~ Rethinking Women and Heart Disease, Case Studies and References

Patient Case Study #1

A 50-year-old Caucasian woman presented with the following complaints during her initial visit in April 1999: high blood pressure that was poorly controlled with prescription drugs; migraine; high cholesterol; depression; severe anxiety; irritability; fatigue; poor libido; low sex drive; genital herpes; poor short-term memory; trouble falling asleep; weight gain; arthritis; and irregular menstrual cycle. Her vital signs: height, 5'4"; weight, 125 pounds; blood pressure, 150/90 mmHg; pulse, 64 beats/minute.

Many of these signs and symptoms are risk factors for CHD, including hypertension, elevated cholesterol, and depression/anxiety. We indicated that broad-spectrum treatment of these risk factors could dramatically reduce her chances of experiencing debilitating or deadly CHD.

The patient had complained of most of her symptoms for the last 10-15 years. She did not exercise, noting that despite her desire to lose some weight, she felt tired all the time.

The patient was taking the following drugs: triamterene/ hydrochlorothiazide, Procardia XL®, and Nifedical XL® (for high blood pressure); Premphase® (for hot flashes and vaginal dryness); Zoloft® (for depression); Butisol Sodium® (sedative) and Ambien® (for sleeping disorder); and Zovirax® and Valtrex® (to manage genital herpes recurrences).

Initial laboratory evaluations revealed high total cholesterol (241 mg/dL). Her profile of basic steroid hormones also was significantly imbalanced. The patient's hormone levels are shown in Table 1 (reference ranges shown in parentheses).

Table 1

Hormone - (Reference Range) - Patient's Result

  • DHEA-S - (65-380 ug/dL) - 66

  • Pregnenolone - (10-230 ng/dL) - 50

  • Total estrogen - (61-437 pg/mL) - 643

  • Progesterone - (0.2-28 ng/mL) - 0.7

  • Total testosterone - (14-76 ng/dL) - 29


The patient had an extremely high level of total estrogen and low levels of the four other steroid hormones. She demonstrated a relative dominance of estrogens, which can stimulate sympathetic system activity and might explain why she had serious difficulties correcting her blood pressure.

The patient's initial treatment program focused on correcting what we considered her "foundational problem": hormonal imbalance. The patient started the following treatment with bioidentical hormones taken in the morning:

  • pregnenolone: 100 mg
  • DHEA: 50 mg
  • Triest gel (containing a 90:7:3 ratio of estriol, estradiol, and estrone): 0.6 ml on days 1-10 following menses, 0.4 ml on days 11-21
  • micronized progesterone gel (50 mg/ml): 0.6 ml on days 1-10 after menses, 0.8 ml until menses begins
  • micronized testosterone gel (50 mg/ml): 0.1 ml daily


Additional supplements included in her treatment were: Life Extension Mix, three tablets taken three times daily; omega-3 fatty acids, 1000 mg taken in the morning; glucosamine sulfate, 2000 mg taken in the morning; phosphatidylserine, 200 mg taken in the morning; and NutriCology® ProGreens® (containing green foods, plant fibers, bioflavonoids, herbal extracts, and probiotics), one scoop taken in the morning. After three days on the program, the patient discontinued her use of Premphase®.

During the first month of treatment, the patient's blood pressure improved to 130/90 mmHg, her migraines decreased in frequency and severity, and her joint pain disappeared completely. We increased her dose of DHEA to 100 mg in the morning and 50 mg at noon, and added 0.2 ml of progesterone and 420 mg of magnesium citrate to be taken one hour before bedtime.

During the next three months, the patient's depression and anxiety were so improved that she decreased and then discontinued her use of Zoloft® and Butisol Sodium®. She later stopped taking Ambien® because her sleeping disorder had resolved. The patient reported that she was on only one drug for hypertension (Procardia XL®) and that her energy level had improved tremendously. She started exercising four to five times weekly. At this time, we added to the patient's regimen human growth hormone (HGH), 0.5 IU daily taken six days per week, and androstenedione, 50 mg taken 30 minutes before exercise. We decreased DHEA to 50 mg and increased pregnenolone to 200 mg taken in the morning.

After one year of treatment, the patient had experienced no recurrences of genital herpes and thus decided to discontinue her prescription medications for herpes. Her quality of life had vastly improved, with no occurrence of migraine, which she described as the "first sustained relief in several years." Her total cholesterol had dropped to 187 mg/dL and her blood pressure was 120-130/70 mmHg, though she no longer was using any medication to control blood pressure. She also reported no memory problems. Today, the patient enjoys a healthy lifestyle, exercises regularly, eats a balanced diet, and continues her hormonorestorative therapy and supplements.




