February 2017 Blog with Durk and Sandy


Thou shouldst not have been old till thou hadst been wise.
— King Lear (Shakespeare)

Gold IS money, everything else is credit.
— John Pierpont (J.P.) Morgan

The modern geography of the brain has a deliciously antiquated feel to it—rather like a medieval map with the known world encircled by terra incognita where monsters roam.
— David Bainbridge

… the modern nation-state, a massive and entrenched insurance company attached to an equally massive and entrenched standing army.
— W. Ben Hunt, Ph.D.
https://epsilontheory.com (posted Nov. 24, 2013)

The future is already here—it’s just not very evenly distributed.
— William Gibson, science fiction author


There are a number of meanings of the word “check,” but, it is said in a recent article, they all come from the same root: the game of chess.

First, the game of chess itself: the king, in Persian, is shah, and shah mat means ‘the King is dead.’ In Russian, the game of chess is itself called shakhmaty, and “check” is said shakh. This becomes scaccus in Latin, and from there you get echec in French, chess in English, and lots of other forms in different languages. (Note that echec is also the French word for ‘failure’—and this also comes directly from the chess concept.

—Sasha Volokh, THE VOLOKH CONSPIRACY, The Washington Post, Jan. 1, 2017 (NOTE: The words in Persian, Russian, Latin, and French do not contain the pronunciation punctuation (marks above letters).


Oh, yes, there is a right way to take high-dose immediate release niacin. Take it at the right time and you can get a host of health benefits, especially reduced triglycerides, LDL, and VLDL and increased HDL—at the wrong time, you lose some of these benefits. Here’s why.

Niacin causes cellular metabolism to switch from primarily using glucose as a fuel to primarily using fats, except in the heart, where lipids are the primary fuel and niacin causes a switch to glucose (Carlson, 2005). This switch takes place postprandially, that is, right after you eat, which is when you experience the highest level of blood fats, high enough to increase the risk of a heart attack. That is why some people have a heart attack after eating a heavy meal.

The process of being able to switch between using metabolic substrates is termed metabolic flexibility … (Virtue, 2012).

After eating, fats are taken up and stored by adipose tissue, which releases fatty acids (a process called lipolysis) to the liver and to muscles. “During the fed state, net lipid flux into adipose tissue increases, whereas in the fasted state net lipid efflux predominates” (Virtue, 2012). Niacin prevents lipolysis, the release of these fatty acids from adipose tissue into the bloodstream. (The liver uses the fatty acids to produce triglycerides. The reduction in the availability of free fatty acids for the liver to make triglycerides is why niacin causes a reduction in triglycerides (Virtue, 2012; Kroon, 2017).

There is a strong negative correlation between plasma triglyceride levels and the concentration of HDL—as the level of triglycerides go up, HDL levels go down. The major components of VLDL (very low density lipoproteins) are triglycerides derived from the liver; the VLDL then carry triglycerides in the bloodstream. Reduction of the synthesis of triglycerides in the liver by niacin importantly increases HDL and reduces VLDL.

During the periods when you haven’t eaten (or at night when you sleep), your cells primarily use fats as primary fuel. Taking niacin can’t “switch” the choice of metabolic fuel to fats when you are already using fats as a fuel, but it can reduce the ability of cells to use glucose, which is why some people have a small increase in blood glucose when they use niacin. “We suggest that postprandial FFA [free fatty acid] lowering is the primary mechanism driving the metabolic improvements resulting from NiAc [nicotinic acid, niacin] timed to feeding. Reduced FFA supply to the tissues lowers substrate competition with glucose and improves insulin sensitivity just when it is needed the most (i.e., during the influx of dietary carbohydrate in the postprandial phase), resulting in reduced postprandial hyperglycemia and hyperinsulinemia (Kroon, 2017).”

Thus, the best way to use niacin as a supplement is to take it during or just after a meal, not at other times.

This, incidentally, is one reason why we do not recommend using extended-release niacin: it does not limit niacin to the times when it is best to take it, during or just after a meal.


