191 Caffeinated Beverages: The Hypertension Paradox
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Dynamic Chiropractic – June 6, 2006, Vol. 24, Issue 12

Caffeinated Beverages: The Hypertension Paradox

By G. Douglas Andersen, DC, DACBSP, CCN

Caffeine is arguably one of the world's most popular drugs. More than 60 kinds of plants contain caffeine which, depending on the species, may be located principally in the plant's leaves, seeds, nuts, beans or fruit.

The amount of caffeine in beverages, specifically coffee and tea, can vary widely depending on source, processing and preparation. Table 1 is a compilation of the amount of caffeine in certain beverages; I found the information in a variety of books and journals. Data was derived from a number of sources, ranging from governmental entities (such as the FDA), trade organizations (The National Coffee Association, The Gatorade Sports Science Institute, The National Soft Drink Organization and The Consumer's Union) and professional bodies (the American Medical Association and the American Dietetic Association). Unless you take caffeine in pill form, the amount contained in beverages is far from exact.

Table 1: Amount of Caffeine in Selected Beverages
Beverage Caffeine Range (milligrams)
Instant coffee 40-108 mg
Drip (brewed) coffee 110-155 mg
Percolated coffee 60-125 mg
Tea, brewed/steeped for 1 minute 9-33 mg
Tea, brewed/ steeped for 3 minutes 20-50 mg
Tea, brewed/steeped for 5 minutes 20-100 mg
Green tea 12-16 mg
Iced tea (12 ounces) 22-54 mg
Cola drinks (12 ounces) - includes diet or regular drinks 36-46 mg

Table 2: Risk of Hypertension Based on Total Estimated Dietary Caffeine Intake
NHS I
Caffeine range (mg/day) 0-45 45-144 144-297 297-417 Over 417
Relative risk* 1.0 1.13 1.13 1.08 1.04
NHS I
Caffeine range (mg/day) 0-45 45-144 144-297 297-417 Over 417
Relative risk* 1.0 1.05 1.12 1.06 1.01
* Adjusted for age, body mass index, alcohol intake, family history of hypertension, physical activity and smoking status.

Table 3: Risk of Hypertension Based on Total Estimated Coffee Intake
NHS I
Cups per day <1 1 2-3 4-5 6
Relative risk* 1.0 1.06 1.0 0.93 .88
NHS II
Cups per day <1 1 2-3 4-5 6
Relative risk* 1.0 1.06 1.0 0.91 0.91
* Adjusted for age, body mass index, alcohol intake, family history of hypertension, physical activity and smoking status.

Caffeine and/or caffeine-containing beverages (specifically coffee) have been shown both to be linked to, and to have no association with, a variety of ailments, including hypertension and heart disease. The evidence continues to be contradictory and, in a new study on caffeine and hypertension, even paradoxical.

Caffeine and Hypertension

Researchers looked at data from the Nurses Health Studies, Part I (NHS I, begun in 1976 with over 120,000 registered nurses ages 30 to 55) and Part II (NHS II, begun in 1989 with over 116,000 RNs ages 25 to 42).1 The authors began by selecting all women in NHS I who were free of hypertension in 1990 (more than 53,000) and all of the women in NHS II who were free of hypertension in 1991 (more than 94,000). Records were analyzed for 12 years. By 2002, over 19,000 subjects in NHS I had developed hypertension; by 2003, more than 13,000 participants in NHS II were hypertensive. Dietary records from NHS I (1990, 1994 and 1998) and NHS II (1991, 1995 and 1999) were reviewed. The findings are indicated in Tables 2-4.

As you can see from Table 2, the results of this trial exhibit a U-shaped curve with regard to caffeine and hypertension indicate a lower risk of hypertension with higher and lower intakes of caffeine, with an increased risk in the middle. In Table 3, the risk of hypertension with coffee declined after one cup to a level whereby those who drank six or more cups daily had a 9 percent to 12 percent reduction compared to nonusers. Tea confirmed the coffee results in NHS I but was contradictory in NHS II, with the risk paralleling consumption (Table 4).

Table 4: Risk of Hypertension Based on Total Estimated Tea Intake
NHS I
Cups per day <1 1 2-3 4-5 6
Relative risk* 1.0 1.04 1.03 0.97 .99
NHS II
Cups per day <1 1 2-3 4-5 6
Relative risk* 1.0 1.05 1.04 1.10 1.11
* Adjusted for age, body mass index, alcohol intake, family history of hypertension, physical activity and smoking status.

Table 5: Risk of Hypertension Based on Total Estimated Daily Cola Intake
NHS I
Cans per day <1 1 2-3 4
Relative risk* 1.0 1.09 1.11 1.44
NHS II
Cups per day <1 1 2-3 4
Relative risk* 1.0 1.13 1.24 1.28
* Adjusted for age, body mass index, alcohol intake, family history of hypertension, physical activity and smoking status.

Table 6: Risk of Hypertension Based on Total Estimated Daily Diet Cola Intake
NHS I
Cans per day <1 1 2-3 4
Relative risk* 1.0 1.07 1.06 1.16
NHS II
Cups per day <1 1 2-3 4
Relative risk* 1.0 1.05 1.09 1.19
* Adjusted for age, body mass index, alcohol intake, family history of hypertension, physical activity and smoking status.

Cola Surprise

Note that both sweetened and diet cola intake were the strongest predictors of increased risk for hypertension in both studies (Tables 5 and 6). Confused? It may take genetics to sort this out. For example, a new study found an increased risk of caffeine-related heart disease only in those who are genetically "slow" metabolizers. "Rapid" caffeine metabolizers did not have a heart disease connection.2 It turns out that people who carry the "slow" 1F allele on the liver enzyme cytochrome P4501A2 metabolize caffeine and have an increased risk of heart disease compared to those who carry the "rapid" 1A allele. There could be some type of genetic influence as to how certain people metabolize coke ingredients, both individually and in combinations. In the meantime, this research adds one more reason for both doctors and patients to reduce soft drink consumption. As far as coffee and tea, these findings indicate the need for further study.

References

  1. Winkelmayer WC, Stampfer MJ, Willett WC, Curham GC. Habitual caffeine intake and the risk of hypertension in women. JAMA 2005;294:2330-2335.
  2. Cornelis MC, El-Sohemy A, Kabagambe EK, Campos H. Coffee, CYP1A2 genotype, and the risk of myocardial infarction. JAMA 2006;295:1135-1141.

Click here for previous articles by G. Douglas Andersen, DC, DACBSP, CCN.

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