A crude estimate of liver insufficiency in America

Liver insufficiency is not liver disease. It is just some kind of liver metabolic insufficiency or impairment due mostly to poor stewardship of the body.

Roughly 20-25% of Americans have a noticeably higher serum cholesterol after a month of consuming 3-5 eggs a day.

Roughly 75-80% of Americans have approximately the same serum cholesterol after consuming 3-5 eggs a day.

Crude estimate of liver insufficiency in America: 20-25%, could be higher, as these data focus on proper bile production from dietary cholesterol, choline, and taurine, and successful bile secretion, i.e. no backup of dietary cholesterol (and/or bile acid salts) into the circulatory system, nearly all dietary cholesterol being confined to enterohepatic circulation in healthy individuals.

The prevalence of liver insufficiency should be considerably greater than the prevalence of cirrhosis, which is estimated to be less than 1% in the US.

The Epidemiology of Cirrhosis in the United States: A Population-based Study.

PMID: 25291348

CDC stats on the prevalence of all types of liver disease:

  • Number of adults with diagnosed liver disease: 3.9 million
  • Percent of adults with diagnosed liver disease: 1.6%


Still a fraction of the number I am estimating, closer to 20%. Are their tests not sensitive enough to see real metabolic problems in liver?

Or is my estimate utter nonsense?






Increasing the burden on the back end of our defenses

Acidity is critical to digestion, but also to our immune system.

When we do not kill germs effectively with acidic digestion of food, coupled with sufficient fat, we increase the burden on our downstream defenses, including our immune systems.

But this problem also occurs during periods of fasting.

Roughly half of our nasopharyngeal mucus backs up into our stomachs. Microbes (possibly including Mtb), viruses, and pollutants drop into a pool of acid at the base of the stomach.

People who take acid blockers (up to 99% reduction in acid production) lose a good deal of their protection. All but unharmed microbes, viruses, and pollutants leave the relatively impermeable stomach, and enter the duodenum, a considerably more permeable environment. An environment that can be rendered still more permeable by a number of mechanisms, including heavy drinking.

This overburdens the downstream defenses, including the immune system. These microbes were supposed to be trapped in mucus and killed by strong stomach acid. Instead, any bacteria that have been freed from mucus, are able to feed and breed, and pose a more serious threat as they move through the intestines, requiring more immune system resources to deal with. If they get into the bloodstream, even more problems develop.

Is this a second route for Mtb to enter the lungs? And to get into places where these microbes might do even more harm?

A possible source of the sex bias in autoimmunity?

I have hypothesized that autoimmunity is a multistep process that may go something like this.

Step I generally requires undernutrition, such as generates a Franken-structure within a normal structure. Example B12 deficiency -> accumulation of methylmalonic acid in myelin. Choline deficiency -> myelin that is choline deficient. myelin with methylmalonic acid and a deficiency of choline is Franken-myelin.

Step 2: antibodies develop to this.

Step 3 is due to non-specific immune system damage to surrounding normal structures, and is aided and abetted by mild vitamin C deficiency.

Step 4: antibodies develop to this, sometimes as sub-clones to the cells that produce the antibodies in step 2.

Any number of steps before the final step, step N.

Step N: in the final step, autoantibodies develop, and this too normally requires either toxins affecting immune system accuracy or under-nutrition or both.

At least in part, the sex bias: more women make the mistake of starving themselves thin. Becoming thin and staying thin must never be at the expense of maintaining bodily pools of nutrients at their proper levels. At the very least, starvation must be accompanied by strong and appropriate supplementation.

Were it not for strong protection of the female by nature, women’s health as a whole might be noticeably worse than men’s. As it is, the natural protection of women leads to a net better health in the female.

Disease is due to toxins’ exploiting weaknesses in our defense systems, and under-nutrition seriously weakens our defenses, including of course, kidney and liver function, and the immune system accuracy, precision, and activity. In addition, under-nutrition leads directly to the accumulation of toxic wastes, such as Franken-myelin in place of normal myelin.

The conditions that favor the development of cancer

A person with dandruff has scalp chemistry that favors the growth of yeast, and a body chemistry that is generally supportive to the growth of yeast. It is not likely that a person has really bad dandruff, while having bodily conditions that aggressively disfavor the growth of yeast.

