NEWFLASH for Chromium, Potassium, Vitamin D, and Galantamine

Don’t Be Nutritionally Deficient

Does It Matter What Type of Chromium You’re Using?

Is it possible to take enough chromium and still be deficient? According to a recently published paper, conducted at the Georgetown University Medical Center in Washington, DC, a comparison of different types of trivalent chromium supports a conclusion that “enough” may be insufficient.1 Scientific studies have found that the average individual becomes chromium deficient with age, a fact that is highly associated with aspects of metabolic syndrome, insulin resistance, and type 2 diabetes. Ironically, while replacement of chromium may reduce harmful manifestations associated with insulin resistance and diabetes . . . it may not. Here’s why.

There are many commercial trivalent chromium compounds available in the marketplace, each with a distinctively different form. (Trivalent chromium, as a class, has a very large safety range, for which there have been no documented signs of side effects in any of the nutritional studies at levels up to 1 mg per day.2 A recent study conducted by Dr. Richard Anderson found no evidence for DNA damage.3) Despite previous reports showing that the location of the negative charges of trivalent chromium can influence effectiveness markedly, no one has investigated this, until now.

The Georgetown researchers (who include famous dermatologist Nicolas Perricone, M.D.*) compared various commercial forms of trivalent chromium commonly used alone or in formulations, to examine whether they are equally effective and non-toxic.


*Dr. Perricone has a potential conflict of interest due to his avocation of one of the six chromiums tested. Another of the authors, Sidney J. Stohs, Ph.D. is an officer in the company that markets that form of chromium.


Two studies were conducted using spontaneously hypertensive lab rats. In the first study, there were five different trivalent chromium forms examined: citrate, amino acid chelate, chelavite, polynicotinate, and nicotinate. In the second study, only the effects of polynicotinate and picolinate were assessed. In study #1, only chelavite and polynicotinate demonstrated the ability to improve insulin sensitivity, and only polynicotinate decreased systolic blood pressure to a significant degree. In study #2, both picolinate and polynicotinate were found to significantly decrease systolic blood pressure when compared to controls.

Of further interest, polynicotinate and picolinate decreased free radical formation (as measured by malonyldialdehyde concentrations) and DNA fragmentation in liver and kidney tissues. There was no evidence of adverse effects with any of the compounds tested and at conclusion, while all the trivalent chromium compounds were deemed safe, only three enhanced insulin sensitivity (polynicotinate, chelavite, and picolinate) and only two decreased SBP significantly (polynicotinate and picolinate). Moreover, both polynicotinate and picolinate were protective in lessening free radical formation and DNA damage in the liver and kidneys.

If You’re Potassium Deficient, You’re Certainly Not a Caveman

As Durk Pearson and Sandy Shaw explain this month in Life Enhancement (see page 11 and page 15), virtually everyone is potassium deficient. Back in the bad old days, everything wasn’t bad. For example, potassium and sodium levels and ratios were nearly the reverse of what they are today, the consequences of the Paleolithic diet, and a good thing for certain aspects of health. Premised on the idea that 50,000 years are not enough to accommodate changes in dietary shifts, Durk & Sandy believe it’s about time to—not necessarily eat exactly like a Caveman—but to shift to some aspects of the Paleolithic diet, and become potassium proficient. Potassium bicarbonate, in their view, opens a doorway to reaping the benefits of significantly improved health by reducing blood pressure, increasing muscle mass, decreasing bone loss, and more.

You May Be Deficient in Vitamin D if You’re Fat

In a study recently conducted in sunny southern California, women with insufficient levels of vitamin D were significantly heavier and had greater body mass than their counterparts with sufficient levels of vitamin D. This is according to Dr. Vicente Gilsanz and colleagues of the Children’s Hospital of Los Angeles.4

As most of you know, vitamin D—a regulator of bone metabolism and instrumental to a great many biological functions—can be obtained through exposure of the skin to direct sunlight. The new report finds that there is a correlation between low levels of vitamin D and obesity. Despite inconstant results in past studies, Gilsanz et al. examined the relationships between vitamin D levels, body fat, and bone structure among postpubertal women in sun-soaked California. Surprisingly, only 37 of the 90 women in the study had sufficient concentrations of the vitamin D metabolite 25-hydroxyvitamin D (30 ng/ml or above). The remainder of the group has such low levels that they were deficient in vitamin D. The researchers concluded, “Our study indicates that vitamin D insufficiency is extremely common in young women living in a sun-rich area of the United States.”

While there was no association between vitamin D levels and bone measurements in young women who were between 16 and 22 years old, same-age counterparts with insufficient vitamin D levels were heavier by about 16.3 pounds on average. The vitamin D insufficient group also averaged 3.4 points higher in body mass measurements. Moreover, the researchers found an “unexplained and intriguing” positive link between height and vitamin D. In other words, higher levels of vitamin D add UP!

