Hypertension and Hyperinsulinemia

By Dr. Brian P. Jakes, Jr.

 

Hypertension is defined as the sustained elevation of either or both systolic and diastolic blood pressure while at rest. There are several different classifications of hypertension, but the two main categories are primary, also called essential hypertension, and secondary hypertension. The majority of all those diagnosed with hypertension fall under the primary category while only a small percentage are classified as secondary hypertensive. Secondary hypertension is the result of some other condition or disease where as primary hypertension is said, by conventional medicine, to have no identifiable cause for development.  

An overwhelming number of studies have revealed that diet, obesity and vitamin and mineral deficiencies are related to primary hypertension. Changes in lifestyle and the uses of specific supplements have proven to be extremely effective in the treatment and reversal of mild primary hypertension and could be considered prior to the use of prescription drugs  

Hypertension is strongly associated with the development of cardiovascular disease and is one of the major factors in the incidences of heart attacks in both the diabetic and non-diabetic population. It can also contribute to the progression of atherosclerosis. Numerous studies show a definite correlation between hypertension, diabetes, hyperglycemia, atherosclerosis and cardiovascular disease.[i] [ii]   

We are most interested in the links between diabetes and hypertension and how to prevent and or treat them accordingly.  

Type I diabetes patients usually develop secondary hypertension while Type II patients are associated with primary hypertension.  Secondary hypertension in Type I patients is usually the result of nephropathy often caused by chronic hyperglycemia. Type II diabetes patients can also develop secondary hypertension from nephropathy, but it is not as common.

The cause of primary hypertension in Type II patients as well as non-patients has been under investigation for some time without any real agreement on the subject.   

Hypertension, like other conditions, has several factors involved in its pathology and just as one individual event probably did not cause it, one type of treatment is not likely to cure it. The greatest single factor in the development of primary hypertension, which had been suggested over 30 years ago, is the condition of hyperinsulinemia.[iii] [iv] [v]  

Hyperinsulinemia can be caused by insulin resistance, which creates elevated glucose levels due to glucose intolerance. The pancreas tries to correct this by massively increasing insulin production, which leaves high levels of serum insulin that are not utilized. One of the many effects of this over production is the increased re-absorption of sodium by the kidneys.[vi] This causes increased extracellular fluid volume, which will demand greater cardiac output and raise blood pressure. There are also several other pathways in which sustained elevated levels of insulin can stimulate the sympathetic nervous system and increase peripheral vascular resistance and raise blood pressure.  

Hyperinsulinemia can also be caused by the uses of injected insulin. The hyperbolized amount of injected insulin needed to eventually make its way to the vascular system can increase insulin resistance. In spite of its extremely limited benefit, large doses of insulin are sometimes used in Type II patients in an attempt to overcome insulin resistance and restore normoglycemia, however this may be just adding to a hyperinsulinemia problem.  

Some studies clearly demonstrate the direct correlation between a decrease in insulin doses and a corresponding drop in blood pressure without deterioration in glucose control.[vii]  

Hyperinsulinemia, insulin resistance and glucose intolerance are the most prominent characteristics of Type II diabetes and Type II patients almost exclusively develop primary hypertension, which also shares identical symptoms.   

We know that exercise; diet modification and weight loss decreases both elevated blood pressure and glucose tolerance. One of the many ways this type of non-pharmaceutical treatment may accomplish these improvements is through an increase in insulin sensitivity.  

This action will cause a decrease in insulin resistance, which in turn will cause a reduction in insulin output. Correcting hyperinsulinemia, the primary root cause of the related conditions, would ultimately lead to improvements in both Type II diabetes and primary hypertension. There are trials that suggest that this process may be expedited with the uses of two trace minerals that enhance glucose uptake, chromium and vanadyl sulfate. 

There are other conditions that can contribute to hypertension and treatments used to correct them.  

Sodium in the form of common table salt increases blood pressure in those with hypertension with abnormal renal sodium handling characteristics.  The removal of added salt in specific individuals can cause up to a 10-15% decrease in overall blood pressure.  

Unsaturated fat to saturated fat intake ratio should be as high as conceivably possible. Monounsaturated fat is the preferred unsaturated fat for both its lower blood sugar impact and its ability to decrease blood pressure.  

