May 2008 Blog with Durk and Sandy

An unconstitutional act is not law; it confers no rights; it imposes no duties . . . it is in legal contemplation, as inoperative as though it had never been passed.
— Norton vs. Shelby County 118 US 425 p. 442

D&S Comment: Of course, unconstitutional acts by Congress and administrative agencies are enforced without regard to the above. The bottom line is that current government is mostly illegitimate.

When the magician says, ‘Watch very closely,’ the trick’s already been done.
— Timothy Zahn, Blackcollar 2: The Judas SolutionTo my dismay, IPCC authors ignored all my comments and suggestions for major changes in the FOD (First Order Draft) and sent me the SOD (Second Order Draft) with essentially the same text as the FOD. None of the authors of the chapter bothered to directly communicate with me (or with other expert reviewers with whom I communicate on a regular basis) on many issues that were raised in my review. This is not an acceptable scientific review process.
— Dr. Madhav Khandekar, IPCC 2007 expert reviewer and
meteorologist, Natural Resources Stewardship Project,
as quoted in The New American, February 18, 2008


As of January 2008, four major temperature-trend sources have reported that January 2008 was the latest in a 12-month period of sharp global temperature drops [Hadley Climate Research Unit Temperature (HadCRUT), NASA Goddard Institute for Space Studies (GISS), University of Alabama, Huntsville (UAH), Remote Sensing Systems of Santa Rosa, CA (RSS)].

“This drop in temperature is certainly very unusual. The fall of 0.595 degree since Jan. 2007 is the largest January-to-January drop in HadCRUT since 1875 and the biggest drop for any 12-month interval since –0.681 degree in Feb. 1974.”

“The January temperature is the lowest for any month since 1994, and the lowest for a month unaffected by volcanic eruptions in 20 years.”

All the above plus lots more (including graphs of the temperature trends from each temperature center) was found at

There is a tremendous amount of perceived threat being expressed on the Web and in Science1 and Nature in the “global warming as human-caused disaster” community in response to a new hypothesis of global climate change based upon the effects of the sun’s magnetic field on cosmic rays, which strongly affect cloud formation. What we expect to see, in response to the temperature-drop data, is that the global warmists will frantically look for some way they can manipulate their hypothesis to “explain” global cooling in the context of global warming. In other words, temperatures can go up or they can go down and it is still global warming. This is a giveaway that “global warming” dogma is a religion, not science: when there is no fact that can falsify the hypothesis.

This period of sharp global temperature drops coincides with a sharp decrease in the sun’s magnetic activity, associated with few or no visible sunspots. A drop in the sun’s magnetic activity results in a decrease in the solar interplanetary magnetic field that would otherwise push cosmic rays away from Earth’s atmosphere, resulting in fewer clouds. The energetic particles of cosmic rays serve as nucleation sites for cloud formation. With fewer clouds, the Earth’s albedo is decreased, and hence less of the sun’s energy is reflected back into space. Conversely, with more cosmic rays reaching the atmosphere under conditions of less energetic solar winds, more clouds are formed, resulting in higher albedo and thus cooling.2,3

A final note: As has been pointed out by many, there are more human deaths during cold than during hot weather. Now that the politicians and bureaucrats have seriously damaged fuel-producing markets in the U.S. and elsewhere, a cold trend (should it continue) could be very costly. Wind and solar power are not going to keep most Americans warm!


  1. Pasotti J. Geophysics: daggers are drawn over revived cosmic ray-climate link. Science, January 11, 2008. “Last year, climate change scientists thought they had driven a silver stake through the idea that fluctuations in solar activity were behind global warming in the last century. Now, a high-profile team led by geophysicist Vincent Courtillot, director of the Institut de Physique du Globe in Paris, has sought to raise the dead in a paper linking changes in Earth’s magnetic field to temperature variations in recent millennia. . . . Climate change researchers have set out to strangle the hypothesized climate-geomagnetism connection in its crib.” [Emphasis added] This is remarkably unobjective language for a news report in a supposed scientific journal. Moreover, they did not give the citation for the paper by Courtillot, only that it “appeared last year” in Earth and Planetary Science Letters.
  2. Carslaw et al. Cosmic rays, clouds, and climate. Science 298:1732-7 (2002).
  3. Medvedev and Melott. Do extragalactic cosmic rays induce cycles in fossil diversity? Astrophys J 664:879-89 (2007).


