Iodine related disorders

This is a very worthwhile review of the importance of iodine in our diet. Zimmermann et al 2008 Iodine-deficiency disorders, Lancet vol 272 pp 1251-62
Iodine is an essential component of the thyroid hormones., and therefore iodine, is essential for mammalian life. Iodine (as iodide) is widely but unevenly distributed in the earth’s environment. Most iodide is found in the oceans (about 50 ug/L), and iodide ions in seawater oxidise to form elemental iodine, which is volatile and evaporates into the atmosphere and returns to the soil by rain, completing the cycle. However, the cycle of iodine in many regions is slow and incomplete, and soils and groundwater become deficient in iodine. Crops grown in these soils will be low in iodine concentration, and man and animals consuming food grown in these soils become deficient in iodine.
In plants grown in deficient soils, iodine concentration might be as low as 10 ug/kg of dry weight, compared with about 1 mg/kg in plants from iodine-sufficient soils. Iodine-deficient soils are common in inland regions, mountainous areas, and places with frequent flooding, but can also occur in coastal regions. Iodine deficiency in populations residing in these areas will persist until iodine enters the food chain through addition of iodine to foods (eg, iodisation of salt) or dietary diversification introduces foods produced in iodine-sufficient regions.
The native iodine content of most foods and beverages is low, and most commonly consumed foods provide 3-80 ug per serving. Major dietary sources of iodine in the USA and Europe are bread and milk.” On the basis of direct food analysis, an adequate mean intake of dietary iodine is about 100-180 ug per day Boiling, baking, and canning of foods containing iodated salt cause only small losses (<10%) of iodine content. Iodine content in foods is also determined by iodine-containing compounds used in irrigation, fertilisers, and livestock feed. Iodophors used for cleaning milk cans and teats can increase the native iodine content of dairy products;
2 billion individuals worldwide have insufficient iodine intake, with those in south Asia and sub-Saharan Africa particularly affected. Iodine deficiency has many adverse effects on growth and development due to inadequate production of thyroid hormone. Iodine intake is very important during pregnancy and lactation. Assessment methods include urinary iodine concentration, goitre, newborn thyroid-stimulating hormone, and blood thyroglobulin. In nearly all countries, the best strategy to control iodine deficiency is iodisation of salt, which is one of the most cost-effective ways to contribute to economic and social development. When iodisation of salt is not possible, iodine supplements can be given to susceptible groups. Introduction of iodised salt to regions of chronic iodine-deficiency disorders might transiently increase the proportion of thyroid disorders, but overall the small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency.

yoghurt to treat hepatic encephalopathy

This leader is very important in the care of marginally encephalopathic patients. Leader 2008 Nature Clinical Practice Gastroenterology & Hepatology 5, 537
Probiotic yogurt can reverse MHE in patients with nonalcoholic cirrhosis
Minimal hepatic encephalopathy (MHE) affects 60–80% of patients with cirrhosis and is associated with poor quality of life, decreased work performance and impaired driving skills. Lactulose has been advocated as the first-line therapy for MHE, but long-term adherence is limited because of adverse gastrointestinal effects. Alternative, long-term therapies are, therefore, needed. Bajaj and colleagues investigated the use of probiotic yogurt for the treatment of MHE in patients with nonalcoholic cirrhosis. Yogurt was chosen because it is a palatable food item that is widely available and does not require prescription, all of which favour long-term adherence.

physical endurance enhancers

This is such an interesting review and highlights the mysteries of endurance and stamina
Baar1 & Hardie 2008 Small molecules can have big effects on endurance, Nature Chemical Biology 4, 583 - 584 (2008)
Adaptation of muscle to endurance exercise training involves the coordinated expression of genes involved in oxidative metabolism, resulting in increased endurance. A recent study shows that small-molecule activators of two pathways thought to transduce these effects can enhance the effects of training, or even substitute for it.
Skeletal muscle responds to repeated exercise by altering its contractile properties and its metabolism. Endurance training results in an increased capacity to generate energy (in the form of ATP) from aerobic pathways. An intriguing possibility is that small molecules that activate the pathways triggering these adaptations might mimic the effects of training without the accompanying sweat and effort
Muscles of transgenic mice expressing an activated form of PPAR- contain a greater proportion of type 1 fibers (characterized by a more efficient form of myosin and a higher oxidative capacity) and display increased endurance. PPAR- is a transcription factor of the nuclear receptor family; its natural activating ligand remains unknown, although one idea is that it is a fatty acid metabolite generated during muscle metabolism. However, small molecules that activate this receptor (for example, GW1516) have been developed. Narkar et al.1 now report that although prolonged treatment of mice with GW1516 induced a subset of genes involved in fatty acid oxidation, it did not increase endurance on its own. However, when the drug was combined with treadmill training, gene expression, mitochondrial mass and endurance all improved more than with training alone
AICAR is a nucleoside that is taken up into muscle and converted into the nucleotide ZMP, which mimics the effects of the natural ligand, 5'-AMP, on AMPK. The latter is produced by adenylate kinase acting on ADP generated from ATP during muscle contraction. Activated AMPK in the nucleus (an heterotrimer) then promotes expression of oxidative genes, in part by upregulating PGC-1 and switching on promoters with binding sites for PPAR- and its partner RXR. PPAR- can also be activated by GW1516, which may mimic a natural ligand produced by increased muscle metabolism. These dual mechanisms trigger expression of genes (including genes involved in fatty acid oxidation) that increase ATP production and hence endurance.
Another signaling pathway that mediates many exercise effects involves the AMP-activated protein kinase (AMPK). Increased ATP use during prolonged muscle contraction is thought to increase the concentration of 5'-AMP, its activating ligand. One target downstream of AMPK is PGC-1 , a transcriptional co-activator recruited to gene promoters by members of the nuclear receptor family, including PPAR- . PGC-1 is known to facilitate many of the adaptations to endurance exercise, including mitochondrial biogenesis and angiogenesis4. Narkar et al. tested whether the additive effect of training and GW1516 on PPAR- target genes could be mimicked using AICAR, a nucleoside that is converted to an AMPK activator inside muscle cells5. Interestingly, they found that four weeks of AICAR treatment caused modest increases in endurance on its own—that is, without training or GW1516.Previous research has shown that shorter periods of AICAR treatment in rats upregulate expression of the glucose transporter GLUT4 and mitochondrial proteins, and increase glycogen content, all of which would be expected to improve endurance. Second, transgenic expression of an activated AMPK mutant in mouse muscle results in an increase in glycogen content and endurance capacity8. Nevertheless, the new paper does provide proof of concept that small-molecule activators can increase endurance. They also report new data suggesting that AMPK is present inside the cell in a complex containing both PPAR- and PGC-1 . However, the finding that treatment with AICAR is sufficient to improve endurance on its own, whereas treatment with GW1516 is not, suggests that AMPK has additional effects not mediated by PPAR- .
The authors caution human athletes undergoing high-level endurance training (as opposed to sedentary mice maintained in a cage), that both of these pathways will already be regularly activated and the drugs may yield no additional benefit. It is also worth pointing out that the increases in endurance seen in these studies were in exercise of moderate intensity, where there is a greater reliance on fat as a fuel. These conditions may magnify any effects of GW1516, whereas in a human athletic event of an hour or less (when carbohydrates would be the primary fuel), any performance benefits of GW1516 would be minimized. The real benefit of drugs that activate PPAR- and AMPK may lie in treating people who would receive health benefits from regular exercise, but who are unable to tolerate it.