Caffeine has a number of undesirable side effects that may aggravate the hypertensive condition through increased calcium excretion.[viii] There appears to be a direct relationship between low serum levels of calcium and primary hypertension.[ix] [x] There is evidence that impaired calcium metabolism and elevated urinary calcium levels may affect blood pressure regulation in hypertensive patients.[xi] [xii] Calcium supplements in the amount of 2 grams a day in the form of calcium lactate may prove helpful in blood pressure reduction. Potassium also has a role in hypertension treatment, for it will cause a modest reduction in blood pressure.[xiii] [xiv] Its intake should be in a higher ratio to that of sodium to be effective.  

Magnesium has one of the strongest correlations between low serum levels and insistences of hypertension.[xv] [xvi] [xvii] The uses of a one-gram a day dietary supplement of magnesium may induce a significant reduction in blood pressure.  

Coenzyme Q10 has been extremely effective in reducing elevated blood pressure in hypertension as well as improving other serious cardiac conditions.[xviii] [xix] [xx] [xxi] A total daily dose between 120-200 mg seemed to deliver the most benefit.  

The amino acid L-carnitine demonstrated its therapeutic value in several clinical trials with primary hypertensive patients.[xxii] [xxiii] It reduced symptoms and like all other supplements was well tolerated with no side effects. The doses varied between 2 to 4 grams a day.  

Several studies using vitamin B6 to treat primary hypertension had very favorable results in decreasing blood pressure.[xxiv] [xxv]  

Also, a vitamin D deficiency may exist in hypertensive patients and its replacement may improve blood pressure by correcting calcium metabolism irregularities.[xxvi] [xxvii] [xxviii]  

The involvement of free radicals and elevated oxidation rates, which are common in diabetes, brings to the forefront the role of antioxidants. There appears to be a correlation between low levels of serum antioxidants and the development of primary hypertension, atherosclerosis and ischemic heart disease.[xxix] [xxx]  

Beta carotene and vitamin A are included in some of these studies, but most of the attention has been focused on vitamins C and E.[xxxi] [xxxii] [xxxiii] These vitamins seem to offer at the very least protection from the fore mentioned conditions.  

Another link to cardiovascular problems that can affect diabetes patients, and the general population is serum homocysteine levels. Over three decades ago a Dr. Kilmer McCully, a Harvard educated researcher, discovered that high levels of serum homocysteine were a direct link to heart disease. At that time though, everyone was focusing their attention on the dangers of serum cholesterol and developing drugs to combat this condition in hopes to reduce associated deaths. It is interesting to note that almost half of the people that suffer heart attacks have normal serum cholesterol, so there must be other pathologies involved. Cholesterol occlusion can be the end result of a process that first begins damage to the intima lining of the vessel due to an inability to repair it from vitamin deficiencies. This damage causes vascular seepage and the body, without raw materials to effect proper repair, mobilizes fibrin and cholesterol to construct a patch and as long as the vitamin deficiency exists cholesterol keeps being produced. I have seen studies and have personally observed a decrease of nearly 60 points in total cholesterol from just an increase in vitamin C and E with no changes in diet, exercise or medications.[xxxiv] [xxxv] [xxxvi]  It was noted that even infants could die from cardiac failure with the only identifiable cause being elevated homocysteine levels. So, the time required for the progression of this condition is extremely brief. Dr. McCully also discovered that homocysteine levels are kept in check effectively and also inexpensively by vitamins B6, B12 and folic acid.[xxxvii] [xxxviii]  

There are studies that suggest that Type II patients have higher serum homocysteine levels than both Type I patients and normal controls.[xxxix] One of the several possible factors that might help explain these results may be that the sulfonylureas have been known to decrease some B vitamins in diabetes patients. Likewise the biguanides class of oral hypoglycemics causes a reduction of serum B12 and folic acid.[xl] [xli] These two classes of oral hypoglycemic drugs are often used together and may create an environment that can host not only an elevated homocysteine level, but may be involved in a number of other complications due to the vitamin loss associated with them.  

When we look for the ways to help our hypertensive, diabetic patients we can begin to evaluate certain nutritional parameters and help maximize each of our patient’s therapy.

 

Dr. Brian P. Jakes, Jr., N.D., C.N.C.  is a Board Certified Doctor of Naturopathy as well as a Certified Nutritional Consultant. In his practice, in Mandeville, LA, Dr. Jakes works with physicians to treat a large number of diabetes patients. This is an excerpt from his upcoming book; "Diabetes: The Essence Of A Cure”  

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 References:


[i] Massi-Benedetti M, Federici MO. Cardiovascular risk factors in type 2 diabetes: the role of hyperglycaemia. Exp Clin Endocrinol Diabetes 1999;107 Suppl 4:S120-3.

