Basic Lifestyle Interventions for High Blood Pressure and Cholesterol. JMikolai. 11.13.13

by | Jan 1, 2014

Basic Lifestyle Interventions for High Blood Pressure and Cholesterol

by Jeremy Mikolai, ND

High blood pressure is the most prevalent cardiovascular disease in America.1 It is the primary risk factor of heart attacks, stokes, and severe cardiovascular morbidity.2 Greater than 95% of high systemic arterial blood pressure is primary hypertension, formerly called essential hypertension. While we can hypothesize some potential mechanisms for primary hypertension, we ultimately do not know what causes it. We do know that there is a general dose-dependent relationship between the elevation of the blood pressure and its negative consequences; the higher the blood pressure, the higher the likelihood of bad outcomes.3–5

A dose-dependent relationship also exists between lipid levels in the blood and the likelihood for poorer cardiovascular health. The higher the lipid levels (cholesterol and triglycerides), the more likely a person is to have bad outcomes. Important genetic dyslipidemias exist and they are more common than is often appreciated (about 1 in 500 for heterozygous familial hypercholesterolemia in the US).6 Yet we know that the majority of dyslipidemias in the developed world are acquired, not genetic.

The metabolic syndrome is a pattern of acquired pathological conditions which create greatly increased risk for type 2 diabetes mellitus and cardiovascular disease, as well as other forms of chronic disease. Several different organizations have suggested definitions and clinical criteria for defining “metabolic syndrome.” Despite their differences, their purpose is to identify central obesity and the insulin-resistance characteristics that accompany it. Those characteristics include hypertension and dyslipidemia.

The majority of cases of metabolic syndrome, hypertension, and dyslipidemia in the US are lifestyle driven. The foundational treatments for addressing them in both the short and the long term also need to be lifestyle driven. Moreover, therapeutic lifestyle modifications are often able to address multiple conditions simultaneously. Take weight loss, for instance, which improves blood pressure, blood lipids, and insulin sensitivity simultaneously. Therapeutic lifestyle changes do something more than address any individual condition or even set of conditions; they create the foundations for health.

Hypertension is the most prevalent cardiovascular disease in the US.1 The risks for cardiovascular disease begin to rise as soon as the blood pressure is greater than 115 mmHg over 75 mmHg. There is a strong association between blood pressure and cardiovascular disease; the risk of cardiovascular disease doubles with each increase of 20 points of systolic blood pressure.3 High blood pressure is the number one risk factor for strokes of any type.5,7 It is associated with coronary artery disease and heart attacks. It dramatically increases the likelihood of heart failure.3

There is some debate in the medical literature about whether we are over-treating mildly elevated blood pressure. A recent systematic review produced by the Cochrane Hypertension Group concerning the use of pharmacotherapy for the treatment mild hypertension demonstrated that there was no difference in mortality, coronary heart disease, stroke, or cardiovascular events over 4 to 5 years of pharmaceutical treatment of mild high blood pressure, defined as 140 to 159 mmHg systolic blood pressure and/or 90 to 99 mmHg diastolic blood pressure.8 This meta-analysis was derived from four randomized controlled trials (RCTs) comprising 7080 participants on the outcomes of coronary heart disease, stroke, and total cardiovascular events and 8912 participants on the outcome of total mortality. The comparison was between participants of RCTs of pharmacotherapy versus placebo for the treatment of mild primary hypertension (less than 159/99 mmHg) in primary prevention. About 9% of participants discontinued pharmaceutical treatment due to adverse events.8

There are some important things to remember about the Diao et al. 2012 Cochrane review. The meta-analysis data was derived from just four RCTs and the total number of participants from those four trials on most of the outcomes was 7080. So this study is much too small to influence our management of patients in the care setting at this time, which is why its authors concluded that more trials are needed to help generate data on this issue. It also tells us that a large number of our patients being treated for mild hypertension with pharmacotherapy, about 9%, experience side effects severe enough to make them want to give up that treatment.

By contrast, the newest set of guidelines from the European Society of Hypertension and the European Society of Cardiology (ESH/ESC) do not recommend any substantial changes in our present management of the condition. In fact, they recommend that all patients under 80 years old maintain a systolic blood pressure (SBP) below 140 mmHg.9 The newest guidelines on blood pressure from the eighth Joint National Committee (JNC-8) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure are expected soon. Most authorities expect the JNC-8 to make very few, if any, changes from the JNC-7 guidelines.

It is important that we distinguish between types of hypertension. Arterial hypertension can be primary or secondary and the type of prevention that it provides can be primary or secondary. Primary hypertension, formerly called essential hypertension, is idiopathic, meaning that we don’t know what causes it. About 95% of cases of hypertension are primary type. There are several hypotheses about the potential causes of primary hypertension, including increased sensitivity of the renin-angiotensin-aldosterone system, increased catecholamine sensitivity, genetics, decreased nephron mass in the kidneys, and endothelial dysfunction.10

Secondary hypertension is high blood pressure caused by another known condition. Most commonly, those secondary causes are chronic kidney diseases, renovascular disease, bilateral idiopathic hyperaldosteronism, sleep apnea, and thyroid disease; but less commonly it can be caused by coarctation of the aorta, neuroendocrine tumors, and others. Secondary hypertension is a complex topic; it is typically more resistant to treatment and occurs alongside other pathologies of the cardiovascular system or other internal organs. Many lifestyle interventions can be appropriate in certain cases of secondary hypertension, but some are contraindicated. Due to the scope and nuance of the topic of secondary hypertension, we will confine ourselves to primary hypertension for this discussion.

