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Nondrug interventions are a valued component of any plan designed for the treatment of hypertension. Such interventions can be quite varied, as was nicely summarized by Woolf and Bisognano1 in their inclusive article on this topic.In their paper, there is discussion on baroreflex stimulation and renal nerve denervation; however, these are not traditionally viewed as nondrug interventions and will not be further addressed in this commentary.

Viewpoint

  1. Top of page
  2. Viewpoint
  3. Coenzyme Q10
  4. Conclusions
  5. References

An appropriate perspective on this topic can be gained from an appraisal of how the Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) addressed the issue of lifestyle changes and their effect on blood pressure (BP):2

“Adoption of healthy lifestyles by all persons is critical for the prevention of high BP and is an indispensable part of the management of those with hypertension. Major lifestyle modifications shown to lower BP include weight reduction in those individuals who are overweight or obese, adoption of the Dietary Approaches to Stop Hypertension (DASH) eating plan, which is rich in potassium and calcium, dietary sodium reduction, physical activity, and moderation of alcohol consumption. Lifestyle modifications reduce BP, enhance antihypertensive drug efficacy, and decrease cardiovascular risk.”2

Lifestyle modifications are the cornerstone of therapy irrespective of the “starting” BP value and/or whether the patient is receiving multiple-drug therapies. A good example of this can be found in the work by Pimenta and colleagues3 where the role of sodium (Na+) intake was assessed in a 12-patient cohort with resistant hypertension as defined by the patient having a systolic BP >140 mm Hg or a diastolic BP >90 mm Hg at ≥2 clinic visits despite the use of ≥3 antihypertensive medications at pharmacologically effective doses. Two diets were studied as to their effect on BP (50 mmol/24 hours and 250 mmol/24 hours, each for 7 days). Low- compared with high-salt diet decreased office systolic and diastolic BP by 22.7 mm Hg and 9.1 mm Hg, respectively, even as these patients were already receiving several antihypertensive medications. Studies such as this one would argue for the utility of a more assertive approach to lowering of Na+ intake even in persons considered resistant hypertensives by a failure to reach goal BP with a conventional pharmacotherapy approach. The lowering of BP with restricting Na+ intake in patients with resistant hypertension can also be complemented by dietary potassium (K+) supplementation, although this has not been formally studied in a large population base.4

How might one best approach implementing lifestyle modification and use of dietary supplements and/or herbal medicines/alternative approaches in the patient with hypertension? Any such line of attack should be well-reasoned and as much as possible evidence-based. Most patients with hypertension can be viewed as suitable candidates for dietary Na+ restriction and increasing K+ intake. Such would also apply to smoking cessation and restriction of alcohol intake.5 Alternatively, only certain patient types are best served with dietary supplements, herbal medicines, and alternative approaches such as isometric handgrip exercises and paced breathing, in part, because their use is of a more customized nature. Such is the case since these therapies are seldom supported by studies with a rigorous study design and success is oftentimes achieved on an n=1 basis.6

Coenzyme Q10

  1. Top of page
  2. Viewpoint
  3. Coenzyme Q10
  4. Conclusions
  5. References

An assessment of the role of coenzyme Q10 (CoQ10) in the treatment of hypertension is useful in how to best understand the complex nature of using any dietary supplement and/or herbal medicine to lower BP. CoQ10 has been proposed as a supplement effective for a variety of disease states, including hypertension and statin-related muscle symptoms. How CoQ10 lowers BP remains unclear even though it has been suggested to increase nitric oxide bioavailability and/or boost the production of prostacyclin.7 The BP-lowering effect of CoQ10 has proven variable with a recent meta-analysis by Rosenfeldt and associates,8 finding CoQ10 to lower systolic BP by up to 17 mm Hg and diastolic BP by up to 10 mm Hg without significant side effects; however, because of the varying study designs with CoQ10, neither a dose-response relationship (drug amount and/or blood level), frequency of dosing, nor the durability of the effect could be definitively established. Moreover, there is not an unambiguous relationship between either achieving supranormal levels of CoQ10 and/or correcting low CoQ10 blood levels and reduction in BP.

CoQ10 is not particularly water-soluble and therein its absorption is slowed in the gastrointestinal tract. Orally administered CoQ10 has a low clearance rate, with an elimination half-life of about 34 hours. One pharmacokinetic study found that peak plasma levels for a single 100-mg dose of CoQ10 ranged from 5 to 10 hours.9 This observation would bring into question the time-course of effect on BP with CoQ10. Of note, the US Food and Drug Administration does not routinely assess the purity or quality of over-the-counter CoQ10 products; as such, there are innumerable forms of CoQ10 with inherently different bioavailabilities and varying meal effects, circumstances that make recommendations for “what to take” a truly untested proposition. In that regard, ConsumerLab.com offers the following comments following an assessment of 31 CoQ10-branded products:

“Among the 31 products in this review alone, the suggested daily serving size ranged from 22 to 400 mg; the cost to obtain 100 mg of CoQ10 ranged from 11 cents to over three dollars; and many of the CoQ10 products reviewed included ‘solubility enhancers’ which may significantly increase absorption. In addition, labels on a few CoQ10 products violated FDA regulations regarding health claims. The good news was that, unlike past results, all of the products in our review contained their claimed amounts of CoQ10 and ubiquinol.”10

Because of absent large well-designed clinical trials with CoQ10, there cannot be a definitive answer as to how best to use this supplement (or for that matter, any supplement) in the patient with hypertension. One should appreciate that even without solid clinical trial evidence for a supplement’s effect of BP, that patients becoming more active in their own health care can enhance the “placebo” effect and therein confound interpretation of any therapy-related reduction in BP.

Conclusions

  1. Top of page
  2. Viewpoint
  3. Coenzyme Q10
  4. Conclusions
  5. References

Where might nondrug interventions, such as dietary supplements, and/or herbal medicines/alternative approaches be best positioned in the arsenal of therapies that we currently have for the treatment of hypertension? Several patient types seem proper candidates for this therapy, including: (1) the prehypertensive or mildly hypertensive individual where modest reductions in BP are all that is needed to bring BP to goal, (2) patients with resistant hypertension in whom all efforts at therapy have been exhausted and adjunctive nondrug therapy is all that can be offered, (3) patients with multiple medication intolerances in whom limited pharmacotherapy options exist, and (4) patients who wish to assume a less passive role in their own care with active drug therapy supported or supplanted by dietary supplements and/or herbal therapies.

Advocacy for such therapies comes from multiple sources, and the health care provider need be ever vigilant in assessing the validity of the sources of such backing. Issues of bioavailability, frequency of dosing, onset and durability of effect, drug-drug interactions, and plasma level monitoring abound with all such substances and beg the question of how a health care provider might get the best response when advising a patient of such therapy options.

References

  1. Top of page
  2. Viewpoint
  3. Coenzyme Q10
  4. Conclusions
  5. References