RNY gastric bypass: in those cured of diabetes, is this evidence for high level duodenal gluconeogenesis?

In the 80% or so of those who are cured of diabetes shortly after RNY gastric bypass and long before significant weight loss:

Could at least part of the explanation be that in these patients, a high level of constitutive gluconeogenesis was occurring in their duodena or a key regulatory/stimulatory event in gluconeogenesis, or both?

At any rate, causation is out of the question. Causation is an over-used, inane, insane function of one variable.

Enough gluconeogenesis to account for most of the excess glucose found in their bloodstream after an overnight fast?

At any rate, more gluconeogenesis than is commonly recognized. Doctors believe that in general the liver does most of the gluconeogenesis, followed by the kidneys, followed by the intestines. Perhaps in most healthy individuals and when gluconeogenesis is not constitutive.

But in everyone else? I doubt it.

Mental illness – so unlike physical illness

About 1/3 of Americans have high blood pressure (systole >140). Most Americans do not have high blood pressure. Similarly for type II diabetes and I should guess most illnesses. Most Americans do not have ‘X’, where ‘X’ is a serious medical condition or illness.

Mental illness is different.

Mental illness is not rare. It is not the exception.

Just the opposite. Mental illness is the rule (more than half, may be much more) – because NOT to be mentally ill, so many things have to be right or nearly so, and this is unlikely, given our present predicaments.

Mental illness also has a scope that is broader than currently recognized. For one, mindless aggressiveness (aggression without reason), so common in today’s world, and likely somewhat less common in the past, is a form of mental illness. For another, suicide is much more common than is currently recognized by the working definition, and because this is the most aggressive form of aggression toward self, that mental illness is underestimated.

Mental health is exceptional. Anyone who is mentally healthy may be one in a ten, or one in a hundred, or one in a thousand. I just don’t know how prevalent mental illness is.

Mental illness is one of the drivers of accelerated ill health. If a person gets type II diabetes in his/her 60s, that is not indicative of serious mental illness. But some children and adolescents who develop type II diabetes have underlying psychiatric ills that create ‘executive deficits’ in decision-making (and human judgment, as I have argued, is generally poor) and accelerate their decline in health. Again, the establishment is in denial of this. The authorities do not even see the widespread nutritional deficits let alone the mental health deficits.

Nature puts low dose poisons to good use

Selective pressures drive this process.

Another example: alcohol.

Yeast is one of the microbial components in our digestive tract. The optimal level of this microbe is debatable.

Yeasts turn some of the abundant sugar in our digestive tract into alcohol.

Even teetotalers have to deal with alcohol – endogenously produced.

Long before man came on the scene, nature found a good use for moderate amounts of this poison.

Thus, it is not surprizing that there is some optimal level of alcohol in the diet – the exact optimum should depend on a lot of factors, including the amount of endogenous production, something scientists pay no mind to.

The fact that additional alcohol in the diet is still net beneficial suggests that the overall level of yeast in the gut may in fact be suboptimal for most people. What if we consumed more raw buttermilk (how much alcohol do these yeasts produce?) and less yogurt?


Who says logical tautologies cannot have profound consequences?


Suppose someone is both depressed and aggressive, with much of the aggression and anger directed toward himself/herself. Such a person is likely at higher risk of suicide (and I believe is more likely to have been born in winter). Further suppose that this person with depression is being treated for depression and lack of sleep without drugs and the person suddenly starts sleeping much better. Would you retest him/her for depression, even if he/she claims his moods are no better?

Treating a significant improvement in sleep as a marker and forerunner of well-being, I believe you would, based on simple logic:

(depressed->poor sleep)->(not poor sleep-> not depressed).

This is the famous (a->b) -> (-b->-a)

In words, if a person is depressed, he has poor quality sleep and/or poor quantity of sleep. If he does not have poor sleep, he is not depressed. Better test!

