the carb loading that low carbers due before blood sugar tests are done because those tests are attempting to measure how insulin sensitive your tissues are in the context of a moderate to high carb diet. The low carbers thus make their diets temporarily moderate to high carb in order to get an accurate reading of insulin sensitivity.

In summary, I am coming to believe that this physiological insulin resistance and elevated NEFAs are nothing to worry about so long as they are not in a context that suggests that they are markers of a pathological state which I believe they are not in the context of a VLC diet. Now, I do not advocate a VLC diet for other reasons and if you do believe these things are to be worried about, the solution is simple. Instead of a very low carb, high fat diet eat a low to moderate carb, high fat diet and there you have it.

Filed under: ASP, Diabetes, Diet, Hormones, Insulin, Macronutrients, NEFAs, Obesity, Pathogenesis, VLC

Maybe the Problem is Stomach Acidity

After reading a few posts over at Whole Health Source I am starting to think that maybe a deficiency in hydrochloric acid in the stomach is a common condition. First of all, this would lead to indigestion, gas, and the ability for pathogenic bacteria to spread rather than die quickly. These are all conditions that are relatively common and which are exacerbated by foods such as wheat and fructose so it would seem that, circumstantially, increasing the acidity of the stomach could stand to benefit a lot of people.

One way to do this is to supplement with Betaine Hcl which some people do. I took a look at Amazon and it was interesting to see that many reviewers reported not only a decrease in digestive discomfort but also less hunger and more energy. It would seem that their nutrient absorption improved, however, I see no reason to supplement with Betaine Hcl unless other options have been explored, namely, drinking dilutions of apple cider vinegar or lime juice with meals. Anecdotally, it appears to relieve gas and bloating which, in any case, are what I tend to have so I shall be trying this first.

This has all been getting me to thinking about eating raw foods again. Perhaps the reason that people sometimes get sick from raw foods has more to do with whether stomach acidity is sufficient to kill the harmful bacteria. As long as your digestion is healthy, raw meat shouldn’t be a problem. This may also be a cause of deficiencies and hyperphagia. If you’re not digesting food properly than it would make sense that you would want to eat more to get the nutrition you’re lacking and if you’re eating deficient foods in the first place, it would stand to reason that this could cause excessive eating.

References:

http://wholehealthsource.blogspot.com/2009/02/sugar-hydrogen-bacteria-and.html

http://wholehealthsource.blogspot.com/2009/02/low-stomach-acid-and-nutrient.html

http://wholehealthsource.blogspot.com/2009/02/more-thoughts-on-hydrogen-gas-and.html

http://www.livestrong.com/article/292143-what-foods-are-high-in-hydrochloric-acid/

Filed under: Diet, Digestion, Hcl, Nutrients, Raw meat, Stomach acid, Supplements

Raw Meat: Good or Bad?

After finishing Aajonus Vonderplantiz’s Recipe for Living without Disease I can understand why so many people think he’s crazy. While he makes some useful and helpful recommendations, he also makes a lot of wild unsubstantiated claims so it ends up being a book that really proves to be very marginally useful since I don’t know what to take seriously and what not to. I never imagined I would implement his diet but I was really looking for more information on the safety of eating raw meat and ways in which to implement it well. Instead all I found were dismissals of all concerns in regards to raw meat which, considering how unreliable the book is, I don’t really trust.

After a cursory look online it seems that with raw meat as with raw vegetables there are any number of food poisoning possibilities. But, so what? That’s how food is. What I want to know is how to decrease the likelihood of these things. For instance, people always say that you have to cook pork all the way through because of trichinosis but trichinosis is virtually eliminated in pork products and is really something that’s in the past now. I don’t want to be worried about things that are no longer real issues. The possibility of toxoplasmosis was raised by one blogger but after researching it cursorily it seems that it appears primarily in cats and from there can be transferred to other animals via exposure to feline feces and from there travel to other animals via consumption of raw or undercooked meat of animals exposed to feline feces and that generally toxoplasma gondii is more common in pork and lamb. So if you source your meat well, you should have a very low risk of toxoplasmosis since a good source will have sanitary conditions and if you also choose a meat type less likely to have it then that’ll be even better. It seems then that raw beef is probably the best choice for raw meat consumption.

Bacteria seems to grow on the surface area that is exposed so if you buy whole meat cuts instead of ground then less surface area is exposed. A recipe I found for carpaccio online calls for the meat to be seared on all sides for 30 seconds to kill bacteria appearing at the surface and then to trim this part off and proceed with the recipe. Additionally, vinegar and lime juice act as sanitizing agents so soaking meat in a vinegar or lime marinade will likely also kill any surface bacteria making it safer for consumption. But is this at all really necessary if you’ve sourced your meat well? I don’t know. If you were to ask Aajonus Vonderplanitz he would tell you that none of this is a big deal and that raw meat is fine in virtually any condition including severely putrefied or fermented (“high meat”) and that all that bacteria is just going to improve gut health and body ecology. We don’t have this same fear over vegetables after all but we do still wash them.

Now why raw meat? It seems to me like a balanced diet should also have a balanced preparation of foods. With most vegetables it pays to cook them since they are immobile and thus develop toxins to deter predators though some have pretty low toxin levels like cucumbers and lettuce. With meat, however, endogenous toxin levels are nil which means we should be able to eat meat cooked or raw and since these states can be extremely different from one another as far as the chemical structure of the protein, production of AGEs, enzyme availability, and so on it would make sense to me to eat both raw and cooked meats in a diet. I still need to do some more research on the issue of enzymes but, in any case, I do not see any reason why raw meat should be 100% forbidden from a diet when, presumably, we’ve been adapted to it. Even with fire, I cannot imagine every single meal was cooked and, besides, we have the example of the Inuit who did fine on raw meat and high meat.

Unfortunately, if you look up “raw food diets” online all you find are raw vegan websites and if you look up “raw meat diets” all you find are raw meat diets for cats and dogs so this quick summary will have to do for now but hopefully I’ll find a more reliable guide somewhere to raw meat consumption since I do not want to do anything risky but neither do I want to live in fear of something imaginary. For now, raw meat in acid marinades will have to do.

Filed under: Diet, Raw meat