Another potential benefit from taking niacin is that niacin has been shown in healthy human subjects to reduce the elevated fatty acids and triglycerides that resulted from 2 hours of emotional stress as compared to similar human subjects receiving the same emotional stress but no niacin. (Carlson, 2005, p. 99)


Carlson. Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J Int Med. 258:94-114 (2005).

Kroon et al. Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats. J Lipid Res. 58:31-41 (2017).

Virtue et al, A new role for lipocalin prostaglandin D synthase in the regulation of brown adipose tissue substrate utilization. Diabetes. 61:3139-47 (2012).


(Sandy adapted a recipe from one in POTATO SALAD by Debbie Moose (John Wiley & Sons, 2009))

For about 6 servings, you’ll need

2 pounds of sweet potatoes, cut into 1 – 1 1/2” long pieces

1/2 cup of crumbled blue cheese

1/4 cup chopped fresh chives

1/2 cup coarsely chopped walnuts (or any nuts of your choice)

3/4 cup sour cream

1/4 cup mayonnaise

1/2 tsp. salt

1/2 tsp. freshly ground black pepper

1 tsp. Ineffable Essence (optional—we ALWAYS use it)

1/2 cup chopped celery (or, a tsp or two of celery seed)

1/4 cup chopped onion (shallots are nice)

Cook sweet potatoes until they are soft when you poke them with a fork, 10 to 12 minutes (longer if you live at high altitude). Drain. Chop them coarsely until the texture is something like VERY lumpy mashed potatoes. Then put the lumped potatoes and all the other ingredients into a large bowl. Mix thoroughly.

This recipe is great either at room temperature or after refrigeration. (But do refrigerate the leftovers, if you have any.)

NOTE: Ineffable Essence is a condiment, one of our formulations, consisting of disodium inosinate (a nucleotide found naturally in foods such as meats, cheeses, and vegetables) and monosodium glutamate (yup, the supposed disaster area is found naturally in foods such as meats, cheeses, and vegetables at doses that have never caused any problems and that is how we use it). Ineffable Essence adds natural substances that degrade in foods that contain them, to restore them to levels of fresh food and that add importantly to the flavor of fresh food.


EGCG is connected to lifespan
Lifespan is connected to stress
Stress is connected to obesity
Obesity is connected to cancer
Cancer is connected to diet
Diet is connected to eating
Eating is connected to drinking
And drinking—tea that is—
Is connected to Y O U.

—this silly ditty written by Sandy

The reality is that green tea (in particular, its major polyphenol EGCG (epigallocatechin 3-gallate), is an amazingly inexpensive source of important health benefits, which may include protection against neurodegenerative diseases and cognitive decline with aging to reducing stress-induced disorders to reducing the risk of cancer and cardiovascular disease to increasing lifespan of C. elegans and possibly even to reducing scarring after burns.



Among its many benefits, EGCG has been reported in a number of studies to have anti-inflammatory activity. In one recent study (Kumaran, 2009), 3 months old and 24 months old male albino Wistar rats were studied. They were made hypercholesterolemic by being fed a diet of normal rat chow supplemented with 4% cholesterol and 1% cholic acid. Treated rats also received EGCG (100 mg/kg body weight/day) orally for 30 days. Unsurprisingly, the untreated old rats had abnormally elevated lipid levels, marker enzymes, and inflammatory enzymes in serum, as compared to the young rats. This EGCG dose is roughly equivalent to one of our green tea booster capsules taken three times a day, or 6 cups of green tea a day.

Results showed that treatment with EGCG partially reversed the elevated lipid levels and the inflammatory changes seen in the old rats. For example, elevated levels of TNF-alpha (tumor necrosis factor alpha), CRP (C-reactive protein), and fibrinogen (a clotting factor) were “reverted back to near control values upon supplementation of EGCG.” The authors add, “Plasma CRP, an acute phase reactant has proven remarkably robust as a marker of cardiovascular risk… (Kumaran, 2009). ”

As the researchers (Kumaran, 2009) noted in the introduction: “The lesions of atherosclerosis represent a series of highly specific cellular and molecular responses that is described best as an age-related inflammatory disease.”


