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?


Causation is a fine one dimensional representation

in which every other important factor is abstracted or filtered out.

Triggers and aggravators are hardly causes, but they are not non-factors.

Ameliorators are not anti-causes, but are hardly irrelevant.

Necessary conditions are always relevant as well.

Put it together and the one causal dimensional representation of the problem becomes a three dimensional realistic representation that does not violate Ockham’s razor – it has no more than sufficient complexity to describe the phenomenon within scientifically accurate bounds.

A six foot line is a perfectly adequate one dimensional representation of my physical being. It is certainly not wrong, but it is utterly inadequate to characterize even my physical being, let alone me.

Defining cancer as being caused by nuclear mutations is a perfectly adequate one dimensional characterization of the disease.

Defining type II diabetes by insulin resistance is a perfectly adequate one dimensional picture of the medical condition/disease.

Defining hypertension as caused by too much salt consumption is a perfectly adequate one dimensional representation of the medical condition/disease.

Defining human longevity in terms of total calories consumed is a perfectly adequate and perfectly quantitative one dimensional representation of a problem that has certain dimensions that are difficult even to quantify.

Etc., etc.

An adjunct cancer therapy?

In addition to limiting the growth rate of tumors by safe mechanisms (limiting glucose, but probably not glutamine, which immune cells need to fight tumors), and killing tumor cells, try to create conditions within the body that make it inhospitable to tumor growth.

Develop a real time method of measuring tumor growth and study every change in internal bodily condition that limits the growth of tumors. By combining a lot of these little nothing internal changes, one can make the environment inside a body a downright rude host to tumor growth, thus aiding and abetting the other methods of fighting cancer.

Analogy: one can make one’s whole body anything from being a good host for the growth of yeast to being an environment downright inimical to the growth of yeast.

The body tells us we are wrong over and over again: when are we going to listen?

The body is telling us we are wrong.

Give the body a squalene supplement and it efficiently absorbs it.

The body makes squalene and puts it to numerous good uses, but it does not make enough to meet its needs; “so” it tries to absorb whatever we give it.

Doctors prescribe statins to those who have high serum cholesterol, regardless of the reasons behind the high cholesterol. Doctors would mistakenly prescribe statins to those eating the traditional Polynesian diet.

Because statins inhibit our CoQ10 synthesis, doctors recommend that those on statins take CoQ10 (another substance the body readily absorbs “because” we do not make enough of it). What about all of the other important products made by the mevalonate pathway?

Including squalene.

Including dolichols. Want to bet the body avidly absorbs these too?

Including isoprenyls.

Including so many other useful compounds.

When are we going to get a clue? Equivalently, when are we going to take our clues from what the body is doing?

How to know when psychological health has declined

The hard way – look for unusual behaviors and try to get the person to admit he is behaving irrationally.

The easy way – the other drivers of health, so visible to everyone, even the person suffering from psychological ills – drop off when psychological ailments lay a person low and a person’s psychological health deteriorates faster and more thoroughly because of these second winds. It is common medical practice to treat mental illness and none of these other factors – naïve to the point of ludicrousness.

As an example, think of Nietzsche’s lifestyle in the decade before he went insane. His “insanity” was an intermittent medical condition, with all kinds of warning signs, long before it was diagnosed as a mental illness. Of course nothing was done about it; medicine does not know what to make of intermittent medical conditions. It was likely that paresis was a driver and the negative lifestyle variables accelerators of the development of outright insanity.

Those drivers of overall health that contribute to psychological health (a driver of overall health as well) and that fall off during the decline in psychological health and accelerate and aggravate the process of mental illness:
1. Quality/quantity of sleep – people with psychological ills are almost all taking drugs to help them sleep and even then the quality is poor, the side effects noxious, and they live in a stupor.
2. Quality/quantity of exercise – people with psychological ills rarely even go for walks. When someone used to enjoy a good stroll and no longer derives enough pleasure to continue to do so, something is wrong.
3. Quality of diet – catch as catch can, virtually no effort made in this area when psychological ills take over. May be accompanied by significant weight loss as well as outright nutrient deficiencies. When the person used to take great joy in preparing and enjoying delicious and nutritious meals, and no longer makes any effort or seeks the same thing in good restaurants, something is wrong.
4. Daily fasting – the vast majority of even psychologically healthy people do not do this; this counts only if the person used to fast or at least calorie restrict. Lack of fasting -lack of effort is the common denominator in mental illness- is easily concealed by the weight loss due to irregular eating habits that may look like an effort is being made to control food intake and weight gain. No – next to no effort is a hallmark of mental illness.

Barking up the wrong tree

If scientists were reincarnated as hunting dogs, many would be used in humorous skits because the rest of us can easily see and hear where the birds are hiding, but the scientists-turned-dogs would invariably be barking up the wrong tree.

Consider this piece of cluelessness about an important vitamin but an obviously wrong thesis:

Acta Ophthalmol. 2016 May;94(3):e170-6. doi: 10.1111/aos.12688. Epub 2015 Mar 4.

Association of vitamin C with the risk of age-related cataract: a meta-analysis.

Author information

  • 1Department of Ophthalmology, The Second Artillery General Hospital, Beijing, China.



Whether vitamin C is a protective factor for age-related cataract remains unclear. Thus, we conducted a meta-analysis to summarize the evidence from epidemiological studies of vitamin C and the risk of age-related cataract.