Similarly, a diabetic has at least two things that favor the development of tumors: high glucose and high lactic acid. The more hypoxic tumor cells need glucose, which they convert to lactic acid, and the less hypoxic tumor cells utilize lactic acid from the body and the more hypoxic tumor cells, much the way slow twitch muscle fibers utilize the lactic acid from fast twitch muscle fibers. More hypoxic and less hypoxic tumor cells are symbiotic, nutritionally speaking, and perhaps in other senses.

Conditions that favor tumor growth include conditions that disfavor a strong, alert, responsive immune system. For example, rather infrequent fevers. For example, less glutamine and more glutamate. A higher glutamate/glutamine ratio than is normal. Another example: low circulating vitamin C levels.

High circulating fatty acid levels favor the growth of tumors because fatty acids increase insulin resistance, and thus baseline glucose levels.

Successful tumors convert prodigious quantities of glutamine to glutamate and free fatty acids, favoring their own survival at the expense of the body.

The body metabolism that favors the development of tumors I call “degenerative metabolism,” and it may be visible with quantitative urinalysis years before tumors develop. Some markers of degenerative metabolism, all potentially readable in quantitative urinalysis: high glucose, high glutamate/glutamine ratio, low vitamin C, high fatty acids, high lactic acid, high methylglyoxal.

A strong program to reverse course could be instituted before cancer develops.

Arsenic, Oh Arsenic!

Doctors’ conception of arsenic is too narrow: it is just a poison.

However, on a weight/weight basis, arsenic is not that much more poisonous than other common substances, roughly comparable to vitamin D3, sodium fluoride, piperidine (from black pepper), and nicotine. Arsenic has a median lethal dose, LD50, in the ppm range, the milligram per kilogram body weight range, the exact value depending on the chemical form.

No – arsenic is more than just a poison. Arsenic is a versatile inorganic catalyst. While it has an LD50, and too much is toxic, when deprived of arsenic during their formative years, animals (and likely humans), do not develop properly.

Likely: as Nielsen reasoned, arsenic is an essential nutrient, and thus deficiency symptoms likely exist, though they are under-recognized and accordingly under-treated.

Until the wrong idea that arsenic is just a poison actually dies, it is not likely that deficiency symptoms will become recognized and treated, and it is unlikely that arsenic will be included in the formulation of multi-mineral pills or tablets anytime soon.

Arsenic deficiency is probably rare in the US, if Nielsen’s estimate that the average diet normally contains roughly 4x more arsenic than we supposedly require.

It is possible that arsenic and selenium are a biological push-pull pair. Since selenium is supplemented, arsenic deficiency may be more common than thought, among those with marginal consumption of arsenic, and/or those with absorption/utilization problems. The term “utilization problems” references my hypothesis that each essential nutrient has its own ADME network, containing other essential nutrients and some non-essential nutrients. Thus, deficiencies in arsenic’s ADME network can create functional arsenic deficiency even in those ingesting recommended amounts.

More thoughts on hypertension

Roughly 90% of hypertension is “essential hypertension” or “of cause unknown.”

Reasonable assumption: with so much etiological mystery, doctors must have misunderstood hypertension nearly completely. What else is new? An animal who looks at things backwards is a reasonable definition of man.

Rule: doctors misunderstand evolution and the human body that evolution created.

The first salient fact to explain: why is there so much more hypertension than hypotension?

It could be that the mechanisms that tend to reduce blood pressure are more fragile than those that raise it. That is very possible and may be the true explanation. But if it is, then the same would have to be said for diabetes and hypercholesterolemia. Why such a prevalence of overly high values of blood sugar and blood cholesterol? Seems too much of a coincidence, unless there is a common evolutionary ground. Is there an evolutionary explanation of why things tend toward the excessively high? Is nature running away from the clearer and more present danger of excessively low? All things considered, animals that tend toward higher blood pressure, higher blood sugar, and higher blood cholesterol, have a survival advantage as compared to those with similarly lower levels, and optimal is always better, when it can be safely and stably maintained.