One way that EGCG protects against cancer is to reactivate tumor suppressor genes that have been silenced by being methylated. DNA methylation is a method used in the body to make genes inaccessible for the purpose of being expressed. This can be reversed by reducing DNA methylation, which is what EGCG did in a recent study (Nandakumar, 2011). This is important, as DNA methylation increases with aging, one likely reason for the increasing susceptibility of older persons to get cancer.

Studies of green tea have revealed anti-cancer effects in a variety of different cancers, including stomach, small intestine, colon, lung, bladder, prostate, breast, oral cavity, prostate, melanoma, multiple myeloma, acute myelogenous leukemia, and chronic myelogenous leukemia, among others (Kumazoe, 2016). Several studies have shown that the active compounds in green tea extract are the catechins, with EGCG (epigallocatechin-3-gallate) as the most common form (Kumazoe, 2016).


Despite some progress in the treatment of cancer, prostate cancer is still a major killer. Although it can often be brought into remission by blocking androgens, the cancer usually becomes insensitive to androgens and recurs in a different form—it can no longer be controlled by blocking androgens and is then very difficult to treat. Indeed, as of 2006, prostate cancer had become the second leading cause of cancer-related deaths among men in western countries (Bettuzzi, 2006).

A double-blind, placebo- controlled study of 60 men with high-grade prostate intraepithelial neoplasia, 30% of whom would be expected to develop prostate cancer within a year, reported that after a year only one tumor was found in the thirty men treated with green tea catechins (of which EGCG is the major component). The men took three capsules of 200 mg green tea catechins per cap each day for a year. The 30 men who received placebo had 9 tumors diagnosed. (Bettuzi, 2006) This study was particularly impressive considering that the men ALREADY had a form of early prostate cancer that was highly likely to progress to full blown prostate cancer.

In an epidemiological study of 49,920 Japanese men aged 40-69, consumption of green tea (5 or more cups a day) was associated with a dose dependent decrease in the risk of developing advanced prostate cancer, but not of local prostate cancer. The men were followed from 1990 (or 1993) to the end of 2004 (Kurahashi, 2008). These results show an association between green tea and a reduced risk of advanced prostate cancer but cannot be considered proof of causality.


The famous model organism, C. elegans, a free living soil nematode worm, subject of numerous studies including studies of various treatments on lifespan, was in this study (Abbas, 2009) treated with EGCG (220 µm daily) throughout their complete lifespan. The mean lifespan of the treated worms was 16.11% greater than the untreated worms. In addition, when the animals were exposed to lethal oxidative stress, the EGCG-treated worms had a 65.05% increased survival.


For many people, their greatest fear of aging is a loss of mental capabilities or outright dementia. Hence, protecting the brain from decline with age is a powerful motivation.

One study of green tea catechins (with EGCG being the most abundant of these in the tea) followed SAMP10 mice especially bred to have accelerated brain aging (Unno, 2004). The treated mice received free access to food and tap water containing 0.02% green tea catechins for 12 months, while controls had free access to food but plain tap water during the same period. This is roughly equivalent to 400 mg per day of green tea catechins for an adult human (as calculated by body surface area to convert from the mouse dose). The animals were tested for their learning and memory abilities.

One of their memory tests involved the mice receiving a shock when they entered a dark area. Mice normally prefer the dark, so it was instinctive for them to seek darkness and avoid light. However, receiving a shock in dark areas caused the mice to learn to avoid dark areas. Staying in the light area for 300 seconds was used as a measure of the animals’ memories of the shock. Entering the dark area of a chamber divided into dark and light areas was consider a “failure.” The results showed that “[t]he failure ratio [the number of failures out of the total number of entries into the chamber] was significantly lower among the 12-month-old mice that had received GT-catechins than among similarly aged control mice.”