CONVENTIONAL AND COMPLEMENTARY APPROACHES TO PREVENTING CORONARY HEART DISEASE

Clinical experience and the medical literature suggest the following general guidelines for preventing coronary heart disease (CHD):

  • Maintain blood pressure of less than 140/90 mmHg (120/80 is optimal)

  • Maintain blood glucose of 80-120 mg/dL (less than 100 is optimal)

  • Maintain total cholesterol of less than 200 mg/dL (and not less than 160) and LDL (low-density lipoprotein) of less than 130 mg/dL (less than 100 is optimal)

  • Exercise regularly (30-60 minutes of aerobic exercise three to five times weekly is optimal).


When it comes to preventing CHD in women, an ounce of prevention may be worth a pound of cure. A general approach to preventing CHD should include modification of risk factors that play important roles in the disease's development and progression.

While factors such as aging, race, and family history of the disease cannot be controlled, the good news is that you can modify critical risk factors such as high cholesterol, high homocysteine, high blood pressure, diabetes, smoking, physical inactivity, stress, and being overweight or obese.

Diabetes and high cholesterol, homocysteine, and blood pressure can be improved through diet, exercise, medication, and supplements. High C-reactive protein (CRP), an inflammatory biomarker, may help to identify those who would benefit from anti-inflammatory intervention. Diet, lifestyle changes, positive adaptation to stress, and supplements can assist in weight loss and help decrease stress. Quitting smoking will also reduce CHD risk. The scientific data strongly suggest that modification of these multiple risk factors can help to lessen CHD risk and thus total mortality in women.


Patient Case Study #2

A 56-year-old Caucasian woman presented in September 1999 with a history of chronic fatigue syndrome, obesity, severe shortness of breath, hypertension, type II diabetes, depression, anxiety, panic attacks, insomnia, arthritis, body aches, hot flashes, vaginal dryness, no sex life, vaginal yeast infection, short-term memory problems, and "chocoholism." Her height was 4'10," her weight 232 pounds, her blood pressure 168/86 mmHg, and her pulse 72 beats/minute.

The patient began having most of these symptoms after the age of 44, soon after her divorce. Her body weight at that time was 118 pounds. At the age of 30, she had a complete hysterectomy secondary to fibroids. This patient had numerous risk factors that, left untreated, could lead to a major cardiovascular event. Heart disease does not happen in isolation, but instead results from a system-wide breakdown in the body. We indicated that by intervening and diminishing her risk factors, we could help her decrease her risk for CHD.

At the time of her first visit, she was taking Glucophage® and glyburide (for type II diabetes), Zestril® and hydrochlorothiazide (for high blood pressure), Wellbutrin® (for depression), Premarin® (for hot flashes and sex disorder), Tylenol® (for pain), multi-vitamins, liquid minerals, vitamin E, niacin, and two weight-loss supplements.

In this case, we again found a high estrogen level (699 pg/mL) and low levels of progesterone (0.2 ng/mL), testosterone (16 ng/dL), DHEA-S (35 ug/dL), and pregnenolone (less than 10 ng/dL). We recommended the following program (all taken in the morning except where noted):

  • vitamin E: 1000 mg
  • selenium: 200 mcg
  • pregnenolone: 200 mg
  • DHEA: 100 mg
  • Triest gel: 1 ml on days 1-14, 0.8 ml on days 15-25, and 0.4 ml on the last five to six days of each month
  • micronized progesterone gel (50 mg/ml): 0.8 ml on days 1-14, 1 ml on days 15-25, and 0.6 ml on the last five to six days of each month
  • micronized testosterone gel (50 mg/ml): 0.2 ml every day
  • phosphatidylserine: 200 mg
  • Nutribiotic® MetaRest® (containing 3 mg of melatonin, 250 mg of kava root extract, and 10 mg of vitamin B6 per capsule): one capsule at bedtime
  • chromium: 400 mcg twice daily


After two days on the program, the patient discontinued her use of Premarin®. We recommended that she decrease her carbohydrate intake and begin an exercise program.

One month later, she returned to the clinic, reporting no complaints whatsoever. Her energy levels had improved significantly, she had lost 10 pounds, and she had elected to discontinue her use of Wellbutrin® and Tylenol®. We added to her regimen glucosamine sulfate (2250 mg taken in the morning), androstenedione (50 mg taken 30 minutes before exercise), and 0.2 ml of progesterone and 420 mg of magnesium citrate, taken one hour before bedtime.