Primary prevention refers to intercepting and modifying a risk before the event associated with that risk occurs. We treat people who have hypertension to prevent them from having their first heart attack or stroke; that is primary prevention. Secondary prevention is attempting to stop the recurrence of an event in a patient who has already had one or more events. We treat the hypertension of people who have survived a stroke to prevent them from having another stroke; that is secondary prevention. So, we may be treating a patient’s blood pressure as a means of primary or secondary prevention.

The point about overtreatment is an interesting one. Certainly, overtreatment creates unnecessary burden on the patient in terms of both treatment participation and any adverse events or morbidity from medication use; it incurs financial cost to the payer and imparts cost onto the healthcare system. However, the majority of these burdens pertain to pharmacotherapy and contacts with the healthcare system. We use risk stratification to help us to determine the level of intervention which is appropriate in cardiovascular primary prevention. The benefits of aggressive risk factor modification in secondary prevention or in those patients with very high risk and risk equivalents is more clear than that in primary prevention, but when the interventions in question are lifestyle modifications which address risk factors and create the foundations for health simultaneously, the benefits are apparent across the continuum.

Fortunately, the new ESH/ESC guidelines address a number of lifestyle and dietary therapies, “nonpharmacotherapy” for helping to regulate hypertension. The importance of the lifestyle and dietary foundation for the redress of hypertension, dyslipidemia, and the metabolic syndrome cannot be overstated. We are encouraged to risk-stratify patients on the basis of their likelihoods for future cardiovascular events to help us make management decisions about their cardiovascular targets and the therapeutic strategies used to get them to those targets, yet we should begin every management strategy with underpinning lifestyle and dietary changes. Nonpharmacotherapy interventions are sanctioned as the first-line in redress of any of these three conditions by all of the authorities that create guidelines for their evaluation and treatment. Lifestyle changes can be used to enhance and complement a pharmacotherapy strategy; they may be capable of maintaining primary control over blood pressure and lipids, in some cases; they are the lifelong strategies necessary to rehabilitate the underlying cause of the problem and create the foundations for health moving forward for the patient.

The five basic therapeutic lifestyle changes to address hypertension are straightforward and applicable to the vast majority of cases of primary hypertension. They are: (1) maintain a sodium controlled diet that is rich in potassium; (2) maintain frequent exercise; (3) achieve and maintain and ideal body weight; (4) eliminate or decrease use of substances including tobacco, alcohol (in excess), and over-the-counter pain relievers/nonsteroidal anti-inflammatory drugs (NSAIDs), but also use of sympathomimetic drugs, such as amphetamines, cocaine, even caffeine; (5) maintain sufficient vitamin D levels.10

There has been considerable debate about sodium-restricted diets. The overall prevalence of true “sodium-sensitive” hypertension is thought to be low. On the other hand, the evidence from the DASH diet trials demonstrated that restricting sodium to less than 2300 mg/day resulted in significant decreases in blood pressure regardless of whether a person began with normal or high blood pressure.11 Two recent meta-analyses failed to show the significance of sodium restriction on lowering cardiovascular morbidity and mortality. One of these studies demonstrated that, despite a significant decrease in the number of cardiovascular events in the salt-restricted group compared with the group that had no salt restriction, there was no difference in mortality between the two groups.12,13

The new ESH/ESC guidelines recommend daily salt (sodium chloride) restriction to 5 to 6 g salt/day, as a reduction from a typical 9 to 12 g/day diet. Those 6 grams of salt (sodium chloride) are equivalent to 2300 mg/day of sodium. This is the same amount of sodium restriction that was recommended in the JNC-7 guidelines from 2003.14 Previous ESH/ESC 2007 guidelines recommended limiting sodium to under 2000 mg/day.15 The United States Departments of Agriculture and Health and Human Services dietary guidelines from 2010 recommend further sodium restriction down to less than 1500 mg in any patient: over the age of 51 years, of black race, or with a history of hypertension, diabetes mellitus, chronic kidney disease.16

Several studies demonstrate that a reduction of approximately 1700 mg/day of sodium intake correlates with a decrease in blood pressure of about 5 mmHg SBP and about 3 mmHg DBP (5/3 mmHg).17 Benefits from a sodium conscientious diet seem to extend to further BP reduction and control for patients on pharmacotherapy. Sodium restriction appears to increase the efficacy of pharmacotherapy, in some studies demonstrating a further reduction of 9/3 mmHg in blood pressure.18 Calcium channel antagonists appear to be affected least by this relationship while diuretics and angiotensin converting enzyme inhibitors (ACEIs) appear to be most affected.18–21