“Among the 12-month-old SAMP10 mice that had been given catechin water, there were fewer individuals with both marked cerebral atrophy and a longer learning time.” The authors discussed possible mechanisms for these results. They explained that green tea has potent antioxidant effects, but in addition to that, they induce increased expression of antioxidant enzymes. The researchers concluded that the preventive effects of GT catechins on brain senescence in these senescence-accelerated mice “may indicate a beneficial effect in maintaining the quality of life during old age.”


After reading about the benefits of EGCG described above, it may not seem nearly as important that it may reduce scarring after burns. But severe (hypertrophic) scars can, in addition to being unsightly, result in “itching, redness, and hard nodular scar tissue often with abnormal sensation.” Worst of all, they “can result in functional loss especially over joints such as in the hand.” This loss of function is the result of contracture as the hard scar tissue inhibits motion (Mehta, 2016).

The prevention and treatment of hypertrophic scars has not improved during recent years, even though survival following extensive burns has improved. Remedies for these severe scars are not readily available. Hence, it is good news that a widely available, inexpensive, and safe constituent of green tea (EGCG, epigallocatechin 3-gallate) has been shown “to inhibit a number of intracellular signalling pathways and reduce expression of pro-fibrotic molecules…” such as vascular endothelial growth factor (VEGF), TGF-beta1 (transforming growth factor beta-1), and CTGF (connective tissue growth factor) which promote the development of hypertrophic scars. (Mehta, 2016)


Abbas and Wink. Epigallocatechin gallate from green tea (Camellia sinensis) increases lifespan and stress resistance in Caenorhabditis elegans. Planta Med. 75:216-21 (2009).

Bettuzzi et al. Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study. Cancer Res. 66(2):1234-40 (2006).

Kumaran et al. Attenuation of the inflammatory changes and lipid anomalies by epigallocatechin-3-gallate in hypercholesterolemic diet fed aged rats. Exp Gerontol.44:745-51 (2009).

Kumazoe and Tachibana. Anti-cancer effect of EGCG and its mechanisms. Func Foods Health Dis. 6(1):70-8 (2016).

Kurahashi et al. Green tea consumption and prostate cancer risk in Japanese men: a prospective study. Am J Epidem. 167(1):71-77 (2008).

Nandakumar et al. (-)-Epigallocatechin-3-gallate reactivates silenced tumor suppressor genes Cip1/p21 and p16INK4a, by reducing DNA methylation and increasing histones acetylation in human skin cancer cells. Carcinogenesis. 32(4):537-44 (2011).

Nehta et al. The evidence for natural therapeutics as potential anti-scarring agents in burn-related scarring. Burns Trauma. 4:15 (2016).

Unno et al. Suppressive effect of green tea catechins on morphologic and functional regression of the brain in aged mice with accelerated senescence (SAMP10). Exp Geront. 39:1027-34 (2004).


The fear of terror from terrorists could be processed in the brain like fear from many severe sources of unpredictable danger. In each case, there are similar mechanisms, one of which is inflammation.

Israel is a place where the fear of terror is chronic, present on a day-to-day basis. Scientists from Tel-Aviv University and other Israeli institutions studied the effect of the fear of terror in 1,152 apparently healthy employed adults (721 men and 431 women aged 20-70) to test the hypothesis that “chronic fear of terror may be associated with low-grade inflammation” by measuring high sensitivity C-reactive protein (CRP), a commonly used indicator of inflammation (Melamed, 2004). (Chronically high levels of inflammation, as indicated by increased C-reactive protein, are associated with an increased risk of cardiovascular disease.)

The results were sexually dimorphic: “Chronic fear of terror in women, but not in men, is associated with elevated CRP levels, which suggests the presence of low-grade inflammation and a potential risk of cardiovascular disease.” “They [the women] not only appraised the situation as more threatening and expressed higher fear of terror, but this also appears to have negative implications to their physical health.” “Elevated CRP levels (>3.0 mg/L) were found in 24.5% of the men and 31.1% of the women.”

Since there is no way for an individual to control the uncertain occurrence of terrifying incidents, preventing the low-grade inflammation that mediates much of the negative health aspects of chronic fear is a possible way to maintain health while living in a state of fear. As noted above, EGCG has been shown in a study to reduce the level of CRP, C-reactive protein, in old rats.