Synthesis of opposing views: a syncretic view of the many contradictions re vitamin C


A model that makes sense of opposing views about vitamin C has the following “tenets” (by definition, tenets are tentatively held ideas, modifiable with every piece of data that does not fit the model):

  1. Pauling focused on the high rate of synthesis of vitamin C in animals that make it. He focused on the fact that if we ingest grams of vitamin C, we absorb grams of vitamin C. He noted that we absorb even more vitamin C when we are ill. Pauling focused on the proven utility of high dose vitamin C in the work of Dr. Frederick Klenner. He more or less ignored the high rate of urinary excretion of vitamin C.
  2. The US government focused on the high rate of urinary excretion and the fact that total body pools of vitamin C cannot be increased stably beyond about 1500-3000 mg. The government scientists ignored the fact that animals of our size make 200 times our RDA and that we absorb grams of vitamin C before we excrete all but about 100 mg of it per day and that we absorb more vitamin C when we are sick.
  3. As a rule, animals make about what they need of various nutrients. Exception: we make less choline than we need. As a consequence, animals do not make 200 times what they need.
  4. Both Pauling and the government scientists are making valid points. What is the explanation of these contradictory viewpoints?
  5. A possible explanation of the paradox is that vitamin C is accidentally absorbed (for example, oxidized vitamin C is absorbed by a glucose receptor) and deliberately excreted. This fails to explain why vitamin C is absorbed better when we are ill.
  6. Optimal tissue levels of vitamin C are at or near SL (saturating or near saturating levels). This explains why goats make 13 grams of vitamin C a day and why we absorb grams per day even though we need but 100 mg or so to replace losses of vitamin C (at 2-4% loss per day with a total body pool size of 1500-3000 mg).
  7. Supersaturating levels in serum and tissues occur for a short period of time following injection with high levels of sodium ascorbate.
  8. Chosen properly, an injection that achieves a therapeutic window of proper supersaturating levels of serum and tissue vitamin C, which I will call SSL1 (supersaturating level 1), avoids most of the toxicity and allows some antitumor, antiviral, antibacterial, and antifungal action, as well as some high level chelating of heavy metals. This explains the effectiveness of the use of injectable vitamin C as an adjunct cancer therapy and the many anecdotal results (more than 30 diseases treated) of Dr. Frederick Klenner re injection of high doses of vitamin C followed by high oral doses. Before even getting a diagnosis, Dr. Klenner treated everyone prophylactically with a high dose of injectable vitamin C, followed by multiple oral high dose vitamin C. When they came back for their diagnosis and treatment, they were in many cases on the road to recovery.
  9. Chosen improperly, there is a level of serum and tissue super-saturation, SSL2 (supersaturating level 2), at which there could be heavy damage to normal cells, especially if the kidneys are compromised. Possible mechanism: a catalytic cycle in which vitamin C binds regions in the genome in which copper is bound to cellular DNA, and creates single and double stand breaks. Vitamin C can be regenerated by various cellular antioxidants like glutathione (at 5-10 mM, glutathione is many times higher in concentration than cellular vitamin C), making this a highly destructive catalytic event.
  10. This toxic reaction or something like it or both explains why evolution has favored those animals whose kidneys excrete vitamin C so well and so rapidly, and this rapid excretion explains why vitamin C cannot ordinarily be driven to still higher concentrations in tissues (>=SSL2), given reasonably healthy kidney function.
  11. This explains the US government’s position – why take more than about 100 mg a day if it is all going to be excreted? Well yes, after tissue saturation has been achieved. I doubt that 100 mg a day can always maintain saturation in all tissues. When we are sick we absorb more vitamin C (as evidenced by higher bowel tolerance) and we consume more vitamin C when we are sick. When goats are sick they make twice as much vitamin C as when they are healthy.
  12. Nature’s program is to overdose the vitamin, thus achieving tissue saturation, and then excrete the excess as rapidly as possible to sidestep the toxic side reaction(s).
  13. Because of the toxic reaction(s) at SSL2, at inappropriately high supersaturating concentrations of vitamin C, no one with impaired kidney function should take Pauling type doses (18 grams a day).
  14. Re the government’s position: I would argue that vitamin C passing through the bowel may be doing us a world of good in keeping stools somewhat looser rather than too hard. I would also argue that vitamin C in urine is definitely doing us a world of good. First, in solubilizing substances like calcium (calcium oxalate and calcium phosphate stones are much less likely in someone taking high dose vitamin C). Second, and this is more speculative, in reducing the likelihood of UTI – the acidity of urine with lots of vitamin C likely makes it very uncomfortable for fimbriated bacteria trying to colonize the urinary tract.
  15. Also, re the government’s position: the total requirement for vitamin C cannot be deduced merely from mass balance studies. Two reasons – vitamin C is likely a member in a number of other nutrients’ ADME networks, and it will have an optimal dose for functioning there that is in addition to its own optimal dose (since a vitamin C molecule cannot be in two places at once). In addition, we need to write the total requirement of any nutrient as the sum of at least 4 independent parts: 1. the requirements of the entire gut. 2. the requirements of the blood stream and lymphatic systems. 3. the sum of the requirements of all tissues. 4. the requirements of the urinary system.