Eating a potassium-rich diet and increasing the potassium-to-sodium ratio in the diet are also pillars of importance in the low-sodium diet. The ratio of urinary sodium to potassium excretion correlates with a dose-dependent increase in systolic and diastolic BP.22 Eating sufficient potassium in the diet may be preferable to potassium supplementation in many individuals, especially based on electrolyte status and medication regimen. However, there is some evidence to demonstrate that potassium supplementation may decrease BP about 4.4/2.5 mmHg in hypertensive patients.23

It is worth mentioning that manipulation of electrolytes and electrolyte balance is not always appropriate or straightforward in many circumstances of hypertension. The various pharmaceuticals being used in the treatment, the type of hypertension that the patient has, and the other conditions that the patient has, such as diabetes or chronic kidney disease, all play important contributions to our choice and determination of interventions. When patients have hyponatremia, low sodium, for example, we do not ask them to limit their salt intake. When patients are taking multiple drugs which raise their potassium levels, for instance, we are typically advising them to decrease the potassium in their diets, even if they have high blood pressure. So, each of these recommendations are still context dependent and have to be viewed and used in light of the other conditions and complications. Yet our focus is on those interventions that are the basic lifestyle changes, are available to almost all of our patients, have a good level of evidential support for their use, and form the foundations of health for the patient.

The second basic therapeutic lifestyle intervention for hypertension is exercise. Aerobic exercise does make the greatest impact on BP, but resistance exercise also reduces it. The evidence from meta-analyses of RCTs shows that aerobic exercise decreases BP by up to 6/3 mmHg, while moderate-intensity resistance training (dynamic or isometric) lowers BP by about 4/4 mmHg.24–27 Ideally, we would have each patient on a combination of aerobic and resistance exercise. Clinically, it is very useful not to have to depend on one type of exercise or another, since any patient may be more or less able to perform exercise of one type or another at any given time. Regardless of patients’ status of health and mobility, there are exercise recommendations that are appropriate to them and can help decrease BP.

The third basic lifestyle intervention is achieving and maintaining an ideal body weight. ESH/ESC guidelines recommend maintaining a BMI less than 25 kg/m2 with a waist circumference less than 102 cm (40 in) for men and less than 88 cm (35 in) for women.9 For each kilogram of body weight that is lost the blood pressure decreases 0.5 to 2.0 mmHg.28 Even a 10% reduction in body mass can make a substantial impact on blood pressure.

The fourth lifestyle intervention for management of hypertension is to eliminate or limit the use of substances known to exacerbate blood pressure. Excess alcohol intake appears to be of greatest concern. Alcohol consumption in excess of 2 drinks per day in women and 3 in men is correlated with increased incidence of high blood pressure. Higher alcohol consumption is correlated with a stronger response on the blood pressure; the strongest response is seen in those with use in excess of 5 drinks per day. Limitation or cessation of alcohol use in those who drink excessively lowers blood pressure.29

All NSAIDs can cause increased BP and a decreased response of antihypertensive medications. The effect size is variable, but the average BP increase from NSAID use has been stated as 3/2 mmHg.30–32 There is conflicting evidence about the effect of acetaminophen on BP, but it is reasonable to expect that it may increase blood pressure when used at typical doses.33 Low dose aspirin therapy does not appear to interfere with antihypertensive treatment or to raise blood pressure.34

The fifth basic lifestyle intervention in high blood pressure is to address the vitamin D status of the patient. Frank deficiency of vitamin D3 can result in high blood pressure. Those with deficiencies or insufficiencies of 25-hyrodoxyvitamin D should be supplemented.35

Patient education alone can make a substantial change in the blood pressure. Clinician-patient education interventions have been shown to substantially lower BP, in some cases by up to 6.6/3.8 mmHg.36 A peer-mediated sharing experience about hypertension has also been shown to produce similar BP reductions.37

Several therapeutic diets may be relevant to the control of high blood pressure, and several of them may help us to address other elements of the cardiovascular risk profiles of our patients. Particular dietary interventions can be powerful both in addressing a pathological condition as well as in helping establish the foundations for health and promoting behaviors that encourage health and prevent further chronic disease. Many of the basic lifestyle interventions relevant for addressing elevated blood pressure overlap with the interventions which address dyslipidemia and other elements of the metabolic syndrome.

The National Cholesterol Education Program (NCEP)/Adult Treatment Panel III (ATPIII) guidelines define “metabolic syndrome” as the presence of any 3 out of the following 5 of: abdominal obesity with a male waist circumference greater than 40 in (102 cm) or a female greater than 35 in (88 cm), elevated serum triglycerides greater than 150 mg/dL, serum HDL cholesterol less than 40 mg/dL for males or less than 50 mg/dL for females, blood pressure greater than 130/85 mmHg or on treatment for blood pressure, fasting plasma glucose greater than 100 mg/dL, or known history of type 2 diabetes.38