Doctors tend to blame hypertension (10% or so) on too much salt consumption and essential hypertension (90% or so) on what they can see. If a person is obese, obesity is the cause of essential hypertension, ignoring the fact that many other patients are obese and have normal blood pressure. This is just senseless, but all-too-common. If the essential hypertension patient loses weight and normalizes blood pressure, then it is QED for doctors. For the rest of us, that is still nonsense – we are looking at salt water weight loss, not fat, and a partial normalization of lifestyle with respect to proper diet, including reduced salt consumption, but also a diet that is higher in nutrients, essential and non-essential, as being most responsible.

I have hypothesized that as a rule, most diseases, and most essential hypertension begins not as a disease, but a medical condition, freely reversible by readjusting lifestyle, and in fact, in the case of essential hypertension, as a “normal” (given some loss of regulatory powers) bodily response to the inability to regulate blood pressure properly within the normal range. That is right, if this hypothesis is true, the body is electing/selecting to fight hypertension rather than to fight a riskier battle against hypotension. By analogy, this tendency also explains why the body tries to absorb substances like choline, cholesterol, and taurine from its diet, when it can make these from essential nutrients or other components. All things considered, the body would rather cope with excesses of nutrients (yes, dietary cholesterol is a nutrient) than deficiencies, when the quotidian quantities that it can make suddenly are not enough to meet a “clear and present danger.”

This hypothesis may be false in any case, but surely it can be true only, if in fact, for an equivalent deviation from normal, low blood pressure poses a greater imminent danger than high blood pressure. From evolution, the body has inherited a focus on short-term survival. To the body, long-term survival is a series of successful short-term survivals. Long-term survival is never the body’s natural “aim.” No processes are, as a rule, optimized to meet this imaginary aim of long-term survival. It is survival through the early and middle reproductive years that is important.

Consider Marburg disease, Ebola, and a third, possibly related disease, sweating sickness. In the first two, the fatality rate averages around 50% per outbreak, with a wide standard deviation. In addition, mortality is rather quick. Surely, then whatever is responsible for so much mortality is a serious problem indeed, a grave and imminent danger. It is believed that the event that immediately precedes death is a sudden drop in blood pressure due to extreme blood/fluid loss from hemorrhaging, and circulating fluid/electrolyte loss due to vomiting, diarrhea, edema* (a retention of fluid that reduces circulating fluid ,useful in situations of high blood pressure), and sweating.

The blood volume, hydration, and electrolyte state of a person going into one of these episodes is critical to his/her survival, and if sweating sickness is like the other two, one can see why it was so devastating, before the modern era of proper water purification, when so many people drank alcohol all day to wash down their food and to “hydrate” themselves. Hydration, electrolytes, and indeed addition of blood of the proper blood type were essential, if death from sweating sickness was to be prevented, long enough until the immune system could neutralize the agents, but of course none of these was done. Add to that the fact that doctors back then, if they did anything for a victim of sweating sickness, it was to bleed them, making their blood loss, fluid loss, electrolyte loss, and hypotension worse. Way to go, doctors!

Doctors’ view at the time was that bleeding sometimes helps a victim of the sweat recover. More likely, in some who were going to survive anyway, bleeding did not kill them. How backwards our thinking is!

Hypotension is responsible for a nearly immediate death, at a rate of about 50%. The equivalent hypertension is fatal many years later and at a rate of less than 50%, though with so much time until death, other things besides hypertension kill the people off first.

Can there be any doubt which is more dangerous?

The same goes for low blood sugar vs high blood sugar – again, doctors misunderstand diabetes. The same probably goes for low cholesterol vs high cholesterol.

In all likelihood, in all three cases, low x is much less common than high x and this must be explained, likely by a single unifying hypothesis. The animal body responds appropriately to the inchoate inability to regulate blood pressure, blood sugar, and blood cholesterol, and perhaps many other things, by regulating them to a higher level, putting immediate death at bay, reducing the odds of the grave and immediate danger of extremely low values.

Modern doctors, like their counterparts of old with their exsanguination, are opposing nature and evolutionary pressures, as they often do, and thereby subtly increasing the odds of a rapidly fatal event. Doing nothing makes more sense than that. But still more sense is to chart a reverse of the errant lifestyle course, and reverse the reversible medical condition, before it is too late and is no longer reversible, re-establishing proper regulation within the normal levels. for an even longer, healthier life.

