PharmacoNutrition Reviewed

While I am still struggling to digest Richard Dawkins’ “Ten Commandments” raised in his new book “The God Delusion”, I just found on Ouroboros - Research in the Biology of Aging a hint regarding another list of “Ten Commandments”, this time for the future of aging research in the UK.
As I am particularly interested in diet & nutrition, the 6th commandment caught my attention as is states the word “nutrient” in connection with an individuals’ genetic make-up and response to enviromental impact.
The original article is freely availabe at BMC Geriatrics.

Source: Lancet 369: 1876-1882
Article Type: Meta Analysis
Authors: X Wang et al.

More than a decade ago, homocysteine has been suggested to act as an independent risk factor for the development of cardiovascular disease (CVD). Luckily, homocysteine levels can easily be modified, i.e. reduced, in states of adequate folic acid/folate (FA) intake. Whereas nobody doubts that FA supplementation is able to significantly reduce homocysteine levels in humans, there is an ongoing debate of whether homocysteine is indeed a risk factor or an innocent bystander.
The recent meta analysis by Wang an colleagues argues for a beneficial effect of FA supplementation on human health, here stroke prevention. The risk of stroke was reduced by 18% and the effect of FA supplementation was greater in those studies with longer duration. Although this meta analysis aimed to establish a link between FA supplementation and primary stroke prevention, there are several confounders that ought to be considered (for details see CM Carlsson’s comment, Lancet 369). To get a better picture of the true potential of increasing FA intake in terms of health outcome, I also recommend reading another meta analysis which has been published in 2006 in JAMA 296 and confirmed that FA supplementation did not reduce the risk of CVD or all-cause mortality in patients with pre-existing disease.
Last but not least, for all who would like to get a quick overview on homocysteine, you might want to go to the following wepage www.homocysteine.net run by Axis-Shield, a diagnostic company based in the UK.

Image taken from: strokecenter.org

Source: The Journal of Nutrition 137: 1493-1495
Article Type: Opinion
Author: H. Sies

Several times we discussed already the pros and cons of measuring “total antioxidant capacity” in food or biological fluids.
Today, I would like to somewhat conclude this issue by referring you to a recent article by Helmut Sies from Düsseldorf University, Germany. As there’s nothing to add, I would like to cite the article’s abstract as it is:

“In this contribution, I discuss the applicability of total antioxidant capacity (TAC) data obtained from plasma to human health issues and the use of TAC data for dietary items in epidemiological applications. Against the background of knowledge that major antioxidant defense is enzymatic, the use of the term “total” is not appropriate. Because dietary phytochemicals undergo uptake and metabolism, extrapolation to health effects requires direct molecular information, not a global parameter that uses an arbitrarily selected prooxidant source. Suitable alternatives are given in measuring functional biomarkers (surrogate endpoints). Although using TAC may be helpful in comparing different food items, the extrapolation to their contribution of antioxidant defense in vivo and, further, to health issues, should be discouraged, with the possible exception of the gastrointestinal tract. This is of particular importance because dietary phytochemicals and other small molecules have nonantioxidant activities. Direct assay of urate, ascorbate, and tocopherol, the major small-molecule contributors to TAC, is recommended.”

Image taken from: Crodausa

In March this year Coca Cola announced in a press release the launch of Diet Coke Plus. This new member of the Coke beverage family will provide the consumer with 15% Daily Value of the vitamins B3, B6 and B12 as well as with 10% Daily Value of zinc and magnesium (calculated per eight-ounce serving).
Well, maybe this offers a great opportunity for a prospective, large scale health trial - considering the 1.4 billion servings Coke sells each day. I just worry somewhat about the data collection………

Out of interest I quickly searched Pubmed and here’s what I found (selection):

Belpoggi F et al.:
Results of long-term carcinogenicity bioassays on Coca-Cola administered to
Sprague-Dawley rats.
Ann N Y Acad Sci. 2006, 1076:736-52

Ladas SD et al.:
Gastric phytobezoars may be treated by nasogastric Coca-Cola lavage.
Eur J Gastroenterol Hepatol. 2002, 14:801-3

Malhotra S et al.:
Effect of an acidic beverage (Coca-Cola) on the pharmacokinetics of carbamazepine in healthy volunteers.
Methods Find Exp Clin Pharmacol. 2002, 24:31-3

Ellertson C:
History and efficacy of emergency contraception: beyond Coca-Cola.
Fam Plann Perspect. 1996, 28:44-8

Image taken from: wikimedia.org

Source: Nutrition Journal (2007), 6:10
Article Type: Original Research
Authors: G McNeill et al.

Image taken from: http://www.buzzle.com/img/articleImages/431619-54med.jpg

Just recently, I discussed the possibility of mutivitamin supplementation negatively affecting mortality. And there’s more bad news.
In their randomised controlled trial, Mc Neill and colleagues again confirm the inefficiency of multivitamin/-mineral supplementation (duration: 12 months) for the improvement of cognitive function in elderly (>65 years of age) subjects. As the article is freely available I will leave it to you to read the details.
I just wonder if we ever will have the chance to read the report of a prospective study assessing the impact of at least 15-20 years of multivitamin/-mineral supplementation starting well before (!) ongoing biological havoc prevents any possible health-beneficial effect of such intervention.

Image taken from: http://homepage.ntlworld.com/
andrew.lipson/escher/relativity.jpg

If you want to know why science too often goes down the drain, I recommend you check out the BadScience blog written by Dr. B. Goldacre.
Although the content of some posts, like the recent one on the vitamin-guru Matthias Rath, should be sufficiently known to the public, the response quackery science attracts keeps me wonder about the incidence of common sense.