Other metabolic syndrome criteria are defined slightly differently; the International Diabetes Federation makes abdominal obesity and essential part of their definition. The World Health Organization (WHO) makes insulin resistance a defining and essential component to its criteria. In any of its guises, metabolic syndrome raises the individual risks of type 2 diabetes and cardiovascular events, as well as other chronic diseases, in the individual who presents with it. The metabolic syndrome raises an individual’s risk for type 2 diabetes mellitus 2- to 3.5-fold.39 Metabolic syndrome increases the relative risk of cardiovascular disease by 1.5- to 2.2-fold and increases the all-cause mortality risk by 1.27- to 1.6-fold.40–42 Metabolic syndrome is also associated with fatty liver disease fibrosis and cirrhosis, polycystic ovarian syndrome, chronic kidney disease, gout and hyperuricemia, sleep disordered breathing, and hepatocellular and cholangiocarcinomas.43–53

Lifestyle interventions are crucial in the redress of metabolic syndrome. Many of the therapeutic lifestyle interventions for addressing hypertension will overlap or intercalate synchronously with the basic interventions that we will use for dyslipidemia and the metabolic syndrome. Debate exists, of course, about the relative importance of the hazard created by elevated total cholesterol and low-density lipoprotein cholesterol (LDL-c) in the absence of other cardiovascular risk factors and the degree of real risk reduction that is offered by statin therapy in the primary prevention of cardiovascular events. Again, in the arenas of secondary prevention and in primary prevention for those with high-risk features and with risk equivalents such as diabetes type 2, the data are stronger and there appears to be more clear benefits to restrictive LDL-c and total cholesterol (TC) targets. Moreover, risk factors are additive, and with each addition of another risk factor, the contributions of the others become more hazardous. Fortunately, if we begin our treatment strategy with lifestyle interventions that address several conditions simultaneously and promote the foundations for health, we will be doing our patients a service on several fronts.

We begin addressing dyslipidemia by introducing a TLC diet format and several individual dietary recommendations to reduce cholesterol and triglycerides. We encourage a plant-based diet that adheres to the TLC fat restrictions or less. TLC dietary restrictions emphasize less than 20% to 30% of daily calories from fat, less than 7% of those from saturated fat, and less than 200 to 300 mg of dietary cholesterol per day. The TLC diet has been shown to lower LDL-c by 10%.54

Recommendations for various therapeutic diets overlap substantially in the setting of high blood pressure, dyslipidemia, and metabolic syndrome and demonstrate how several therapeutic dietary strategies can be used simultaneously. The TLC dietary guidelines coexist nicely with the DASH, Mediterranean, and plant-based dietary guidelines. It is widely acknowledged that there are several important health-promoting eating behaviors present in the Mediterranean-style diet, including high monounsaturated to saturated fat ratio; low to moderate red wine consumption; high consumption of legumes, grains and cereals, fruits, and vegetables; low consumption of meat and meat products; increased consumption of fish; moderate consumption of milk and dairy products; dining in community; and other behaviors. The two features considered most defining are the exchange of saturated fats for monounsaturated fats and increased fruit and vegetable intake.55 The DASH diet also defined increased fruit and vegetable intake as part of that dietary strategy. Plant-based diets emphasize the intake of fruits and vegetables as the primary source of dietary calories. As such, they naturally include increased consumption of dietary fiber and plant sterols. In a comparison of Mediterranean diet versus low-fat diet, the Mediterranean group had greater weight loss; lower blood pressure; improved lipid profiles; and improvements in insulin resistance, endothelial function, and inflammation.56 Whereas a DASH diet, which had a sodium restriction to 2400 mg/day and permitted more dairy intake than in the Mediterranean diet study, demonstrated improved triglycerides, diastolic blood pressure, and fasting glucose than in the comparison diet, a weight-reducing diet emphasizing healthful food choices.57

In fact, none of these therapeutic diets are necessarily incompatible with one another. They can be combined appropriately or along with other strategies to meet therapeutic targets. Patients on a TLC diet can decrease their lipids by 10%.54 A Mediterranean diet can be made to meet the TLC guidelines, the DASH guidelines, or other dietary guidelines such as gluten-free, diary-free, plant-based, or other necessary interventions.

We encourage patients to work toward several other small daily dietary interventions that can accumulate to large changes in the lipid profile, blood pressure, and metabolic syndrome traits. We help patients to move in the direction of a dietary intake of 40 to 50 grams per day of fiber. Many are starting from a daily intake that is only a fraction of this amount, so it is important to assess where a person is starting and work on manageable goals for increasing dietary fiber. We advise patients to get 50% of their fiber as soluble fiber and 50% as insoluble. Insoluble fiber helps to bind up cholesterol; insoluble fiber keeps cholesterol moving out of the body in the stool. Increased dietary fiber can lower LDL-c 5 to 10% as well as help decrease blood pressure and body weight.54

We encourage patients to work toward consumption of 2 to 2.5 grams/day of plant sterols and stanols, in the absence of contraindications. Plant sterols and stanols compete with cholesterol for absorption in the intestines. Plant sterols and stanols can help to lower cholesterol by 10% or more. Several other small, strategic additions to the diet can help to make impacts on the cholesterol: increasing consumption of nuts decreases LDL-c by about 5% to 8% and consumption of soy protein decreases cholesterol about 3% to 10%.54

The strategic success or failure of lifestyle interventions is in putting them all together. The most difficult part of change is maintenance. Most practitioners have observed that, the more changes that we ask a patient to make, the fewer will be made. Lifestyle changes are habitual: we have the power of old habits working against us; eventually we have the power of new habits working for us. Therefore it stands to reason that the more of these lifestyle modifications that we can incorporate into as single behavior, the higher its probable long-term success. On that front, there are two powerful lifestyle interventions that most people can introduce and maintain with relative ease and which can get done a great deal of the important work to be done.