How general is this model? Might the same not be true of selenium and other nutrients in which the therapeutic window is rather narrow?

Nature plays with fire – it has to; life would never have come to be without doing so – and avoids getting burned most of the time thanks to many rounds of selective pressure that was at times so great that scientists estimate that ~90% of all species were extinguished. That is how nature comes up with such nearly flawless solutions to working with substances that can be as beneficial at one set of doses, between SL and SSL1, and so harmful at another set of doses, that is, >=SSL2.

Is there an inverse correlation between ingested natural chelators and heavy metal toxicity?

Natural chelators such as citrate and vitamin C can be ingested in large quantities and then safely excreted. Drug based chelators are a different story. Lipoic acid is a pretty good chelator, but it should be taken with an RDA worth of biotin or more if quantities exceeding 100 mg lipoic acid are taken per day.

The amount of heavy metal chelated by natural chelators such as vitamin C and citrate is probably small in most individuals because their body burden of heavy metals is low.

But when the body burden is high, the amount of ingested chelator and the amount of chelated heavy metals in the urine may be high enough to measure with ultrasensitive techniques.

Would it not be a hoot if all the worry about mercury in fish -especially during pregnancy -could have been avoided by co-ingestion of higher levels of natural chelators such as citrate and vitamin C? Fish has so much going for it to let concerns about mercury be blown out of proportion.

The rule: the multi-hit a-causal model of disease

Rule: The multi-hit a-causal model of disease

Exception: The one-hit causal model of disease, which most people view as the rule and some view as the rule with no exceptions.

Complications: Sometimes deficiencies, a type of “hit” (see below), help with dread diseases. Example: low red blood cell lifetimes (due to sickle cell anemia, any of various thalassemias, G6PDH deficiency, other genetic deficiencies, and all other types of anemias, including iron deficient anemia) increase the odds of survival to at least the reproductive age against the dreaded malarial parasite. Nature is incredibly and intrinsically complex – a deficiency is not always the worst thing in the fight for life and reproduction; an excess of a toxin is not always the worst thing in the fight for life. Everything depends on other things, on the exact conditions. Nothing is simply good or bad, especially when survival is at stake.

The cause of the effect” is a succinct definition of the causal, one hit model of disease and it seems to have some applicability as the exceptions to the rule.

A possible exception to the rule: Vitamin C deficiency alone appears to be completely responsible for the symptoms of scurvy and high dose vitamin C alone can completely reverse all of the symptoms of scurvy.

However, I think this is a bit of medical gerrymandering. There are a lot of scurvy associated symptoms that are not considered manifestations of scurvy. These are not curable by adding high dose vitamin C. What is curable by adding high dose vitamin C are just those symptoms attributable to vitamin C deficiency. In other words, scurvy is caused solely by vitamin C deficiency by definition, and by definition, scurvy is curable by high dose vitamin C alone.

