PharmacoNutrition Reviewed

Source: J. Pediatr. (152) 2008: 79-84
Article Type: Original Research
Authors: Aaltonen et al.

 

Alcohol consumption and smoking have long been the only concerns regarding the time we spend in utero. This, however, changed with the publication of the so-called Barker hypothesis in the 1980s. Barker postulated that maternal under-/malnutrition might have long-lasting effects on the susceptibility and occurrence of various diseases (especially cardiovascular disease) in the life of their children (’fetal or in utero programming‘).

Aaltonen et al. studied the effect of fat-modified diets consumed during pregnancy on the blood  pressure of 6-month old infants (n=256). After dividing the dietary intake into quartiles and correcting for various confounding variables, the authors found:

1) a U-shape association maternal mono-unsaturated fatty acid (MUFA) intake and infant diastolic blood pressure

2) a U-shape association between maternal carbohydrate intake and infant diastolic and systolic blood pressure

“One of the most interesting findings in our study was the complex interaction between maternal carbohydrate intake and infant blood pressure. This finding may be linked to the pathogenesis of gestational diabetes in which altered glucose metabolism in the mother exposes the fetus to high levels of blood glucose and subsequent hyperinsulinemia. Due to the anabolic properties of insulin, hyperglycemia (even in temporary peaks) may lead to cardiac hypertrophy and functional abnormalities. Therefore, a high maternal carbohydrate intake, particularly consumption of refined carbohydrates in the diet, could result in subclinical maternal hyperglycemia and mild fetal hyperinsulinemia, resulting in higher blood pressure in infancy. This concept is supported by the observation that the higher systolic blood pressure in the neonatal period is linked to increased umbilical cord insulin concentrations, which may be driven by even minor maternal hyperglycemia. In view of the adverse fetal metabolic programming of intrauterine hyperglycemia in gestational diabetes in combination with a postnatal nutritional imbalance manifesting itself in a clustering of the cardiovascular risk factors at even early ages, the long-term sequelae of our finding warrant further investigation.”

Taken together, this study again indicates that the environmental conditions (i.e. maternal diet, body weight, etc.) we are exposed to in utero might be a lot more important for our teenage and adult life than many of us previously thought.

Image taken from: pregnancy.about.com

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?