Will this ever be done? Your guess is as good as mine. I’m not betting on it, as long as the rule above holds, or until medicine comes up with proper bi-specific or tri-specific drugs. The current mono-specific drugs (that only lower x) are losers compared to nature’s tri-specificity (nature can raise or lower x, or adopt a completely different regulatory scheme in an emergency). When doctors understand evolution properly, they will understand the human body properly – they will understand that as a rule, they must stop opposing the human body (by rule, evolution usually gets it right), and start helping the body to do the right thing, and they will oppose the human body, only when evolution could not get it right, likely due to the chief limitation of evolution, the fact that evolution can work only with what variation it has at the moment. Evolution cannot create more optimal solutions ex nihilo the way the omnipotent god of the theologians is alleged to.

  • Some scientists think that lung edema was the key event that may have killed victims of sweating sickness. Certainly possible, but if the lung edema did not actually kill them, it -and any other edemas- certainly added to the loss of circulating fluids and the consequent decrease in blood pressure.

An anecdote that says that vitamin C deficiency does not cause scurvy

High dose vitamin C is a therapy for scurvy precisely because vitamin C deficiency is NOT the cause of scurvy.

What? Huh?

Some background:

By definition, the cause of something is completely responsible for it. There can be only one cause of something.

By definition, the driver of something is predominately responsible for it. There can be only one driver of something and there must also be at least one contributor.

By definition, a contributor to some effect is partly responsible for it. There can never be one contributor if there is no driver and no cause.

Statistics and common sense tell us that in nature there are many more contributors than drivers, and many more drivers than causes.

If vitamin C deficiency is the cause of scurvy, then only vitamin C can cure scurvy.

If vitamin C deficiency is a contributor to scurvy or a correlate of scurvy, and not the cause, or even the driver of scurvy, then a therapeutic dose of vitamin C might cure scurvy.

If vitamin C deficiency is a correlate of scurvy, not a cause, then simply increasing bodily pools of vitamin C to above the level seen in scurvy will not cure scurvy.

On the contrary, it will take quite a bit higher doses to do that. This is what is observed and was in fact the second thing that made me suspicious of the one-hit causal model of scurvy. The anecdote below, while not reliable, would disprove conventional wisdom, if the anecdote could be verified and established by rigorous experimentation.

If scurvy is a multi-hit a-causal disease, as I believe is the rule for diseases, then any number of things might cure it, including large doses of a single agent, vitamin C – because even single agents are multifactorial in their actions.

Scurvy could also be an exceptional one-hit causal disease or it could be a case of medical gerrymandering, making the statement somewhat trivial, as being true by definition. Gerrymandering means that only those symptoms attributable to vitamin C deficiency are included within the scope of the disease known as scurvy. Yet those who suffer from scurvy have more things wrong with them than that definition allows, including more deficiencies than just one vitamin.

As scientific evidence goes, anecdotes are weak, really weak. But they are not NOTHING. They are not controlled experiments and those reporting the anecdotes may even lack credibility. The anecdotes need to be investigated and the work repeated, scientifically. Most scientists just ignore anecdotes and go on about their business, but they do so at their own peril, the peril of the scientific error of promulgating and perpetuating overly simplistic univariate models.

Many an underpowered model, one that is too causal, too univariate, has arisen by ignoring anecdotes.

Here is a widely ignored anecdote about scurvy that if it is true, blows the theory that vitamin C deficiency is the cause of scurvy right out of the water because scurvy was cured rapidly without vitamin C. The two keys, which dispute scientists claims to the contrary, are the rapidity of the effect and the heat stability of the factor(s) responsible.