Much has been published of late on the fact that HDL levels alone do not tell you how much protection HDL is affording your cardiovascular system. Under inflammatory conditions and under oxidative stress, the main HDL protein, apolipoprotein A-I, can be modified by reactive oxygen species, and HDL becomes proatherogenic rather than atheroprotective.1

That’s why we were so excited by a recent paper showing that albumin-bound quercetin repairs vitamin E oxidized by apolipoprotein radicals in native HDL3 and LDL2. As the authors explained, the oxidation of tryptophan and tyrosine by hydroxyl radicals may be involved in the myeloperoxidase-induced loss of apoAI structure and activity.2 Vitamin E can repair, but incompletely, the apoAI damage by reduction of tyrosine radicals but not tryptophan radicals. The researchers then found that quercetin bound to albumin, its physiological carrier, “can indeed repair the portion of [tryptophan] and [tyrosine] radicals generated in apoAI, apoAII, and apoB not repairable by [vitamin E].” In fact, it also effectively repairs the tocopheryl radicals formed when the vitamin E scavenges radicals, thereby replenishing the supplies of vitamin E in LDL and HDL3. These were test tube studies that used human HDL3 and LDL.

We include quercetin (130 mg in the recommended 12 capsules daily) in our Personal Radical Shield™.

This effect could be very important; we hope to see more published on it.


  1. Navab et al. Mechanisms of disease: proatherogenic HDL—an evolving field. Nature Clin Pract Endocrinol Metab 2(9):504-11 (2006).
  2. Filipe et al. Albumin-bound quercetin repairs vitamin E oxidized by apolipoprotein radicals in native HDL3 and LDL. Biochemistry 46:14305-15 (2007)


A group of scientists has published a paper on age-dependent gene expression in humans and mice.1 On p. 3244, the authors say, “. . . we identify the transcription factor NF-kappaB as a major regulator of gene expression programs associated with mammalian aging. . . . Here we provide evidence for widespread involvement of NF-kappaB in mammalian aging and demonstrate a reversal of many features of aging upon acute blockade of NF-kappaB in aged skin.”

We have written about NF-kappaB before [Life Extension News, December 2006, published in Life Enhancement, February 2007], as it is importantly involved in the regulation of innate and adaptive immunity, inflammation, apoptosis, and (as suggested by in vitro studies) regulation of cell senescence.1 Excess NF-kappaB activity is also involved in the induction of muscle atrophy, insulin resistance, and neurotoxicity (as in Alzheimer’s disease). An earlier paper reported on NF-kappaB constitutive activation (always turned on) in an animal model of aging.2

Since an NF-kappaB knockout mouse would suffer from embryonic lethality, the authors used a sophisticated technique to allow site-specific inducible or inhibited NF-kappaB activity in mouse skin, but not in other tissues. These animals had normal development, lifespan, and age-dependent induction of NF-kappaB activity in the skin.

They used a compound, 4-OHT (4-hydroxytamoxifen), that inhibited NF-kappaB activity. “Upon NF-kappaB blockade in old skin, expression of 225 of these 414 genes [differently expressed in old as compared to young skin] (54%) was reduced to expression levels indistinguishable from those of the young samples. . . . No gene was significantly altered by 4-OHT treatment that was not also reciprocally altered by aging (FDR<0.05 cutoff).” Markers of cell senescence (SA-beta-gal, p16INK4a) that were induced in aged skin were significantly decreased upon NF-kappaB blockade.

