High magnesium in bones correlates with greater bone strength

Since magnesium is mostly on the surface of bones, the correlation between the level of magnesium in bone and the resistance of bones to breakage is probably indirect.

If bodily pools are adequate to very good, magnesium deposits on the surfaces of bones.

If bodily pools of magnesium are adequate to very good, so are many nutrients that parallel magnesium, and overall, metabolism -including inner bone metabolism and the breakdown and rebuilding of bones- simply runs better.

When bodily pools of magnesium are inadequate, so are its correlates (including other nutrients), metabolism is off, and bone deposition of magnesium decreases, and as bones are continually remodeled, the level of magnesium in bone decreases.


A world from nothing might just be attractive to theologians

Theologians puzzle over the thorny problems inherent in the idea that god created the world and everything in it.

Yet no one ever considers that god is off the hook as the ultimate source of a lot of evils – not just sins but all of the suffering even the best of men suffer needlessly from a parasitic and predatory nature, if we make one simple assumption, that the world came into existence on its own out nothing.

If that assumption is true, then certain things must also be true, and so far, experiments bear these out. The prediction of this theory of mathematical nihilism, that a single absolute reality does not exist, and that no one will ever propose such an absolute reality that will ever be universally accepted by pundits does not mean that there is no god, provided that god is defined simply as the noblest, most exalted, and best of all beings and perhaps the best of all possible beings, perhaps even an ideal yet to be realized.

To most theologians if god did not create the world, that would make god irrelevant, more irrelevant than Aristotle’s “prime mover” – but they forget that through revelation god could educate us to a higher standard and yes, god could still judge us on our efforts to become better people. Hopefully, these theologians would see that eternal punishment is infinite punishment and does not fit the finite nature of our crimes and sins, and that any being applying such punishments is not worthy of our devotion let alone our worship.

What if autoimmunity isn’t “auto”?

What if we are all chimeras? – After all, one cannot verify that all hundred trillion cells of each of us have the same DNA. Then it is possible that so-called autoimmune disease is actually regular immunity, with one or more sets of cells attacking the other(s). In some cases, the majority cell of the organ or tissue loses out. For example, the majority cell that made up the part of the pancreas that is destroyed in Type I diabetes may have been a minority cell in the body.

Worst case of mosaicism: When twins are born, or multiple embryos are implanted in in vitro fertilization, we may have cells of our sibling or could-have-been-a-sibling, respectively, as well as cells from our mothers and cells from our older maternal siblings.

This could explain why even in the worst cases of autoimmunity, complete obliteration of an organ is rare. If true, then our mosaicism literally extends to every organ.

This could explain the positional specificity of disease – why atherosclerosis starts in one specific spot. It is an “autoimmune” attack that the cholesterol patch is trying to prevent from becoming a hemorrhage. Naturally, doctors blame cholesterol. If cholesterol were the cause of atherosclerosis, all of our arteries would be attacked equally. Why a cavity starts in one specific spot. Why an ulcer starts in one specific spot – the cells were under immune attack; the weakened cells were then killed off by acid plus pepsin after the barrier was eroded by NSAIDS, alcohol, and/or bacteria. Why irritable bowel disease and ulcerative colitis are all initially positional. All “auto”- immune attacks.

This could explain male pattern baldness, vitiligo, and conditions like them.

Each of us can be a chimera – at the very least, we may all have had or still have cells of our mother in us. Some of us may have cells from our older maternal siblings, left over from the after-birth, still alive or even still growing inside the mother (sibling cells may multiply during the immuno-tolerance that pregnancy requires in order not to kill the fetus). They join the developing embryo, and really mess things up.

Everything else being equal, older siblings may thus show less autoimmunity. Primogeniture would have a real genetic basis. Hah. But where older siblings result from fusion of two embryos, they could be even more messed up than their younger siblings.

Could at least some of the excess male homosexuality (male:female homosexual ratios being about 2:1?) be due to cells from the mother or an older sister being the developmental precursors of the cells that control sex drive? Interestingly, the probability of homosexuality goes up as more and more children are born to a mother. Female homosexuality may in some cases result from her older brother’s cells developing into her cells that control sex drive.

The people who suffer most devastatingly from “autoimmune” disease may have the most trouble with their chimeric cells and self-cells battling for immune supremacy.

Method of estimating endogenous ethanol production

Use people with typical carbohydrate consumption, but suffering from yeast overgrowth. This blocks most of the conversion to acetaldehyde and acetaldehyde adducts. It allows a significant concentration of ethanol to build up in the blood stream for accurate kinetic measurements.

Still more accurate, but a more limited sample: add poor liver function to the yeast overgrowth to slow down the liver’s conversion of blood alcohol to acetic acid.

Now take that estimate of total alcohol produced from the fermentable carbohydrate and multiply by the correction factor, which would be =  (level of alcohol producing organism activity in the test subject / level of yeast in those suffering from over-growth). Further corrections could be made, such as for total fermentable carbohydrate consumption.