A person eating only pizza will develop scurvy (the small amount of vitamin C in the tomato sauce is basically obliterated by high temperature cooking) and he can be cured of scurvy for the rest of his life by taking a dose of vitamin C every day, but he will not live healthily the rest of his life if he does stop this pure pizza diet. Rather, he will in time develop other deficiency diseases, each of which has a contour of associated symptoms that are not directly addressable by taking single supplements.

As I have argued before, it is impossible for anyone to be deficient in just one nutrient, given that there are thousands of unique sites in the human body and thousands of important substances in each of those sites, each of which has an optimal level, and any one of which can be in either excess or in deficiency. So with millions of measurables, it is simply impossible to have no more than one deficiency (to be below the optimal level) in just one location in the body. Simply impossible. A person develops scurvy by not supplementing and by avoiding entire food groups and thus develops multiple nutrient deficiencies that characterize such poor dietary choices. A person with scurvy and scurvy-associated symptoms can normalize his health only after adopting a sensible diet, if even then.

The multi-hit model is a-causal because the causal model is a one-hit model, and the multi-hit model necessarily involves two or more hits to the same target. This model assumes that our animal ancestors and early hominids went through sufficient rounds of selection to be generally resistant to single hits, provided the hits are not overly aggressive.

A hit may be either an excess or a deficiency in a particular site, including of course nutrient deficiencies and deficiencies in our defense systems.

So for example, most of us are very tolerant of low level mercury or low level arsenic toxicity (types of modest excesses) because we have adequate defenses (that is, no obvious deficiencies in our defense systems) against higher levels. But someone whose defenses are compromised may succumb to disease with just a moderately toxic dose.

This may be happening with certain kids who are getting rather closely spaced multiple doses of vaccines, which normally contain at least three toxins, though each is at a low level. The vaccine compromises the health of only those kids with a serious deficiency in our natural defenses against one or more of those toxins, potentially aggravated by too much of a particular toxin. Unless the authorities are looking for it, they might miss such toxic reactions. The vaccines harm the most vulnerable kids: those with the weakest defenses against one or more of the toxins and those who already had the highest levels of one or more of the toxins.

Think of kids with the highest levels of mercury in their bodies, who also have the weakest defenses against mercury poisoning (one reason why their levels got so high in the first place), who are in fact already struggling with subclinical mercury toxicity, and who then receive a closely spaced series of vaccines, each of which has a dose of ethyl mercury. Not a lot of kids, but a small cohort of highly vulnerable kids. To be able to detect these kids in a large pool of non-vulnerable kids, the authors of studies must classify the kids properly and make basic measurements of all of these parameters. This has never been done right and it probably will not be done right for some time to come. It may be easier to start with kids who develop autism shortly after a series of vaccines.

Here are more examples:

