PharmacoNutrition Reviewed

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/
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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/
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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!

Source: Nutrition & Metabolism (2007), 4: 5 (Open Access)
Article Type: Original Research
Authors: W Zhou, P Murkerjee, MA Kiebish, WT Markis, JG Mantis, TN Seyfried

Image taken from:
http://3quarksdaily.blogs.com/3quarksdaily/images/brain_21.jpg

Ketogenic diets have been in clinical use for more than 80 years, primarily for the symptomatic treatment of epilepsy. In contrast to other organs, the brain almost exclusively needs glucose to satisfy its energy requirements. As an alternative, the brain can utilize ketone bodies for generating energy and fuelling its metabolism. Normal, healthy brain cells can better cope with this shift in energy source than tumour cells. Admittedly, to combat malignant brain cancer this way is a smart idea, especially as it appears so simple by using principles of evolutionary biology. And the concept works well, at least in this preclinical study on mice with implanted brain tumours. Mice fed a ketogenic diet displayed reduced glucose and enhanced ketone levels, finally causing the starvation of cancer cells. Cancer cells are also quite susceptible to oxidative stress; ketones, however, reduce the production of reactive oxygen species (ROS), as shown in neurons exposed to glutamate excitotoxicity (Maalouf et al.).
Of note, the same, i.e. the shift from glucose to ketone body metabolism, also happens in times of caloric restriction which has been shown to enhance the life span of many animal species.
All in all, the issue of using ketone bodies and ketonic diets for improving human health is quite promising, although much still needs to be done to fully understand the nature of their biological action.