[ii] Hano T, Nishio I. Hypertension in the patients with impaired glucose tolerance. Nippon Rinsho 1996 Oct;54(10):2687-91.

[iii] Asch S, Wingard D, Barrett-Connor E. Are insulin and hypertension independently related? Annals of Epidemiology 1:23-44, 1991.

[iv] Gutin B, Islam S, Treiber F, Smith C. Pediatrics 1995;96:1123-1125.

[v] Swislocki ALM, Hoffman BB, Reaven GM. Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension. AM J Hypertension 2:419-23, 1989.

[vi] Rocchini AP, Katch V, Kveselis, Martin M. Insulin and renal sodium retention in obese adolescents.

Hypertension 14:367-74, 1989.

[vii] Tedde R, Sechi A, Pala A, Scano L. Antihypertensive effect of insulin reduction in diabetic hypertensive patients.

Am J Hypertension 2:163-70, 1989.

[viii] Wise KJ, Bergman EA, Sherrard DJ, Massey LK.  Interactions between dietary calcium and caffeine consumption on calcium metabolism in hypertensive humans.  Am J Hypertens 1996 Mar;9(3):223-9.

[ix] Reichel H, Liebethal R, Hense HW, Schmidt-Gayk H, Ritz E.  Disturbed calcium metabolism in subjects with elevated diastolic blood pressure.  Clin Investig 1992 Sep;70(9):748-51.

[x] Sowers JR, Zemel MB, Standley PR, Zemel PC.  Calcium and hypertension.  J Lab Clin Med 1989 Oct;114(4):338-48.

[xi] Zoccali C, Mallamaci F, Psotorino M, Cuzzola F.  Hyperfiltration and calcium metabolism in essential hypertension.  Am J Hypertens 1991 Dec;4(12 Pt 1):944-50.

[xii] Young EW, Morris CD, McCarron DA.  Urinary calcium excretion in essential hypertension.  J Lab Clin Med 1992 Oct;120(4):624-32.

[xiii] Kawano Y, Minami J, Takishita S, Omae T.  Effects of potassium supplementation on office, home, and 24 hour blood pressure in patients with essential hypertension.  Am J Hypertens 1998 Oct;11(10):1141-6.

[xiv] Wu X, Tolvanen JP, Hutri-Kahonen N, Kahonen M.  Comparison of the effects of supplementation with whey mineral and potassium on arterial tone in experimental hypertension.  Cardiovasc Res 1998 Nov;40(2):364-74.

[xv] Peacock JM, Folsom AR, Arnett DK, Eckfeldt JH.  Relationship of serum and dietary magnesium to incident hypertension:  the Atherosclerosis Risk in Communities (ARIC) Study.  Ann Epidemiol 1999 Apr;9(3):159-65.

[xvi] Sanjulianai AF, de Abreu Fagundes VG, Francischetti EA.  Effects of magnesium on blood pressure and intracellular ion levels of Brazilian hypertensive patients.  Int J Cardiol 1996 Oct ;56(2):177-83.

[xvii] Kawano Y, Marsuoka H, Takishita S, Omae T.  Effects of magnesium supplementation in hypertensive patients: assessment by office, home and ambulatory blood pressures.  Hypertension 1998 Aug;32(2):260-5.

[xviii] langsjoen H, Lansjoin P, Lansjoin P, Willis  R, Folkers K.  Usefulness of coenzyme Q10 in clinical cardiology: a long term study.  Mol Aspects Med 1994;15 Suppl:s165-75.

[xix] Digiesi V, Cantini f, Oradei A, Bisi G.  Coenzyme Q10 in essential hypertension.  Mol aspects Med 1994;15 Suppl:s257-63.

[xx] Singh RB, Niaz MA, Rastogi SS, Shukla PK, Thakur AS.  Effect of hydrosoluble coenzyme Q10 on blood pressures and insulin resistance in hypertensive patients with coronary artery disease.  J Hum Hypertens 1999 Mar;13(13):203-8.

[xxi] Folkers K, Drzewoski J, Richardson PC, Ellis J.  Bioenergetics in clinical medicine. XVI. Reduction of hypertension in patients by therapy with coenzyme Q10. Res Commun Chem Pathol Pharmacol 1981 Jan;31(1):129-40.

[xxii] Digiesi V, Cantini F, Bisi G, Guarino G, Brodbeck B. L-carnitine adjuvant therapy in essential hypertension.  Clin Ter 1994 May;144(5):391-5.