Source: Neurobiology of Aging (2007), in press
Article Type: Original Research
Authors: A Bender et al.

Image taken from: http://www.scienceinafrica.co.za/pics/06_2004/brain.jpg

Creatine (an amino acid derivative) is a widely used food supplement due to its putative ergogenic, i.e. exercise capacity enhancing, effect. In terms of exercise performance, a recent review by Paddon-Jones and colleagues (J. Nutr. 134) concludes that creatine is suggested to be of benefit to exercise lasting 30 seconds or less; in contrast, no direct effect of creatine supplementation on muscle protein synthesis has been found. Nonetheless, creatine sales still reached US$ 220 million in 2005.
So whereas creatine might do rather little to improve exercise performance, it still seems to improve health. And not only this, but also survival – at least in mice. Based on previous reports demonstrating protective effects for creatine in models of neurodegeneration, Bender et al. tested the hypothesis whether creatine might also facilitate healthy aging, particularly of the brain, in wild-type mice. In essence, feeding mice a diet containing 1% creatine from 12-month of age onwards, significantly increased both mean and maximum life span in comparison to control mice. Somewhat confirming what was said already above, the creatine-fed mice did not differ in the rotarod and grip strength analyses; however, creatine feeding improved (p<0.05) several markers of memory performance such as object recognition. Also, biomarkers of brain aging due to oxidative stress tended to be lower in the creatine-fed group. Based on gene expression profiling experiments, the authors conclude that creatine not only reversely regulates gene expression altered in aging, but also concordantly affects gene expression as in mice on caloric restriction. Whether this effect of creatine is due to the induction of mild stress like in the case of caloric restriction is unknown. Another potential mechanism of creatine-induced neuroprotection might be the prevention of ROS (recative oxygen species) generation due to enhanced activity of mitochondrial creatine kinase activity, as recently shown by Meyer et al. (JBC 281).
In light of the rather minor safety concerns raised regarding creatine supplementation, it might be worth to further explore the potential of this amino acid derivative to improve healthy aging.

Source: Breast Cancer Research (2007), 9: 201
Article Type: Review
Authors: M Gago-Dominguez, X Jiang, JE Castelao

Image taken from: http://www.massgeneral.org/cancer/crr/types/breast/
illustrations/images/breast_lymph.jpg

In most experimental settings and disease states, lipid peroxidation, notably HNE, MDA or isoprostanes, are considered to be detrimental for the survival of the affected cells/tissue/organ.
The review by Gago-Domingeuz et al., however, summarizes compelling evidence that, at least in the case of breast cancer, in might just be the other way around.
Whereas enhanced lipid peroxidation promotes the onset of liver, kidney and skin cancer as well as of neurodegenerative diseases, the same process seems to protect women from falling ill with breast cancer. Even more surprising is the fact that quite a number of food constituents well known to reduce harmful oxidative and nitrosative stress appear to promote lipid peroxidation in breast cancer cells. Let’s look, for example, at marine omega-3 fatty acids and green tea. The authors refer to a previous publication “of results in humans implicating the peroxidation products of marine omega-3 fatty acids as the proximal anticarcinogens.” In terms of tea, Gago-Dominguez and colleagues conclude “that the protective effect of tea on breast cancer was confined to those possessing the low-activity genotype of the antioxidant catechol-O-methyl transferase (COMT), putatively because more beneficial peroxidation agents could reach the cancer cell and cause damage”.
Admittedly, this is a hypothesis, but one really worth thinking about, especially as the presented evidence is quite strong. What I am missing, though, is a bit more elaboration on how the dietary constituents exert their antidromic biological activities, which are nonetheless always in favour of an individual’s health.
Is it maybe still just a matter of our genes?

Source: The Journal of Nutrition (2007) 137: 979-984
Article Type: Original Research
Authors: MS Golub, CE Hogrefe, SL Germann

Image taken from:
http://content.answers.com/main/content/wp/en-commons/thumb/f/fe/
180px-Views_of_a_Foetus_in_the_Womb_detail.jpg

Iron deficiency (ID) during pregnancy, especially the third trimester, is common throughout the world. Aside from affecting maternal heath, ID already at moderate levels has been shown to hamper brain development and cognition not only in animal but also human subjects.
In their current paper, Golub et al. report on the impact of iron deprivation during foetal development (third trimester) on behaviour in juvenile rhesus monkeys. Athough ID compromised haematological status, no effect was seen on growth or neurological function at birth (Golub et al., AJCN 2006). However, when animals were reassessed from 6 to 12 months of age, prenatally iron-deprived juveniles had significantly “altered behavioural regulation in learning and memory tasks. (…) In relation to conceptualization of childhood behaviour, they demonstrated lower reactive control, greater impulsivity, reduced harm avoidance, and greater novelty seeking.” As possible explanation, the authors suggest changes in the brain dopamine D2 receptor system, which has been reported to be decreased upon states of prenatal ID.
In light of the above mentioned data, the widespread occurrence of ID and anemia in women of child-bearing age is really unfortunate, and just reminds one that interventions such as supplementation and fortification are obviously still not efficient enough to ensure adequate dietary iron intake in this particularly vulnerable part of the population.

Image taken from: http://content.grin.com/binary/hade/14889/4.gif

Today, I would like to draw your attention to a recent post on Marc Joseph’s Nutrition Blog where he’s featuring a hot topic article (published in Neuron) on how epigenetics might drive information storage in the brain.

Looking for more information? Try Epigenetics News!