“Interestingly,” the authors note, “seven NF-kappaB target genes identified in this study possess homologs that extended lifespan when inactivated in C. elegans.

As we wrote in our earlier article, there are a number of natural products that suppress NF-kappaB activity (not necessarily by the same mechanism), as reported in Reference 3, including alpha-lipoic acid, astaxanthin, capsaicin, curcumin, EGCG (found in green teas), L-ascorbic acid, alpha-tocopherol, quercetin, resveratrol, silymarin, theaflavin (found plentifully in fermented teas), aged garlic extract, apple juice, blueberry and berry mix, Ginkgo biloba extract, red wine, glucosamine sulfate, melatonin, fish oils, and others. Reference 4 also adds glutathione, aspirin, and others. Reference 5 reports a new study in which cinnamaldehyde, the major component of cinnamon, suppressed age-related inflammatory NF-kappaB activation in rats. [Suggestion: Add three teaspoons of cinnamon to a batch (one container) of LifeByChocolate™ chocolate pudding. Delicious way to get cinnamaldehyde!]

A note of caution: You do not want to inhibit NF-kappaB entirely; if you didn’t have it at all, you’d die. (Remember, the NF-kappaB was knocked out only in the mouse skin because a global knockout would have been embryonically lethal owing to the importance of NF-kappaB in development. The inflammatory activity of which NF-kappaB is an important part is also essential to proper immune activity against bacteria, viruses, and cancer cells.) The idea here is to prevent excessive and chronic activation of NF-kappaB, an important part of the increased inflammatory activity with aging. The substances we take for this and other purposes (below) have not been reported to impair immune activity, increase the risk of cancer (in fact, they generally reduce the risk), or have cytotoxic effects at the doses we use them. But this is still an experiment because there are no data in animals, let alone humans, on such complex combinations of substances.

The fly (or, perhaps, the elephant) in the ointment is that there is limited information on what is a healthy range of NF-kappaB levels, nor is there a readily available lab test that would provide NF-kappaB levels for specific knowledge of your systemic NF-kappaB status. Thus, moderation is essential. The substances that we take that moderate our NF-kappaB levels (though they have many other effects) are the following. Follow the label-recommended dosages. Alpha-lipoic acid (from AGEless™); melatonin (found in Serene Tranquility™ nighttime formulations); vitamin C [from Double C™ and Personal Radical Shield™ (PRS)]; alpha-tocopherol; curcumin (we take turmeric itself, as it contains 40% curcumin; also found in nutritional supplements); quercetin (from PRS); resveratrol (from MealMate™); fermented teas (black, pu-erh, oolong, from ShapeShifter Teas™); green tea (EGCG source, from ShapeShifter Teas™); silymarin; Ginkgo biloba; red wine; fish oils (from Omega-3 HeartFelt™); and cysteine (to increase glutathione levels; from Root Food™).


  1. Adler et al. Motif module map reveals enforcement of aging by continual NF-kappaB activity. Genes Devel 21:3244-57 (2007).
  2. Spencer et al. Constitutive activation of NF-kappaB in an animals model of aging. Int Immunol 9(10):1581-8 (1997).
  3. Aggarwal et al. Nuclear factor-kappaB: a holy grail in cancer prevention and therapy. Curr Signal Transduc Ther 1:25-52 (2006).
  4. Garg and Aggarwal. Nuclear transcription factor-kappaB as a target for cancer drug development. Leukemia 16:1053-68 (2002).
  5. Kim et al. Suppression of age-related inflammatory NF-kappaB activation by cinnamaldehyde. Biogerontology 8:545-54 (2007).



Many raw materials used in dietary supplements, such as herbs and vitamins, are produced in China and frequently dominate the market, owing to lower prices. Unfortunately, problems with Chinese quality control in, for example, children’s toys and generic drugs, have made the use of Chinese raw materials problematic. Now there is good news to report!