As mentioned above, a recent study found that a “highly traumatized civilian population” had elevated levels of C-reactive protein, an inflammatory marker associated with high levels of stress and a biomarker for increased risk of cardiovascular and metabolic diseases. The “highly traumatized civilian population” were 2692 men and women who were recruited from an inner city hospital (Grady Memorial Hospital in Atlanta, GA) that treated primarily African Americans (Michopoulos, 2015).

Increased CRP was associated with PTSD (posttraumatic stress disorder) symptoms and fear physiology, including “hyperarousal” symptoms, all sounding very much like a “highly traumatized” population. “Individuals with PTSD show elevated levels of the inflammatory cytokines IL-6, IL-1beta, and IL-2…[and] peripheral levels of inflammatory molecules correlate with PTSD symptomology (Michopoulos, 2015).”

A second paper (Shenhar-Tsarfaty, 2014) also studied the relationship between C-reactive protein (CRP) and physiological correlates of chronic fear in a highly traumatized population, 17,380 apparently healthy adult volunteers in Israel. While average maximal pulse values tend to decrease with age (Shenhar-Tsarfaty, 2014), here they found 4.1% of the volunteers had annual pulse increases. Moreover, the observed pulse increases were correlated with elevated CRP levels. The authors concluded: “…consistent exposure to terror threats ignites fear-induced exacerbation of preexisting neuro-immune risks of all-cause ­mortality.”

They explain these results, in part, by noting that pulse is controlled by a number of genetic, environmental and other endogenous factors that “include excessive inflammation, shown to associate with pulse increases [and] to be controlled by cholinergic imbalance (decreased vagal tone or increased sympathetic activity), and to increase mortality (Shenhar-Tsarfaty, 2014).”


Melamed et al. Association of fear of terror with low-grade inflammation among apparently healthy employed adults. Psychosom Med. 66:484-91 (2004).

Michopoulos et al. CRP genetic variation and CRP levels are associated with increased PTSD symptoms and phy siological responses in a highly traumatized civilian population. Am J Psychiatry. 172(4):353-62 (2015).

Shenhar-Tsarfaty et al. Fear and C-reactive protein cosynergize annual pulse increases in healthy adults. Proc Natl Acad Sci U S A., published online Dec. 22, 2014, pp. E467-71.


Increased systemic inflammation has been linked to certain stress-induced psychopathologic disorders, such as posttraumatic stress disorder. In a recent paper (Michopoulos, 2015), researchers found that increased CRP (C-reactive protein) levels were associated with fear-related psychopathology and PTSD in subjects recruited from an inner city public hospital (Grady Memorial Hospital, Atlanta, GA) that primarily served African Americans.

(In addition, CRP levels were found to differ depending upon CRP gene variants, single nucleotide polymorphisms (SNPs). One particular SNP, rs1130864, was found to be significantly associated with increased PTSD symptoms.)

Since C-reactive protein is increased under inflammatory conditions and is itself a promoter of inflammation, a substance that can reduce the levels of C-reactive protein could possibly be beneficial to those under extreme stress or who have a stress-related disorders such as PTSD.

Delayed inhibition of stress or its prolongation can increase susceptibility to many conditions, including cardiovascular disease, diabetes, allergy, immune system disorders, cancer, schizophrenia, Alzheimer’s disease, and depression (Wong, 2010). In fact, C-reactive protein is considered a marker for increased risk of cardiovascular disease and is included in most lab test panels to evaluate CVD risk.

As mentioned above, EGCG was shown to reduce C-reactive protein levels in old rats.


Michopoulos et al. CRP genetic variation and CRP levels are associated with increased PTSD symptoms and physiological responses in a highly traumatized civilian population. Am J Psychiatry. 172(4):353-62 (2015).

Wong et al. Stress and adrenergic function: HIF1alpha, a potential regulatory switch. Cell Mol Neurobiol. 30:1451-7 (2010).