Two high-yield lifestyle interventions that can bring rapid improvements in blood pressure, lipids, and blood sugar with minimal dietary changes are the optimization of flaxseed and cinnamon in the diet. Small clinical trials have shown that 30 grams per day of ground flaxseed added to the diet over 6 months result in BP reductions of up to 10/7 mmHg in the flaxseed group when compared with controls. Participants who started the trial with the most severe high blood pressure showed even greater reductions in blood pressure of 15/7 mmHg.58 Flaxseed, when ground, is an excellent source of soluble and insoluble fiber. This not only helps to lower cholesterol, but also helps to decrease the body’s absorption of carbohydrates eaten together with that fiber; this is the principle of the glycemic index. Ground flax seed contains plant sterols and parent omega-3 oils, chiefly alpha-linolenic acid. Therefore, eating ground flaxseed daily is a way to decrease your blood pressure and the glycemic index of your meal while helping to provide soluble and insoluble fiber and plant sterols to your diet. We recommend about 6 to 8 tablespoons (Tbsp) of ground flaxseed per day to patients. With that amount, we can ensure that we are getting a blood pressure benefit, a boost of about 10 grams in daily fiber intake, and about 40 mg of plant sterols. There are plenty of other ways that patients can negotiate to get adequate daily fiber through use of psyllium supplements, oatmeal or barley consumption, or others; flax is simply and inexpensive and user-friendly way to meet several goals simultaneously.

Optimizing a patient’s daily cinnamon intake is another straightforward, inexpensive, and user-friendly way to achieve intervention simultaneously on several aspects of dyslipidemia and metabolic syndrome. In the past, the evidence on cinnamon has been conflicting. Recent past meta-analyses have showed no benefit to the use of cinnamon in the treatment of high blood sugar and metabolic syndrome. However, the most recent and updated systematic review and meta-analysis of trials of cinnamon for decreasing blood sugar demonstrate fairly impressive effects and include several important effects on cholesterol.

Allen et al. (2013) published their review and meta-analysis of 10 randomized controlled trials of the use of cinnamon as an intervention for fasting plasma glucose levels, glycated hemoglobin (HbA1c), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), and/or triglycerides. The doses of cinnamon varied from 120 mg to 6000 mg/day for 4 to 18 weeks. The analysis demonstrated that cinnamon consumption significantly decreased: fasting plasma glucose levels by 24.6 mg/dL, TC 15.6 mg/dL, LDL-c 9.4 mg/dL and triglycerides by 29.6 mg/dL. Cinnamon mildly raised HDL-c levels and there was no significant change in HbA1c levels. There was a high degree of heterogeneity among the studies, meaning that the various studies in the review and meta-analysis used different types and amounts of cinnamon, measured different outcomes and conducted their studies in slightly different ways. That may partly account for why significant changes in HbA1c were not seen.

High heterogeneity will lead conventional authorities to argue that the results of this study are not yet applicable to patient care; that we do not have enough information yet to know the correct dose, duration, and form of treatment; that we do not have a standardized and reliable source; and that we cannot be sure if its interactions with other medications. These are all important points to be taken into account and monitored. Yet with appropriate monitoring and follow-up, it is likely that we can feel good about recommending cinnamon at doses equivalent to culinary use on a daily basis. We typically recommend ground cinnamon at one-quarter to one-half of a teaspoon three times daily with meals.

Pharmacologic and nonpharmacologic treatments have their place in the clinical redress of hypertension, high cholesterol, and metabolic syndrome. As integrated providers and practitioners of complementary and alternative medicine (CAM), we have an opportunity to create the foundations for health and disease reversal in the interventions which we recommend for patients with these conditions. Therapeutic lifestyle interventions are available to virtually all patients with high blood pressure and high blood lipids. Therapeutic lifestyle changes form the foundations for healthful living that not only help patients overcome their present health concerns but also give them the possibility of living a more healthy life for the future, one more free from chronic disease.

To contact the author or for further information:

Jeremy Mikolai, ND

Heart & Lung Wellness Center of Excellence in Naturopathic Cardiovascular Medicine

Center for Natural Medicine Inc. (CNM)

1330 SE Cesar E Chavez Blvd.

Portland, Oregon 97214

503-232-1100

CNMWellness.com

drmikolai@cnmwellness.com

This author has no financial conflicts of interest to declare.