The United States Pharmacopeia (USP), a private standards-setting organization for prescription and over-the-counter drugs, as well as dietary supplements, opened its third international facility in September 2007 in Shanghai, China. In HerbalGram issue 77, 2008 (, it was reported that “The new USP-China facility will also implement a new program of the Natural Products Association (NPA) for testing Chinese raw materials for conformity to their specifications, including identity, purity, and composition.” Of course, Chinese suppliers will need to submit ingredients if they want the USP testing (which will not be free), and not all will do so. Presumably, there will be a certification process, perhaps with a label designation, to identify the USP-tested and approved ingredients.



There has been considerable research done and many papers published on the medicinal properties of various mushrooms, mostly exotic varieties. A new paper now reports enhanced immune function in C57BL/6 mice eating the common white button mushrooms, which account for 90% of all mushrooms consumed in the U.S.1

Mushroom powder was added to the base diet at levels of 2% by weight or 10% by weight. The controls received the base diet that was adjusted with additional ingredients to equalize the levels of total energy and macronutrients (carbohydrates, protein, and fiber) in the experimental diet.

Natural killer (NK) cell activity was significantly enhanced by mushroom supplementation in a dose-dependent manner. “Similar results (data not shown) were obtained when NK activity was expressed as killing activity per given number of NK cells . . .” NK cells are specialized lymphocytes, part of the innate immune system, that spontaneously kill pathogen-infected cells and tumor cells. IFNgamma (interferon gamma) is “the most important cytokine in mediating NK activity.” IFNgamma was increased in splenocytes in the experimental mice. The study found that “Con A- and PHA-stimulated IFNgamma production and NK activity in splenocytes were significantly and positively correlated.” As the authors explain, “IFNgamma is thought to play an essential role in NK cell-mediated suppression of viral and bacterial infection and the inhibition of tumor initiation and metastasis.” (References in quote not included here.)

White button mushrooms may not be as tasty as some exotic medicinal mushrooms, but they are much less expensive, a great advantage at a time of soaring food prices.


  1. Wu et al. Dietary supplementation with white button mushrooms enhances natural killer cell activity in C57BL/6 mice. J Nutr 137:1472-7 (2007).



Autophagy (“self-eating”) is an important process in which defective organelles (such as mitochondria), aggregated proteins, and other undesirable cellular contents are “eaten” in autophagosomes and the constituents recycled. In fact, autophagy is not just important in the context of getting rid of “garbage.” Between meals, the liver and other organs routinely get some of the raw materials they need, such as amino acids and energy, via autophagy.1 As such, autophagy is important for survival during starvation.

As the authors of Reference 1 explain, “. . . the requirements for autophagy is [sic] even more evident under disease conditions. Recent studies reveal that degradation of disease-related mutant proteins is highly dependent on autophagy in addition to the ubiquitin-proteasome system.” Autophagy function is known to decline with aging and cancer has been genetically linked to autophagy malfunction.1 Moreover, loss of autophagy in the central nervous system has been shown to cause neurodegeneration in mice.2,3

A very recent paper4 reports that lithium, at least in part by inducing autophagy, delayed the progression of amyotrophic lateral sclerosis (ALS) in 44 human patients affected by ALS. The patients received either riluzole (a standard drug treatment) or the same amount of riluzole plus two daily doses of 150 mg of lithium carbonate. Lithium delayed the development of ALS in the patients receiving it. “In fact, all subjects treated with lithium were alive at the end of the follow up (15 months) . . . By contrast, ~30% of the patients receiving [only] riluzole died during the study.” This survival difference was significant at 12 and 15 months. “When we compared the groups at the end of the follow up, the mean decrement in the normalized Norris score [a measure of disease progression] was 46.1% in patients receiving riluzole only and 10.6% in those receiving lithium.” The authors conclude that the patients receiving lithium had “very slow” progression in their disease as compared to those not receiving lithium.