…You need to know that not all forms of selenium are equally effective in doing so and that selenite is likely to be more effective than some other forms, including ­selenomethionine.


Selenium has anticarcinogenic effects, which is a major reason why the mineral is taken as a supplement by so many people. A recent paper (Olm, 2009) explains why, in terms of cancer prevention, selenate, selenocysteine, or selenomethionine may be less preferable than selenite. There, the authors explain what they have discovered about how different forms of selenium can exert different cytotoxic effects against cancer cells.

The researchers found that there is a reductive (anti­oxidant) microenvironment around cancer cells due to the secretion from cancer cells of cysteine that occurs as part of a cystine/cysteine redox cycle. This cycle is under the control of multidrug resistance protein pumps that operate in cancer cells to pump out intracellular molecules cytotoxic to cancer cells such as cysteine. This reductive extracellular microenvironment, in turn, activates selenium into forms that are cytotoxic because they are taken up into the cancer cells where they release deadly hydroxyl radicals. Selenate and selenomethionine were reported (Olm, 2009) to be less able to enter the cancer cells (less redox active). While selenocysteine is redox active, it has to be enzymatically degraded by the enzyme beta-lyase to selenide to achieve its full toxic potential. Moreover, selenocysteine may, the authors suggest, be partly secreted back to the extracellular compartment along the same pathway as cysteine.

The bottom line of this complex mechanism of selenium cancer protective effects is, as proposed in this paper, that there might be a “… possibility of a cancer-specific high-affinity selenium uptake mechanism that might explain cancer-specific selenite cytotoxicity at therapeutic selenite concentrations (μM range) (Olm, 2009).”

We hope that research is done on the use of sodium selenite as an adjunct to cancer chemotherapy. At least some of the cancer cells that are most resistant to chemotherapy will be particularly susceptible to selenite. The reason that chemotherapy so often eventually fails is that the cells that remain alive after that therapy are those that are able to pump the drugs out and, hence, are resistant and can continue to proliferate. The new resistant population is no longer treatable with the original chemotherapeutic regimen. These cells may be especially susceptible to the effects of selenite.

Meanwhile Back at the FDA the Selenium Evidence is Receiving Short Shrift

While considerable evidence supports a role for selenium in cancer risk reduction, the FDA has denied qualified health claims that selenium MAY have anticancer effects and MAY reduce the risk of several types of cancer. In the rarified atmosphere at the FDA, the belief persists that nothing can be communicated to the public as true about dietary supplements or foods unless the FDA first gives you their permission.


Interestingly, the concentration of Se in the Earth’s crust is actually lower than that of gold, making it rarer than gold (Whanger, 2004). It should be no surprise, then, that there are many areas of the world where people live in a low-selenium environment.


The Institute of Medicine of the National Academy of Sciences (2000) has set 400 µg of selenium as the upper tolerable (safe) limit.


Olm et al. Extracellular thiol-assisted selenium uptake dependent on the xc-cystine transporter explains the cancer specific cytotoxicity of selenite. Proc Natl Acad Sci U S A. 106(27):11400-5 (2009).

Whanger. Selenium and its relationship to cancer: an update. Br J Nutr. 91:11-28 (2004).


Vitamin D deficiency has been linked to many chronic disorders, such as multiple sclerosis, inflammatory bowel disease, infections, immune deficiency, cardiovascular disease, hypertension, heart failure, sudden cardiac death, cancer, and Alzheimer’s disease (Gruber, 2015). But, even more than that, low vitamin D levels in serum are associated with increased mortality. In fact, in a recent meta-analysis of 42 randomized trials, taking vitamin D for three years or longer resulted in a significant 6% reduction in all-cause mortality.

In another meta-analysis (this one included 73 observational studies and 22 randomized controlled trials with 849,412 and 30,716 participants respectively), the observational studies were reported to show that “[e]ach decline of 25(OH)D [vitamin D] by 10 ng/mL was associated with a 16% increased risk of all-cause mortality (Gruber, 2015).”