Good News for Galantamine Users

Galantamine Can Prevent the Neuronal Oxidative
Damage Induced by Amyloid-Beta Peptide

The legendary phytonutrient galantamine, woven into Homer’s story of memory recovery in The Odyssey, is currently used for the treatment of Alzheimer’s disease spanning mild-to-moderate-to-severe (see the March issue). As we have recently learned, galantamine’s action goes beyond helping with cholinergic transmission, a key factor in memory. It can also protect neurons against amyloid-beta peptide, which is involved in Alzheimer’s swathe of pathogenesis. In a new study, researchers at the University of Coimbra in Portugal treated cultured rat cortical neurons with two forms of amyloid-beta peptide, and found that galantamine prevented neurodegeneration induced by both peptide forms in a concentration-dependent manner.5

Furthermore, when neurons were co-incubated with fresh amyloid-beta peptide, plus galantamine, the amount of amyloid aggregates was reduced.* Because oxidative conditions influence Abeta aggregation—indeed fresh or aged amyloid-beta peptide significantly increases reactive oxygen species and lipoperoxidation, the researchers investigated whether galantamine prevents oxidative stress induced by this peptide. And indeed galantamine prevents it. How? The amyloid-beta peptide causes the depletion of reduced glutathione in neurons, which appears to be related to the decrease in glutathione peroxidase and glutathione reductase (valuable antioxidants made in the body) activities. These alterations in the reduced glutathione antioxidant system were prevented by galantamine. When taken altogether, these results represent the first evidence that galantamine can prevent the neuronal oxidative damage induced by amyloid-beta peptide. They provide in vitro support for the beneficial actions of galantamine in the Alzheimer’s neurodegenerative process.


* Incidentally, these aggregates— as well as lysosomal lipofuscin, ceroid bodies, advanced glycation end-products (AGEs), and cytoplasmic inclusions observed in senescent cells—are caused by misfolded proteins, which can be controlled to some degree by supplementation with osmolytes (see the Sept. 2008 issue).


Acetylcholinesterase Inhibitors May Slow the Progression to Alzheimer’s

Individual randomized clinical trials with acetylcholinesterase inhibitors (AChEIs) aiming to delay the progression from mild cognitive impairment (MCI) to Alzheimer’s disease (the leading dementia) have not rung loudly in its favor. So a group of Brazilian scientists, wanting to know the truth, conducted a meta-analysis of the AChEIs randomized clinical trials at the University of São Paulo to assess whether pooled analysis could show the benefit of these drugs in delaying the progression from MCI to Alzheimer’s disease.6

The researchers searched for references of published and unpublished studies in electronic databases (Medline, Embase, Web of Science, and Clinical Trial Database Registry, particularly the Clinicaltrials.gov [www.clinicaltrials.gov]). They retrieved 173 references, which yielded three references for data extraction. A total of 3,574 subjects from four studies were included in the meta-analysis. Among 1,784 subjects (nearly 50%) allocated in the AChEI-treatment group, 275 (15.4%) progressed to Alzheimer’s/dementia, as opposed to 366 (20.4%) out of 1,790 subjects in the placebo group. The relative risk for progression to Alzheimer’s/dementia in the AChEI-treated group was 0.75. The patients in the AChEI group had a significantly higher all-cause dropout risk than the patients on the placebo group. The relative risk for serious adverse events in the AChEI-treated group showed no significantly statistical difference from the placebo group. In their conclusion, the researchers found that the long-term use of AChEIs in subjects with MCI may lessen the risk of progression to Alzheimer’s/dementia, and that this finding may alter public health and pharmaco-economic policies with regard to AChEI endorsement.

References

  1. Preuss HG, Echard B, Perricone NV, Bagchi D, Yasmin T, Stohs SJ. Comparing metabolic effects of six different commercial trivalent chromium compounds. J Inorg Biochem 2008 Nov;102(11):1986-90. Epub 2008 Jul 31.
  2. Anderson RA. Chromium as an essential nutrient for humans. Regul Toxicol Pharmacol 1997 Aug;26(1 Pt 2):S35-41.
  3. Hininger I, Benaraba R, Osman M, Faure H, Marie Roussel A, Anderson RA. Safety of trivalent chromium complexes: no evidence for DNA damage in human HaCaT keratinocytes. Free Radic Biol Med 2007 Jun 15;42(12):1759-65. Epub 2007 Mar 24.
  4. Kremer R, Campbell PP, Reinhardt T, Gilsanz V. Vitamin D status and its relationship to body fat, final height, and peak bone mass in young women. J Clin Endocrinol Metab 2009 Jan;94(1):67-73. Epub 2008 Nov 4.
  5. Melo JB, Sousa C, Garção P, Oliveira CR, Agostinho P. Galantamine protects against oxidative stress induced by amyloid-beta peptide in cortical neurons. Eur J Neurosci 2009 Feb;29(3):455-464.
  6. Diniz BS, Pinto JA Jr, Gonzaga ML, Guimarães FM, Gattaz WF, Forlenza OV. To treat or not to treat? A meta-analysis of the use of cholinesterase inhibitors in mild cognitive impairment for delaying progression to Alzheimer’s disease. Eur Arch Psychiatry Clin Neurosci 2009 Feb 17. [Epub ahead of print].


Will Block is the publisher and editorial director of Life Enhancement magazine.

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