As we age, we need more parenteral nutrition

As we age, the efficiency of both our digestion of food and the absorption of nutrients from the digested food declines. Doubtless, so does the efficiency of our cellular uptake of nutrients from the blood stream (and not just because of lower concentration of nutrients in the blood due to poorer digestion and absorption), a problem that even parenteral nutrition won’t fix.

Parenteral nutrition would get us past the digestive and absorption inefficiencies. I’m thinking of regular self-administered shots of nutrients, not an IV hookup.

We also need an invention to get us past the inefficiencies of cellular uptake from the blood stream. Something that generically pushes much-needed nutrients into cells, and then deep inside them to the subcellular compartments. As we age, I wonder whether our mitochondria are even getting all of the oxygen that they need, or whether our cells are even getting all of the water that they need.

Persistent High Blood Pressure: Due to excess salt or nutrient deficiency?

One of the salient facts about high blood pressure is that about three-quarters of people cannot completely control it even with drugs (Berlowitz DR, Ash AS, Hickey EC, et al. Inadequate management of blood pressure in a hypertensive population. N Engl J Med 1998;339(27):1957–1963. [PubMed: 9869666]; Med Sci Monit. 2010 January; 16(1): RA1-RA8). That is, their high BP is persistent. One explanation of the persistence is that the central nervous system has reset the baseline pressure higher, and all regulatory mechanisms operate to re-establish the higher baseline, not the doctor’s 120/80. A reasonable explanation of the resetting is that due to chronic (years and years) nutrient deficiency, the major arteries with baroreceptors, the aorta and the carotids, lose a sufficient quantity of their elasticity. This reduced distention is read by the CNS as blood pressure being too low and it “permanently” dials it up. Two solutions are (1) to reprogram the CNS to dial BP down (quick and dirty, probably lots of side effects, including inadequate GFR) or (2) to adopt a healthy diet and wait about 2-5 years for the arteries to be re-built with sufficient flexibility. I favor the latter as the only genuine solution to blood pressure problems. It is the only solution I would even consider if my 100/50 BP were to get dangerously high.

In this model, high salt (i.e. about 10 grams/day) has only a minor role to play – it is another challenge, another stressor on a system that already is not coping well. But a cause of the problem? Not reasonable to assume so, not without nutrient deficiency to slow down the proper coping mechanisms that kick in when salt intake is ridiculously too high (20-30 grams/d). It is all a question of rate – each 24 hour period, salt balances must be achieved or the consequences are very painful. Given nutrient deficiency and extreme salt intake, salt balance may not be achieved in 24 hours without dialing up the blood pressure. But this change in BP is not expected to be long-lasting; it should go away soon after salt levels are reduced. This cannot be the majority of cases unless nearly everyone on a salt-restricted diet is in fact cheating.

In essence, this is what is wrong with a recently proposed model for salt-induced hypertension via CNS involvement that employs digoxin-like compounds. (Hypertension Research (2011) 34, 1147-1160.) This model fails to identify the level of NaCl required to initiate the problem. It does not consider whether that level is personal and specific. It does not consider the role of nutrient deficiency or the role of loss of sufficient elasticity in key arteries. It fails to explain why BP is not simply controlled by the low salt DASH diet. If excess NaCl per se caused the problem, why does a removal of the excess salt from the diet not reverse the problem? The high BP not only does not reverse quickly on DASH, as would be expected in their salt-induced model, it does not reverse after YEARS, when healthier arteries could have been rebuilt by a proper diet (together with psychological help, more exercise, and better sleep).

Personal anecdote:  My own systolic blood pressure has not budged one point – a steady 100 – in 40 years of adulthood, all while enjoying tasty high salt meals, and smiling at the accepted theory that high sodium dieting causes high blood pressure.

Lack of quantitative methods: a real hindrance to research

Biologists and medical doctors are not the most quantitative of scientists.

This hurts their disciplines a lot.

Consider carcinogenesis.

Some doctors consider “cancer” to be an umbrella term for many distinct diseases. In which case, different terms should be invented and used. One term – one condition or disease.

Cancer is a condition, not a disease. Cachexia is a disease. Gradual loss of function of a tissue or organ due to invasive cancer is a disease.

If doctors developed methods for simultaneously quantifying multiple variables on a cell-by-cell basis in tumors, they might find the following, everything else being equal:

1. The more tumorigenic or malignant a cell from a tumor is, the more cytoplasmic dysfunction – for example, the more malignant a cell is, the less competent it is in electron-transport-dependent respiration.

2. The more reliant a cell from a tumor is on non-respiratory energy-generating metabolism (such as utilization of glutamine, alanine, or glucose), the more transforming it already is or is likely to become.

3. The stronger the mutator phenotype, the more likely the tumor cell is resistant to selective mechanisms, from immune surveillance to radiation to chemotherapy.

4. Any many, many more – lots of quantitative relationships, cell-by-cell. But no tumor will be truly heterogeneous. That is why multiple quantitative cell-by-cell assays must be performed simultaneously (and deftly to avoid changing the phenotype during the analysis) to get a clear picture of the process.

Right now, without these methods, confusion reigns supreme. Scientists can’t even agree on what cancer is due to, let alone what best to do about it, or how best to prevent it in the first place.