A contributor to poorer quality sleep?

Eating too often. Not too much (which is also a problem, and may be as relevant to sleep quality, especially in the extremely obese via sleep apnea).

Eating too often. The point is that one can eat the right amount of food, but eating too often will still lead to unexpected problems.

Many Americans eat 3 meals a day and some eat 3 meals plus snacks.

This is too often – it does not allow time for important repair processes, particularly those dependent on autophagy, which is stimulated by glucagon, and inhibited by insulin (and hence by every episode of feeding).

My guess is 1-2 meals per day is optimal for overall health and for optimal repair processing.

There are other problems that arise from eating too often. For example, because those who eat 3 meals plus snacks suffer the inevitable post-prandial slump, they consume more caffeinated beverages than they would if they ate just once per day, and this has the effect of reducing overall quantity and quality of sleep.

The Fast-5 diet format recommended by Dr. Bert Herring suggests having one meal a day of about 5 hour duration just before bedtime, followed by a 19 hour fast. As long as there is no reflux, this seems to me to be the best time for the single meal (and I am trying it out now). Because no caffeinated beverages need be consumed to combat the slump just before retiring, less caffeine is needed during the productive waking hours (I’m trying 100 mg every few hours in the AM – 400 mg MAX), meaning that all other things being equal, sleep will tend to be of better quality and longer in duration.

I wonder if there are data to support this. Probably very little, since the Fast-5 is not a particularly popular diet format – and who would study such a topic? I would – if only I could.

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.