weight changes in a Scottish population

Ebrahimi-Mameghaniet al Changes in weight and waist circumference over 9 years in a Scottish population
European Journal of Clinical Nutrition (2008) 62, 1208–1214; doi:10.1038/sj.ejcn.1602839; published online 11 July 2007
This study looked at patterns of measured weight and waist circumference (WC) change and the increase in overweight and obesity over a 9-year period in a Scottish population..
A total of 1044 subjects from two age-defined cohorts aged 39 and 59 in 1991. Height, weight and WC were measured in 1991, 1995 and 2000 and body mass index (BMI) was calculated. Pattern of weight and WC change was studied over approximately 9 years.
The prevalence of overweight and obesity increased markedly and the younger cohort showed greater increases in weight and WC than the older cohort. There was no significant difference in mean BMI and/or mean 9-year weight change between men and women in either age cohort, and mean weight gain was similar for all occupational groups. Only 20% of subjects maintained a stable weight ( 2 kg), while 42.2 and 17.6% gained greater than 5 and 10 kg over the 9-year period, respectively. The rate of weight gain appeared to be relatively steady over the 9 years among younger subjects but declined in the older subjects in the second half of the observation period.
Health promotion strategies to prevent weight gain need to be population-based, targeting all social and age groups, but particularly those in their early middle-age.

dietary selenium intake measurements

Yoneyama et al 2008 Dietary intake and urinary excretion of selenium in the Japanese adult population: the INTERMAP Study Japan European Journal of Clinical Nutrition (2008) 62, 1187–1193;
This study examined the relationship between dietary selenium intake and 24-h urinary selenium excretion in Japanese population samples participating in the INTERMAP Study.
Using highly standardized methods, they assessed individual dietary selenium intake from four 24-h dietary recalls and measured urinary selenium excretion in two timed 24-h urine collections in 1145 Japanese participants (574 men and 571 women) ages 40–59 years in four areas of Japan.
The medians of dietary selenium intake were 177.5 g/day in men and 139.8 g/day in women; the medians of 24-h urinary selenium excretion were 127.9 g/day in men and 109.4 g/day in women, that is, urinary excretion was estimated to be 73% of dietary intake in men and 77% in women. Dietary selenium intake was significantly correlated with 24-h urinary selenium excretion (r=0.24 in men, r=0.18 in women; P<0.001).
They concluded that dietary intake and 24-h urinary excretion of selenium are related in the Japanese adult population.

measuring polyunsaturated acid dietary intake

P Astorg et al 2008 Plasma n-6 and n-3 polyunsaturated fatty acids as biomarkers of their dietary intakes: a cross-sectional study within a cohort of middle-aged French men and women European Journal of Clinical Nutrition (2008) 62, 1155–1161;
Astorg and colleagues have measured the correlations between habitual intakes of individual n-6 and n-3 polyunsaturated fatty acids (PUFA) and their percentages in total plasma fatty acids in a French population of adult men and women.
Fifteen 24-h record questionnaires were used to estimate the habitual intake of energy, total fat and linoleic, alpha-linolenic acid, arachidonic, eicosapentaenoic (EPA), n-3 docosapentaenoic (DPA) and docosahexaenoic (DHA) acids. Fatty acid composition of fasting plasma total lipids were determined at baseline.
Dietary intakes of linoleic acid, arachidonic acid, EPA and DHA were weakly but significantly correlated (0.16They concluded that the percentages of linoleic acid, arachidonic acid, EPA and DHA in plasma total fatty acids, but not that of alpha-linolenic acid, are acceptable markers of their habitual levels of intake. The plasma levels of long-chain n-6 and n-3 PUFA are not influenced by the intake levels of their precursors, linoleic and alpha-linolenic acids.