Jeremy Mikolai, ND, is the NERC Integrative Cardiovascular Medicine Fellow for 2013–2015. Along with Drs. Tori Hudson, Martin Milner, and Sheryl Estlund and the Naturopathic Education and Research Consortium (NERC), he has designed the first-ever clinical fellowship program for naturopathic physicians to develop special expertise in areas of medical emphasis. Dr. Mikolai is an assistant professor of naturopathic medicine, clinical medicine, and research at the National College of Natural Medicine (NCNM) and adjunct faculty/professor of cardiology in the naturopathic medicine department at Universidad del Turabo in Gurabo, Puerto Rico. He is also a lead faculty member at the Heart and Lung Wellness Center of Excellence in Naturopathic Cardiovascular Medicine at NCNM and at the Naturopathic Institute of Cardiovascular and Pulmonary Medicine (NICVM).

Notes

1. Egan BM, Zhao Y, Axon RN. US trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA 2. 2010; ;303:2043.

2. Greenland P, Knoll MD, Stamler J, et al. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA 2. 2003; ;290:891.

3. Levy D, Larson MG, Vasan RS, et al. The progression from hypertension to congestive heart failure. JAMA 1996; ;275:1557.

4. Hsu CY, McCulloch CE, Darbinian J, et al. Elevated blood pressure and risk of end-stage renal disease in subjects without baseline kidney disease. Arch Intern Med. 2005; ;165:923.

5. Thrift AG, McNeil JJ, Forbes A, Donnan GA. Risk factors for cerebral hemorrhage in the era of well-controlled hypertension. Melbourne Risk Factor Study (MERFS) Group. Stroke. 1996; ;27:2020.

6. Rosenson RS, de Ferranti SD, Durrington P. Inherited disorders of LDL-cholesterol metabolism. In: Basow DS, ed. UpToDate. Waltham, MA; 2013.

7. Staessen JA, Fagard R, Thijs L, et al. Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. The Systolic Hypertension in Europe (Syst-Eur) Trial Investigators. Lancet. 1997; ;350:757.

8. Diao D, Wright JM, Cundiff DK, Gueyffier F. Pharmacotherapy for mild hypertension. Cochrane Database Syst Rev. 2012;8. Article No. CD006742. doi:10.1002/14651858.CD006742.pub2.

9. Mancia G, Fagard R, Narkiewicz K, et al. 2013 Practice guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC): ESH/ESC Task Force for the Management of Arterial Hypertension. J Hypertens. 2013;31:1925–1938.

10. Kaplan NM, Domino FJ. Overview of hypertension in adults. In: Basow DS, ed. UpToDate. Watham, MA; 2013.

11. Appel LJ, Brands MW, Daniels SR, et al. Dietary approaches to prevent and treat hypertension: a scientific statement from the American Heart Association. Hypertension. 2006; ;47:296.

12. He FJ, MacGregor GA. Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials. Lancet 2. 2011; ;378:380.

13. Taylor RS, Ashton KE, Moxham T, et al. Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review). Am J Hypertens. 2011; ;24:843.

14. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003; ;42:1206.

15. Mancia G, De Backer G, Dominiczak A, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens. 2007; ;25:1105.

16. US Dept of Agriculture and US Dept Health and Human Services. Dietary Guidelines for Americans, 2010. Washington, D.C.: U.S. Government Printing Office; 2010.

17. He FJ, MacGregor GA. Effect of longer-term modest salt reduction on blood pressure. Cochrane Database Syst Rev 2. 2004; ;4:CD004937.

18. Singer DR, Markandu ND, Sugden AL, et al. Sodium restriction in hypertensive patients treated with a converting enzyme inhibitor and a thiazide. Hypertension. 1991; ;17:798.

19. Slagman MC, Waanders F, Hemmelder MH, et al. Moderate dietary sodium restriction added to angiotensin converting enzyme inhibition compared with dual blockade in lowering proteinuria and blood pressure: randomised controlled trial. BMJ. 2 2011; ;343:d4366.

20. Cook NR, Cutler JA, Obarzanek E, et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ. 2007; ;334:885.

21. Ram CV, Garrett BN, Kaplan NM. Moderate sodium restriction and various diuretics in the treatment of hypertension. Arch Intern Med. 1981; ;141:1015.

22. Hedayati SS, Minhajuddin AT, Ijaz A, et al. Association of urinary sodium/potassium ratio with blood pressure: sex and racial differences. Clin J Am Soc Nephrol. 2012; ;7:315

23. Whelton PK, He J, Cutler JA, et al. Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials. JAMA. 1997; ;277:1624.

24. Whelton SP, Chin A, Xin X, He J. Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials. Ann Intern Med. 2002; ;136:493.

25. Dickinson HO, Mason JM, Nicolson DJ, et al. Lifestyle interventions to reduce raised blood pressure: a systematic review of randomized controlled trials. J Hypertens. 2006; ;24:215.

26. Cornelissen VA, Buys R, Smart NA. Endurance exercise beneficially affects ambulatory blood pressure: a systematic review and meta-analysis. J Hypertens. 2013; ;31:639.

27. Cornelissen VA, Fagard RH, Coeckelberghs E, Vanhees L. Impact of resistance training on blood pressure and other cardiovascular risk factors: a meta-analysis of randomized, controlled trials. Hypertension. 2011; ;58:950.

28. Stevens VJ, Corrigan SA, Obarzanek E, et al. Weight loss intervention in phase 1 of the Trials of Hypertension Prevention. The TOHP Collaborative Research Group. Arch Intern Med. 1993; ;153:849.