[xxiii] Digiesi V, Palchetti R, Cantini F.  The benefits of L-carnitine therapy in essential arterial hypertension with diabetes mellitus type II. Minerva Med 1989 Mar;80(3):227-31.

[xxiv] Aybak M, Sermet A, Ayyildiz MO, Karakilcik AZ.  Effect of orla pyridoxine hydrochloride supplementation on arterial blood pressure in patients with essential hypertension.  Arzneimittelforschung 1995 Dec;45(12):1271-3.

[xxv] Duleeva VL, Piatnitskaia In, Bogdanov NG. The vitamin B6 allowance of hypertension patients and the effect of dietotherapy.  Vopr Pitan 1990 May-Jun;(3):20-4.

[xxvi] Duprez D, de Buyzere M, de Backer T, Clement D.  Relationship between vitamin D3 and the peripheral circulation in moderate arterial primary hypertension. Blood Press 1994 Nov;3(6):389-93.

[xxvii] Young EW, Morris CD, Holcomb S, McMillan G. Regulation of parathyroid hormone and vitamin D in essential hypertension. Am J Hypertens 1995 Oct:8(10 Pt 1):957-64.

[xxviii] Lind L, Wengle B, Wide L, Sorensen OH, Ljunghall S.  Hypertension in primary hyperparathyroidism—reduction of blood pressure by long term treatment with vitamin D (alphacalcidol).  A double blind, placebo controlled study.  Am J Hypertens 1988 Oct;1(4 Pt 1):397-402.

[xxix] Rissp C. P;ovoero P. Girelli D, Faccini G.  Anti-oxidant status and lipid peroxidation in patients with essential hypertension.  J Hypertens 1998 Sep;16(9):1267-71.

[xxx] Wen Y, Killalea S, McGettigan P, Feely J.  Lipid peroxidation and antioxidant vitamins C and E in hypertensive patients.  Ir J Med Sci 1996 Jul-Sep;165(3):210-2.

[xxxi] Galley HF, Thornton J, Jowdle PD, Walker BE, Webster NR.  Combination oral antioxidant supplementation reduces blood pressure.  Clin Sci (Colch) 1997 Apr;92(4);361-5.

[xxxii] Yoshioka M, Matsushita T, Chuman Y.  Inverse association of serum ascorbic acid level and blood pressure or rate of hypertension in male adults aged 30-39 years.  Int J Vitam Nutr Res 1984;54(4):343-7.

[xxxiii] Kuznetsov NS, Abulela AM, Neskromnyi VN.  The comparative evaluation of the efficacy of tocopherol acetate in the combined treatment of patients with hypertension and diabetes mellitus.

Lik Sprava 1994 Sep-Dec;(9-12):133-6.

[xxxiv] Ginter E, Zdichynec B, Holzerova O, Ticha E. Hypocholesterolemic effect of ascorbic acid in maturity onset diabetes mellitus. Int J Vitam Nutr Res 1978;48(4):368-73.

[xxxv] Paolisso G, Balbi V, Volpe C. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll Nutr 1995 Aug;14(4):387-92.

[xxxvi] Paolisso G, D’Amore A, Balbi V. Daily vitamin E supplements improve metabolic control but not insulin secretion in elderly type II diabetic patients. Diabetes Care v16, n11 Nov 1993.

[xxxvii] Siri PW, Verhoef P, Kok FJ. Vitamins B6, B12 and folate: association with plasma total homocysteine and risk of coronary atherosclerosis. J Am Coll Nutr 1998 Oct;17(5):435-41.

[xxxviii] Pancharuniti N, Lewis CA, Perkins LL, Go RC. Plasma homocysteine, folate, and vitamin B12 concentrations and risk for early onset coronary artery disease. Am J Clin Nutr 1994 Apr;59(4):940-8.

[xxxix] Chico A, Perez A, Cordoba A, Arcelus R. Plasma homocysteine is related to albumin excretion rate in patients with diabetes mellitus: a new link between diabetic nephropathy and cardiovascular disease? Diabetologia 1998 Jun;41(6):684-93.

[xl] Caspary WF, Zavada I, Reimold W, Deuticke U. Alteration of bile acid metabolism and vitamin B12 absorption on biguanides. Diabetologia 1977 May;13(3):187-93.

[xli] Carpentier JL, Bury J, Luyckx A, Lefebvre P. Vitamin B12 and folic acid serum levels in diabetics under various therapeutic regimens. Diabete Metab 1976 Dec;2(4):187-90

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