J Ethnobiol Ethnomed. 2009; 5: 5.  Published online 2009 Feb 2. doi:  10.1186/1746-4269-5-5 PMCID: PMC2647905.  Arginine, scurvy and Cartier’s “tree of life”

“One of the first documented uses of indigenous medicine in North America was the cure in the winter of 1536 of Jacques Cartier’s crew from a disease he called “Scorbut”(scurvy) [1,2]. Cartier’s second voyage (1535–1536) was undertaken at the command of King François 1er to complete the discovery of the western lands under the same climate and parallels as in France. At Stadaconna, now Quebec City, Cartier’s crew was cured from scurvy by ascorbic acid (vitamin C) obtained as a decoction from the Iroquois. It was prepared by boiling winter leaves and the bark from an evergreen tree. The tree, identified as “Annedda”, became known as the “tree of life” or “arbre de vie” because of its remarkable curative effects. In the winter, scurvy was the most prevalent disease among the Iroquois. This was due to the lack of food and vitamin C [3].

The cure for scurvy was significant for future naval explorations and for the introduction of the tree into France during the Reformation when the Age of Reason began (1558–1648) [4]. The medicinal value of the tree of life contributed to the resurrection of botany, which at that time struggled to free itself from pharmacy when medical men were still its masters. By the eighteenth century, the French naturalists at the Jardin du Roi in Paris knew of Thuja occidentalis as the tree of life and planted an avenue of it in the Jardin itself [5].

The Iroquois referred to the tree as Annedda (l’Annedda, Aneda, Anneda, Hanneda) [2]. Other tribal names for conifers were “ohnehta” for white pine, “onita” and “onnetta” for white spruce (Mohawk, Onandaga). These names represent the evergreen nature characteristic of coniferous trees. Regarding the transmission of the tree of life to France, the earlier one goes, the sparser are the available manuscripts. The pre-Linnaeus terminology for conifers made their precise identity impossible to make. Based on collections by French explorers and the ethnomedicine of indigenous peoples in eastern Canada, the true identity of the tree of life became controversial [2]. The identity of Anneda was narrowed down to eastern white cedar or arborvitae (Thuja occidentalis L.), white spruce (Picea glauca (Moench) Voss), black spruce (Picea mariana (Mill.)), eastern white pine (Pinus strobus L.), red pine (Pinus resinosa Aiton), balsam fir (Abies balsamea (L.) Mill.), eastern hemlock (Tsuga canadensis (L.)), and juniper (Juniperus communis L.) [2,6].

We now know that during late a severe winter and at a similar latitude to Quebec City, the candidate trees of life are a rich nutritional source of arginine, proline and other amino acids [79]. Their physiological fluids and proteins contain amino acids which are essential in the human diet because the body does not synthesize them (viz., phenylalanine, valine, threonine, tryptophan, isoleucine, methionine, leucine, and lysine). Arginine, cysteine, glycine, glutamine, histidine, proline, serine and tyrosine are conditionally essential, meaning they are not normally required in the diet, but must be supplied to specific populations that do not synthesize these amino acids in adequate amounts [10]. Today, these amino acids are used as nutritional support for the recovery of critically ill patients [1114]. In the recovery from scurvy they would help to promote vitamin C-dependent collagen biosynthesis, promote wound healing, reduce susceptibility to sepsis, and contribute to weight gain [10,1517].”

He declares, I believe wrongly, in view of the trivial amount of vitamin C present in heat-treated extracts of Thuja occidentalis bark and needles, the rapidity of the cure, and the heat-stability of the curative agent(s):

“Several conifers have been considered as candidates for “Annedda”, which was the source for a miraculous cure for scurvy in Jacques Cartier’s critically ill crew in 1536. Vitamin C was responsible for the cure of scurvy [emphasis mine] and was obtained as an Iroquois decoction from the bark and leaves from this “tree of life”, now commonly referred to as arborvitae. Based on seasonal and diurnal amino acid analyses of candidate “trees of life”, high levels of arginine, proline, and guanidino compounds were also probably present in decoctions prepared in the severe winter.”

In spite of declaring vitamin C deficiency to be the cause of cancer, this author concludes more sensibly, more multifactorially:

“The history of medicine and clinical practice has involved a succession of blind alleys and detours, mountains of often uninterpretable observations, and a great leap forward as in the discovery of vitamin C as a cure for scurvy. This review takes us centuries back, and turns our attention to the combined values of arginine, NO, proline, other conditionally and essential amino acids, guanidino compounds, and antioxidants as added factors in the food and medicines of indigenous Canadian peoples.”