In the same study, the researchers examined the effects of lithium treatment on the survival of motor neurons in a mouse model of ALS. They found preservation of the size of the motor neurons, preservation of motor neuron number and size in those areas that (in the ordinary course of the disease) degenerate later, and decreased aggregation of alpha-synuclein, ubiquitin, and SOD1. Moreover, the administration of lithium resulted in a marked increase in autophagy vacuoles, signifying induction of autophagy.

The dosage given the human patients, 150 mg of lithium carbonate twice daily, is far more than the low-dose lithium (1–4 mg per day) contained in a normal daily consumption of lithium-containing mineral waters. It is, in fact, within the therapeutic range of lithium taken by those with bipolar disorder for mania. Hence, we would not suggest that such a high dose be used only for the induction of autophagy in those without ALS, in light of potential side effects at therapeutic dosage levels.5 It is not clear whether low-dose lithium can induce autophagy; this would be a worthy subject for an aging research project, since even a small increase in autophagy could be a practical antiaging strategy.

1. Mizushima et al. Autophagy fights disease through cellular self-digestion. Nature451:1069-75 (2008).
2. Komatsu et al. Loss of autophagy in the central nervous system causes neurodegeneration in mice. Nature 441:880-4 (2006).
3. Hara et al. Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice. Nature 441:885-9 (2006).
4. Fornai et al. Lithium delays progression of amyotrophic lateral sclerosis. Proc Natl Acad Sci USA 105(6):2052-7 (2008).
5. Nielsen et al. Proteomic analysis of lithium-induced nephrogenic diabetes insipidus: mechanisms for aquaporin 2 down-regulation and cellular proliferation. Proc Natl Acad Sci USA 105(9):3634-9 (2008).

Sirt1 Inducers Such as Resveratrol May Increase Autophagy

Just as we were nearly finished writing this issue, we read an exciting, newly published paper6 that indicates that Sirt1 also induces autophagy. Autophagy is induced by starvation or chronic caloric restriction, and Sirt1 has been shown to be required for the beneficial changes of caloric restriction in mice.6 The new paper examined the role of Sirt1 in detail in a cell-culture study.

Sirt1 is a histone deacetylase, that is, it regulates whether a gene is turned on or off by modifying the acetylation of histones surrounding DNA to allow or not allow access to gene transcription molecules. The researchers of the new paper found that the absence of Sirt1 leads to markedly elevated acetylation of proteins known to be required for autophagy; the elevated acetylation deactivates them. They show that Sirt1 knockout mice embryonic fibroblasts do not fully activate autophagy under starved conditions. “Reconstitution with wild-type but not a deacetylase-inactive mutant of Sirt1 restores autophagy in these cells.”

The authors propose that Sirt1 can increase the manufacture of new mitochondria and, by inducing autophagy, stimulate the clearance of defective mitochondria. They and others have shown that “Sirt1 can interact and regulate the activity [of] the mitochondrial biogenesis regulator peroxisome proliferator-activated receptor 1alpha (PGC-1alpha). Most evidence suggests that Sirt1 can augment PGC-1alpha activity and thereby increase the supply of new mitochondria. In this report, our data would suggest that by regulating autophagy, Sirt1 may also be important for the clearance of old and damaged mitochondria.”

There is evidence that resveratrol improves mitochondrial function by activating Sirt1 and PGC-1alpha.7 Thus, resveratrol very possibly enhances autophagy. We take resveratrol as a functional component in our MealMate™, a weight-control formulation. Another recent paper8 reports that NF-kappaB activation mediates the repression of autophagy in response to TNF-alpha (tumor necrosis factor-alpha) in three models of cancer cell lines. “In contrast,” the authors report, “in the absence of NF-kappaB activation, TNF-alpha induces macroautophagy (autophagy) . . .”

6. Lee et al. A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy. Proc Natl Acad Sci USA 105(9):3374-9 (2008).
7. Lagouge et al. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell 127: 1109-22 (2006).
8. Djavaheri-Mergny et al. Regulation of autophagy by NFkappaB transcription factor and reactive oxygen species. Autophagy 3:4, 390-2 (July/Aug. 2007).

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