Pertinent studies were identified by searching in PubMed and in Webscience. The random effect model was used to combine the results. Meta-regression and subgroups analyses were used to explore potential sources of between-study heterogeneity. Publication bias was estimated using Egger’s regression asymmetry test.


Finally, 15 articles with 20 studies for vitamin C intake and eight articles with 10 studies for serum ascorbate were included in this meta-analysis. The relative risk (RR) and 95% confidence interval of cataract for the highest versus the lowest category of vitamin C intake was 0.814 (0.707-0.938), and the associations were significant in America and Asia. Significant association of cataract risk with highest versus the lowest category of serum ascorbate was found in general [0.704 (0.564-0.879)]. Inverse associations were also found between serum ascorbate and nuclear cataract and posterior subcapsular cataract.


Higher vitamin C intake and serum ascorbate might be inversely associated with risk of cataract. Vitamin C intake should be advocated for the primary prevention of cataract.


age-related cataract; meta-analysis; serum ascorbate; vitamin C

PMID: 25735187
DOI: 10.1111/aos.12688

How did I know a priori that the thesis is ridiculous? An entire civilization that must have had marginal vitamin C intake was without any significant evidence for excess cataracts.

In the long cold winters, the isolated Swiss had a diet consisting of: 2-3 servings of meat per week (none or negligible vitamin C), raw milk (some vitamin C), raw dairy products derived from milk (mostly cheese and butter, even less due to processing out the vitamin C in the liquid phase), and rye bread (no vitamin C). If these people had glassy eyes like so many peoples do around the world, would Weston Price have failed to notice the problem and report it? No.

Since vitamin C consumption is obviously not a factor in cataract development, does the following study surprise us?

Cochrane Database Syst Rev. 2012 Jun 13;(6):CD004567. doi: 10.1002/14651858.CD004567.pub2.

Antioxidant vitamin supplementation for preventing and slowing the progression of age-related cataract.

Author information

  • 1MetroWest Medical Center, Framingham, Massachusetts, USA.



Age-related cataract is a major cause of visual impairment in the elderly. Oxidative stress has been implicated in its formation and progression. Antioxidant vitamin supplementation has been investigated in this context.


To assess the effectiveness of antioxidant vitamin supplementation in preventing and slowing the progression of age-related cataract.


We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2012, Issue 2), MEDLINE (January 1950 to March 2012), EMBASE (January 1980 to March 2012), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to March 2012), Open Grey (System for Information on Grey Literature in Europe) (, the metaRegister of Controlled Trials (mRCT) (, ( and the WHO International Clinical Trials Registry Platform (ICTRP) ( There were no date or language restrictions in the electronic searches for trials. The electronic databases were last searched on 2 March 2012. We also checked the reference lists of included studies and ongoing trials and contacted investigators to identify eligible randomized trials.


We included only randomized controlled trials in which supplementation with one or more antioxidant vitamins (beta-carotene, vitamin C and vitamin E) in any form, dosage or combination for at least one year was compared to another antioxidant vitamin or to placebo.


Two authors extracted data and assessed trial quality independently. We pooled results for the primary outcomes, i.e., incidence of cataract and incidence of cataract extraction. We did not pool results of the secondary outcomes – progression of cataract and loss of visual acuity, because of differences in definitions of outcomes and data presentation. We pooled results by type of cataract when data were available. We did not perform a sensitivity analysis.


Nine trials involving 117,272 individuals of age 35 years or older are included in this review. The trials were conducted in Australia, Finland, India, Italy, the United Kingdom and the United States, with duration of follow-up ranging from 2.1 to 12 years. The doses of antioxidant vitamins were higher than the recommended daily allowance. There was no evidence of effect of antioxidant vitamin supplementation in reducing the risk of cataract, cataract extraction, progression of cataract or in slowing the loss of visual acuity. In the pooled analyses, there was no evidence of effect of beta-carotene supplementation in reducing the risk of cataract (two trials) (relative risk (RR) 0.99, 95% confidence interval (CI) 0.91 to 1.08; n = 57,703) or in reducing the risk of cataract extraction (three trials) (RR 1.00, 95% CI 0.91 to 1.10; n = 86,836) or of vitamin E supplementation in reducing the risk of cataract (three trials) (RR 0.97, 95% CI 0.91 to 1.04; n = 50,059) or of cataract extraction (five trials) (RR 0.98, 95% CI 0.91 to 1.05; n = 83,956). The proportion of participants developing hypercarotenodermia (yellowing of skin) while on beta-carotene ranged from 7.4% to 15.8%.


There is no evidence from RCTs that supplementation with antioxidant vitamins (beta-carotene, vitamin C or vitamin E) prevents or slows the progression of age-related cataract. We do not recommend any further studies to examine the role of antioxidant vitamins beta-carotene, vitamin C and vitamin E in preventing or slowing the progression of age-related cataract. Costs and adverse effects should be weighed carefully with unproven benefits before recommending their intake above recommended daily allowances.

PMID: 22696344
PMCID: PMC4410744
DOI: 10.1002/14651858.CD004567.pub2
[PubMed – indexed for MEDLINE]

Free PMC Article


Anyone knowing Weston Price’s observational data would not even have done this meta-analysis. A complete waste of time – killer counterexamples are real and smart scientists save time by paying attention to them.