TABLE 5-2 Current Status in U.S. Diet Compared to DRI

 

Percent Less Than EAR

 

Male, Aged 19+ y

Female, Aged 19+ y

Vitamin A

57

48

Vitamin E

89

97

Thiamin

4

10

Riboflavin

< 3

< 3

Niacin

< 3

< 3

Vitamin B6

7

28

Folate

6

16

Vitamin B12

< 3 for ages 19–50

< 3 for ages 19–50

Vitamin C

40

38

Phosphorus

< 3

< 3

NHANES 05–06

< 3

3 (0.7)

Magnesium

64

67

NHANES 05–06

53

56

Iron

< 3

10

Zinc

11

17

Copper

< 3

10

Selenium

< 3

< 3

 

Percent Less Than Adequate Intake

Vitamin K

80

59

Potassium

94

> 97

Dietary fiber

> 97

92

Linoleic acid 18:2

47

44

Linolenic acid 18:3

47

39

SOURCES: Adapted from Moshfegh et al., 2005, 2009.

consumption of beverages and dietary supplements or medications may reduce caffeine’s cognitive and physical performance–enhancing benefits. Furthermore, beverages like energy drinks often contain other methylxanthines and caffeine analogues, such as guarana, in addition to other herbal compounds, like ginseng; the mechanisms of action, potential benefits, and safety concerns of these substances remain unclear.

Emerging evidence suggests that caffeine exerts a neuroprotective effect in animal models of TBI, stroke, and Parkinson’s disease (Sachse et al., 2008). A retrospective study of caffeine concentration measured in cerebrospinal fluid of patients with severe TBI also found an association between caffeine concentration and favorable Glasgow Outcome Scale scores (Sachse et al., 2008). However, the evidence, depending on the dose, model, and timing, is conflicting, and warrants further investigation.

The combination of caffeine and alcohol has been found to be beneficial in experimental TBI and stroke models (Dash et al., 2004). Even on its own, alcohol has also been associated with improved outcomes in patients with moderate to severe TBI (Berry et al., 2010; Opreanu et al., 2010). Despite a possible neuroprotective role of alcohol, it is important to emphasize that alcohol intoxication is a leading factor in civilian cases of TBI, especially among individuals with a history of substance abuse. At the same time, TBI is a noted risk factor for substance abuse (Graham and Cardon, 2008). Excessive and chronic consumption of alcohol has also been associated with negative interactions with certain nutrients, such as impaired absorption (zinc), depletion (magnesium), and depressed fatty-acid oxidation (polyunsaturated fatty acids) (IOM, 2006b).



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