  1. The causal model is so ingrained in human thinking, as Kant noted, that even when the causal model is obviously wrong, people still hold it to be true. For example, the CDC estimates that there are 55 million cases of infectious diarrhea in the US each year and 3,000 deaths that are caused by these infections. Clearly, however, these two facts define an a-causal model in which the infectious agent is just one hit, one that challenges our defenses, and clearly the challenge is easily beatable, with a death rate of only 0.0055%. Weakness in the defenses of the victims, the second hit, is what proves fatal. Among the weaknesses noted are frail health (the victims are often very old), underdeveloped immunity (children under six), immunosuppression, long-term use of antibiotics, and the use of acid blockers. Not even considered, but worth a look, are potassium deficiency, a deficiency of fat in the diet, and deficiencies in hygiene (bio-amplification from re-infection).
  2. Cigarette smoking plus a heavy dose of asbestos constitute an imbalanced toxic load on the lungs, and greatly increase the odds of getting mesothelioma, much more than cigarette smoking alone or heavy exposure to asbestos alone.
  3. Contrary to common belief, alcoholism alone is usually not enough to yield cirrhosis. It takes a second insult to the liver in the form of either hepatitis (especially hepatitis C) or malnutrition (which is often secondary to an excessive alcohol consumption, and for two different reasons: (1) the inflammation in the digestive tract compromises nutrient absorption and (2) detoxification reactions consume nutrients). There is an entire population of heavy drinkers who are also hearty consumers of rich and nutritious foods and who rarely get cirrhosis – the bon vivants.
  4. Cancer is a multiple hit disease, and involves both genetic hits (often requiring hits in both copies of a critical gene), metabolic deficiencies, and immune deficiencies.
  5. Speculative example: could IBD be due to 2 hits (each of which has other hits) – an inflammatory hit plus a hit to the immune system? There is a baseline of gut inflammation in all humans due to uncontrollable factors, including simply the ingestion of food lectins.
    1. Above that there are some serious inflammatory substances that we ingest, some of us in massive quantities. About 17 million Americans (12% of adults) abuse alcohol. This alcohol abuse is also a hit to the immune system and a hit due to multiple nutrient deficiencies that develop, as noted above. In addition, though I have not seen this studied, heavy alcohol consumption should increase the yeast burden in the gut because as a group yeast are more resistant to alcohol than bacteria.
    2. Another hit to the guts involves a direct hit by alcohol to the immune system. Again, there is a huge background to this immuno-inflammation, including of course the food we eat and all of the food allergies and over-reactions by our immune system. But on top of this is the 15 million Americans (about 10.6% of adults) who take acid blockers. This also constitutes a deficiency type of hit to our defenses by reducing total nutrition (the expected hits, some of which have been at least noted in the literature, include calcium, magnesium, iron, B12; and a second wave of deficiency hits, affecting potentially all nutrients somewhat, when the small intestine becomes overgrown with bacteria or fungi that were not killed by stomach acid plus free fatty acids).
    3. Given sufficient free fatty acids, proper acidification of the stomach kills most pathogens that we consume, and allows mostly acidophilus bacteria and acid tolerant yeasts to pass through. The former include beneficial bacteria and I assume the acid tolerant yeast are likely commensals. However, when we allow acid-sensitive pathogens to pass through our guts, we can expect a vigorous battle with our both our innate and adaptive immune systems, constituting a second inflammatory hit in the development of IBD.
    4. According to CDC, only 1-1.3 million (approximately 0.4%) Americans have IBD. As noted above, 5.7% of Americans (17 million/300 million) drink heavily (multiple hits to the guts) and 5% take acid blockers (multiple hits to the guts)? If these are independent events, we would expect 0.3% of Americans do both, and we would expect 0.3% of Americans to suffer the consequences of doing both, which may or may not include IBD. This is close to the 0.4% prevalence of IBD, but of course this is an oversimplified outline of inflammatory insults to the gut. What else is involved? A lot of things.
    5. Unfortunately, I have seen but one study of IBD and alcohol consumption and it was based on surveys. If man were more truthful, this might actually count for something. Man is not – I would run a sequence of random urine samples from people with IBD and people without, and look for a complete spectrum of compounds in their urine, each normalized to creatinine. I would create categorical variables (say dividing populations into tertiles or quartiles and contingency tables, and then use the Chi Squared Test of Independence to look for variables that correlate to IBD, and everything else I was testing.
    6. Would love to know what correlates with depression – I suspect alcohol consumption, the taking of acid blockers, and yeast overgrowth biomarkers may correlate with degree of depression because alcohol itself and the other yeast byproducts both have depressing effects on the CNS.
    7. Yeast overgrowth and chronic fatigue syndrome are probably also linked – a person with yeast overgrowth should feel a bit depressed, a little spacey, a little tipsy, and a little hung over at all times, but especially after high carbohydrate meals and snacks have been converted to alcohol in the gut.