29. Xin X, He J, Frontini MG, et al. Effects of alcohol reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2001; ;38:1112.

30. Grover SA, Coupal L, Zowall H. Treating osteoarthritis with cyclooxygenase-2-specific inhibitors: what are the benefits of avoiding blood pressure destabilization? Hypertension. 2005; ;45:92.

31. Pope JE, Anderson JJ, Felson DT. A meta-analysis of the effects of nonsteroidal anti-inflammatory drugs on blood pressure. Arch Intern Med. 1993; ;153:477.

32. Johnson AG, Nguyen TV, Day RO. Do nonsteroidal anti-inflammatory drugs affect blood pressure? A meta-analysis. Ann Intern Med. 1994; ;121:289.

33. Sudano I, Flammer AJ, Périat D, et al. Acetaminophen increases blood pressure in patients with coronary artery disease. Circulation. 2010; ;122:1789.

34. Zanchetti A, Hansson L, Leonetti G, et al. Low-dose aspirin does not interfere with the blood pressure-lowering effects of antihypertensive therapy. J Hypertens. 2002; ;20:1015.

35. Larsen T, Mose FH, Bech JN, et al. Effect of cholecalciferol supplementation during winter months in patients with hypertension: a randomized, placebo-controlled trial. Am J Hypertens. 2012; ;25:1215.

36. Roumie CL, Elasy TA, Greevy R, et al. Improving blood pressure control through provider education, provider alerts, and patient education: a cluster randomized trial. Ann Intern Med. 2006; ;145:165.

37. Houston TK, Allison JJ, Sussman M, et al. Culturally appropriate storytelling to improve blood pressure: a randomized trial. Ann Intern Med. 2011; ;154:77.

38. Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005; ;112:2735.

39. Ford ES, Li C, Sattar N. Metabolic syndrome and incident diabetes: current state of the evidence. Diabetes Care. 2008; ;31:1898.

40. Ford ES. Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: a summary of the evidence. Diabetes Care. 2005; ;28:1769.

41. Galassi A, Reynolds K, He J. Metabolic syndrome and risk of cardiovascular disease: a meta-analysis. Am J Med. 2006;119:812.

42. Gami AS, Witt BJ, Howard DE, et al. Metabolic syndrome and risk of incident cardiovascular events and death: a systematic review and meta-analysis of longitudinal studies. J Am Coll Cardiol. 2007; ;49:403.

43. Marceau P, Biron S, Hould FS, et al. Liver pathology and the metabolic syndrome X in severe obesity. J Clin Endocrinol Metab. 1999; ;84:1513.

44. Hamaguchi M, Kojima T, Takeda N, et al. The metabolic syndrome as a predictor of nonalcoholic fatty liver disease. Ann Intern Med. 2005; ;143:722.

45. Hanley AJ, Williams K, Festa A, et al. Liver markers and development of the metabolic syndrome: the insulin resistance atherosclerosis study. Diabetes. 2005; ;54:3140.

46. Chen J, Muntner P, Hamm LL, et al. The metabolic syndrome and chronic kidney disease in U.S. adults. Ann Intern Med. 2004; ;140:167.

47. Zhang L, Zuo L, Wang F, et al. Metabolic syndrome and chronic kidney disease in a Chinese population aged 40 years and older. Mayo Clin Proc. 2007; ;82:822.

48. Kurella M, Lo JC, Chertow GM. Metabolic syndrome and the risk for chronic kidney disease among nondiabetic adults. J Am Soc Nephrol. 2005; ;16:2134.

49. Pasquali R, Gambineri A, Anconetani B, et al. The natural history of the metabolic syndrome in young women with the polycystic ovary syndrome and the effect of long-term oestrogen-progestagen treatment. Clin Endocrinol (Oxf). 1999; ;50:517.

50. Vgontzas AN, Papanicolaou DA, Bixler EO, et al. Sleep apnea and daytime sleepiness and fatigue: relation to visceral obesity, insulin resistance, and hypercytokinemia. J Clin Endocrinol Metab. 2000; ;85:1151.

51. Ip MS, Lam B, Ng MM, et al. Obstructive sleep apnea is independently associated with insulin resistance. Am J Respir Crit Care Med. 2002; ;165:670.

52. Choi HK, Ford ES. Prevalence of the metabolic syndrome in individuals with hyperuricemia. Am J Med. 2007; ;120:442.

53. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57:109.

54. Bruckert E, Rosenbaum D. Lowering LDL-cholesterol through diet: potential role in the statin era. Curr Opin Lipidol. 2011;22:43–48.

55. Rees K, Hartley L, Flowers N, Clarke A, Hooper L, Thorogood M, Stranges S. ‘Mediterranean’ dietary pattern for the primary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews 2013, Issue 8. Art. No.: CD009825. DOI: 10.1002/14651858.CD009825.pub2.

56. Esposito K, Marfella R, Ciotola M, et al. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA. 2004; ;292:1440.

57. Azadbakht L, Mirmiran P, Esmaillzadeh A, et al. Beneficial effects of a Dietary Approaches to Stop Hypertension eating plan on features of the metabolic syndrome. Diabetes Care. 2005; ;28:2823.