Importantly, however, different forms of Vitamin D have different effects. In the randomized clinical trials noted in the paragraph above, “where vitamin D2 (dose range: 208-4500 IU/day) or vitamin D3 (dose range: 10-6000 IU/day) were given alone vs placebo or no treatment, vitamin D3 significantly reduced the mortality by 11%, whereas vitamin D2 increase[d] the mortality by 4%.” (The increased mortality seen with vitamin D2 was, however, seen with lower doses (<600 IU/day) and shorter average periods of supplementation (less than 1.5 years).) Vitamin D3 is the form of vitamin D that the two of us take.

A third meta-analysis that included 32 studies from January 1966 to January 2013 with more than 500,000 people (about 55 years old), found that serum 25(OH)D levels less than or equal to 30 ng/mL were associated with greater all-cause mortality, as compared to levels over 30 ng/mL. The authors of this meta-analysis also noted that the cutoff point for a deficient intake of vitamin D (20 ng/mL), as recommended by the federal government’s Institute of Medicine was too low to get all the health benefits of vitamin D (e.g., reduced risk of all-cause mortality and diseases such as cancer, autoimmune diseases, etc.). They suggested that the cutoff point should “not be set at 20 ng/mL, but at 30 ng/mL (Gruber, 2015).”

It is notable that the “Institute of Medicine recommended a daily tolerable upper intake (UL) for vitamin D for persons of nine years and older of 4000 IU and the Endocrine Society recommended for adults an UL of 10,000 IU vitamin D (Gruber, 2015).” We take 16,000 IU/day to attain a minimum-mortality sweet spot value of 60 ng/ml. NOTE: Do not take more than 10,000 IU/day unless you also have a blood test to verify that you are not taking too much.

It is also interesting to know that “obese individuals needed 2.5 times more vitamin D to raise the blood levels of 25(OH)D to the same degree as a normal weight person (Gruber, 2015).”

In conclusion, vitamin D3 is an inexpensive way to obtain a variety of potentially important health benefits, including the possibility of living longer.


Gruber et al. Live longer with vitamin D? Nutrients. 7:1871-80 (2015).


Telomeres are the ends of chromosomes that become shorter with each cellular replication—the shortening is associated with age and accelerated by oxidative stress and chronic inflammation. Arthritis, autoimmune diseases, and coronary heart disease have been associated with shorter telomeres (Richards, 2007).

Telomeres are commonly measured on leukocytes, white blood cells. A study of 2,160 women aged 18-79 years found that “[t]he difference in LTL [leukocyte telomere length] between the highest and lowest tertiles of vitamin D was 107 base pairs, which is equivalent to 5.0 years of telomeric aging (Richards, 2007).” This is a very substantial difference, especially considering that the vitamin D was the dietary source rather than supplemental.

With the advent of mostly indoor employment and the widespread use of sunscreens for outdoor recreation to protect against too much ultraviolet light, vitamin D deficiency has become endemic. It makes sense to take a supplement of D3­!


Richards et al. Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. Am J Clin Nutr. 86:1420-5 (2007).


We have now learned why certain evil characters (such as Gollum, Smaug, and an orc) in J.R.R. Tolkien’s “The Hobbit” were all losers in their battles with humans, elves and dwarves: they had a severe vitamin D deficiency! Yes, they were felled as a result, thus answering a longstanding question concerning how such powerful, evil characters could have been such overwhelming losers.

As reported in the Christmas edition of the Medical Journal Of Australia, Nicholas Hopkinson, a doctor at Imperial College, London, and his son Joseph studied the diet, living conditions, and habitat of the characters in “The Hobbit” and made the Earth-shaking discovery that the evil characters were all living in the dark, with poor diets severely deficient in vitamin D.

Meanwhile the hobbit diet was varied, with plenty of vitamin D, and although Bilbo lived in a hole, he liked sitting in a sunny window as well as gardening, getting plenty of exposure to the sun.

The lesson to be derived from this story, according to the good doctor and his son, was that the triumph of good over evil could be explained to some extent by the poor diet of the evil characters and their lack of exposure to sunlight.


(reported in the YAHOO NEWS, 12/15/13

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