Iron supplementation can be toxic. Monitoring is important. RCT finds 11wk of Fe supplementation (325mg FeSO4 daily) does not maintain iron status in elite female athletes. Low Fe status impairs muscular performance (vs control group) http://ow.ly/GTYl30mhAwR #StatusMatters
A paper entitled “Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis” was recently published in Lancet. The authors identified 51 randomized control trials (RCT) with high- and low-dose vitamin D supplementation. They concluded:
Full disclosure, because of Nature’s paywall I have not read the paper in detail. However, it is my strongly held position that meta-analyses which only evaluate nutrient supplementation miss the point. It is clearly established that essential nutrients, e.g. vitamins, EPA+DHA, lutein, zeaxanthin, iron, etc, provide benefit when nutrient status is insufficient to support normal cell structure and function.
Food fortification is known to improve nutritional status, help prevent deficiency diseases and save lives. This fact isn’t based on dietary intake data. It is based on status measurements and health outcomes, e.g. effect of mandatory folic acid fortification of flour in incidence of neural tube defects.
So, with input from Dr William B Grant (@wbgrant2), here is evidence (4 examples) that it is vitamin D status, i.e. 25(OH)D3 concentrations, which is correlated with outcome and needs to be measured NOT whether an individual is randomized to a supplement or placebo arm of a RCT.
Maternal 25(OH)D3 status and Gestational Age (weeks
After decades of proven benefits from food fortification, the question to be asked isn’t whether additional intake of a vitamin is beneficial. Instead, the answer needed is: ‘what is the optimal blood 25(OH)D level to maintain strong bones and muscles? http://ow.ly/LkTe30mfVOw
More evidence of the importance of measuring status, i.e. vitamin A content of breast milk (also applies to DHA, lutein, etc), and then assessing maternal dietary interventions to see if nutrient intake is adequate to support infant development http://ow.ly/kCMJ30meU7C
And did I mention my frustration with paywalls? Why is a study funded by the German Academic Exchange service (DAAD) not open access nature ? http://ow.ly/NFU430meUIe #SciencePrivilege http://ow.ly/i/IVEMG
Just read an intriguing article entitled Cell-Specific Competition for Calories” Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-human Animals. It is insightful.
Years ago I did lots of animal surgery. I noted, especially in rats which accumulate fat pads as the top of their front shoulders, that these adipose beds were heavily vascularized. Once fat cells are created (hyperplasia), they persist as the most accessible ‘sink’ for postprandial glucose, fatty acids & amino acid excursions. With this metabolic ‘sinkhole’ for glucose, fatty acids, and de-amidated amino acids to ‘fall into’ postprandially, it is easy to see why weight loss and subsequent weight maintenance is so difficult.
Prior to adipocyte hyperplasia in an animal or human, caloric nutrients (glucose, fat, amino acids) have to circulate in the blood until actively transported into muscle cells, liver cells, immune cells, brain cells, etc. Once adipocytes are created, there is a new, ‘easy’ path to remove these metabolites from the blood with the benefit of longterm energy conservation. And after nutrients leave the bloodstream, humans and animals want to eat (manage managing hunger/appetite) or respond to signals to release these same energy sources into the blood to fuel our activities and basic cellular functions.
Thank you to these authors for making this ‘regulatory’ story so much clearer.