58. Rodriguez-Leyva D, et al. Potent antihypertensive action of dietary flaxseed in hypertensive patients. Hypertension. Epub Oct. 14, 2013 .

59. Allen RW, Schwartzman E, Baker WL, Coleman CI, Phung OJ. Cinnamon use in type 2 diabetes: an updated systematic review and meta-analysis. Ann Fam Med. 2013;(5):452–459.

Author

Already Subscribed?

Search

Formatting updates are ongoing for older articles.

Author

Featured Articles

Where are your Clinical Trials?

It has proven to be difficult, if not impossible, to proceed to full-scale randomized controlled trials (RCTs) for most of the natural methods that cannot be patented or otherwise monopolized. 

A Renewed Focus on Self-Help for Healing

As the producer of The Moss Report, the year leading up to the Covid-19 pandemic was filled with anticipation and excitement. We had invested years of hard work and significant resources into two major projects: our feature film, Immunotherapy: The Battle Within, and...

Issue Archives

Event Calendar

  • 2026 Association of Natural Health Conference

    Douglasville Conference Center Douglasville, GA, United States

    "From Practitioner to Leader: Clinical Excellence, Business Mastery & Sustainable Practice" Discover how clinical excellence, business mastery, and sustainable systems can help practitioners grow into confident leaders and build practices designed for long-term impact. Why Attend? Three days of learning, connection, and growth designed for every stage of your practice journey. Learn from Leading Voices Gain insights from top experts in natural health, holistic wellness, and functional medicine. Hands-On Learning Participate in in-depth workshops, real-world case studies, and interactive sessions you can apply immediately. Meaningful Networking Connect with like-minded professionals, students, and exhibitors who share your passion for natural health. Practical Tools & Approaches Explore new strategies and tools to elevate both your practice and your own health journey. Who Should Attend? This conference is built for a wide community of natural health professionals, educators, and advocates - wherever you are in your journey. Licensed & Clinical Practitioners Doctors, chiropractors, acupuncturists, naturopaths, and functional or integrative medicine practitioners looking to sharpen clinical skills and grow into stronger practice leaders. Allied Health Professionals Bio-feedback technicians and other allied practitioners seeking hands-on training and the latest tools in natural and holistic care. Educators & Students Natural health educators and students entering the […]

  • Food as Medicine Global 2026

    Virtual Event

    Join health professionals, farmers, food producers, researchers, educators, nonprofit leaders, chefs, policymakers, community organizers, food advocates, public health practitioners, nutritionists, and other changemakers as we convene to share knowledge, build partnerships, and explore new possibilities for improving health, strengthening communities, and creating more equitable and sustainable food systems. This year’s program features inspiring speakers and practical examples of collaboration at the intersection of food, health, social justice, and planetary well-being. Together, we’ll explore innovative approaches to Food as Medicine, community-led initiatives, nutrition, public health, regenerative agriculture, and equitable access to healthy food. Whether you work in health care, agriculture, food production, education, research, policy, or community development, you will discover new ideas, meaningful connections, and practical strategies to advance healthier, more resilient communities. Virtual  |  Join from anywhere in the world Check out the Program: https://tinyurl.com/Food-as-Medicine-for-All

  • The Midlife Women’s Health Summit: Evidence-Based Menopause Care in the Era of Longevity Medicine

    The Ritz-Carlton, Pentagon City 1250 S Hayes St, Arlington, VA, United States
    Hybrid Event

    Menopause Care in the Longevity Era Longevity medicine is everywhere right now. Supplements, protocols, influencer clinics, patients walking in with questions about interventions their doctors have never heard of. What's missing from most of it is the evidence. The Midlife Women's Health Summit is three days on what the research actually says about menopause care when you add a longevity lens. What works, what doesn't, what's being oversold, and what to tell the patient sitting in front of you. Co-chaired by Lisa Larkin, MD, FACP, MSCP, IF, Jen Gunter, MD, FRCS(C), FACOG, DABPM, ABPMR, and Lauren Streicher, MD, FACOG, MSCP; three of the clearest voices in women's health on separating data from marketing.

    $995 – $1299

Related Posts

Exposure, Activity, Contribution: Reading Epstein-Barr Findings in the Individual Patient

Robert Lamberton, BSc, FNTP – Epstein-Barr virus accounts for roughly 2% of cancers worldwide, approaching 360,000 new cases and as many as 210,000 deaths each year, and about 95% of adults carry it. In the overwhelming majority, it causes nothing at all.

When a test for an agent is positive in nearly everyone, a positive test is not a finding. It is a background condition.

Read More

Before Gerson: The Forgotten Medical History of Coffee Enemas

By Scott Wilson – In 1875, Dr. J.P. Thomas wrote about using coffee enemas for opium and belladonna poisoning. He referred to cases going back to 1858 and 1859 and described coffee enemas as one of the ordinary means of treatment. That word “ordinary” stopped me. He wasn’t describing an experiment. He was describing something physicians already knew.

Read More

0 Comments

Submit a Comment