After four months on the program, the patient had lost an additional 28 pounds and said that she felt like a different person. Her blood pressure had normalized to 120/80 mmHg and her blood glucose was stable. At this time, we added the following supplements to her regime: conjugated linoleic acid (CLA), 8 grams taken in the morning before breakfast; chitosan, two capsules taken before lunch and two capsules before dinner; hydroxycitric acid (HCA), one (1000-mg) capsule taken three times daily before meals (for weight loss); B-complex vitamins, one tablet daily; and omega-3 fatty acids, 3000 mg taken twice daily. We also suggested a one-month parasite-cleansing program using Unicity™ Paraway® Pack.

At the patient's one-year follow-up visit, she reported that she was no longer taking prescription drugs for high blood pressure or type II diabetes, and that her blood pressure and blood glucose levels were normal and stable.

Conclusion

In the cases just described, each woman had several risk factors for CHD before initiating an individualized anti-aging program of hormone restoration therapy.

We believe that hormone restoration may help prevent the development of CHD in women by helping to eliminate cardiovascular risk factors such as high blood pressure, being overweight or obese, elevated blood lipids and blood sugar, and abnormal responses to stress.

We further believe that individualized hormonorestorative therapy using bioidentical hormones applied in a cyclical manner and balancing levels of all the body's major steroid hormones may help women achieve the reduced risk of cardiovascular disease associated with the premenopausal years.

Hormone restoration is not yet widely practiced because it is not always easy to implement, requiring as it does an individualized regimen tailored to the needs of each patient. The two cases just described may help us understand what can be done to reduce or eliminate CHD risk factors in women through the application of hormonorestorative therapy.

References

1. Available at: http://www.americanheart.org/presenter.jhtml?identifier=2859. Accessed May 27, 2005.

2. Lewis V, Hoeger K. Prevention of coronary heart disease: a nonhormonal approach. Semin Reprod Med. 2005 May;23(2):157-66.

3. Baxter JD, Young WF, Jr., Webb P. Cardiovascular endocrinology: introduction. Endocr Rev. 2003 Jun;24(3):253-60.

4. Mendelsohn ME, Karas RH. The protective effects of estrogen on the cardiovascular system. N Engl J Med. 1999 Jun 10;340(23):1801-11.

5. Bush TL, Barrett-Connor E, Cowan LD, et al. Cardiovascular mortality and noncontraceptive use of estrogen in women: results from the Lipid Research Clinics Program Follow-up Study. Circulation. 1987 Jun;75(6):1102-09.

6. Grady D, Rubin SM, Petitti DB, et al. Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann Intern Med. 1992 Dec 15;117(12):1016-37.

7. Mendelsohn ME and Karas RH. Estrogen and the blood vessel wall. Curr Opin Cardiol. 1994 Sep;9(5):619-26.

8. Karas RH, Patterson BL, Mendelsohn ME. Human vascular smooth muscle cells contain functional estrogen receptor. Circulation. 1994 May;89(5):1943-50.

9. Kask E. 17-Ketosteroids and arteriosclerosis. Angiology. 1959 Oct;10:358-68.

10. Bernini GP, Sgro' M, Moretti A, et al. Endogenous androgens and carotid intimal-medial thickness in women. J Clin Endocrinol Metab. 1999 Jun;84(6):2008-12.

11. Ebeling P, Koivisto VA. Physiological importance of dehydroepiandrosterone. Lancet. 1994 Jun 11;343(8911):1479-81.

12. Vermeulen A. Dehydroepiandrosterone sulfate and aging. Ann NY Acad Sci. 1995 Dec 29;774:121-7.

13. Labrie F, Belanger A, Luu-The V, et al. DHEA and the intracrine formation of androgens and estrogens in peripheral target tissues: its role during aging. Steroids. 1998 May;63(5-6):322-8.

14. Wu FC, von EA. Androgens and coronary artery disease. Endocr Rev. 2003 Apr;24(2):183-217.

15. Yager JD. Endogenous estrogens as carcinogens through metabolic activation. J Natl Cancer Inst Monogr. 2000;(27):67-73.

16. Head KA. Estriol: safety and efficacy. Altern Med Rev. 1998 Apr;3(2):101-13.

17. Apgar BS, Greenburg G. Using progestins in clinical practice. Am Fam Physician. 2002 Oct 15;62(8):1839-46, 1849-50.

18. Mosca LJ. Contemporary management of hyperlipidemia in women. J Womens Health Gend Based Med. 2002 Jun;11(5):423-32.

19. Grady D, Herrington D, Bittner V, et al. Cardiovascular disease outcomes during 6.8 years of hormone therapy: Heart and Estrogen/progestin Replacement Study follow-up (HERS II). JAMA. 2002 Jul 3;288(1):49-57.

20. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA. 2002 Jul 17;288(3):321-33.

21. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002 Jan 16;287(3):356-9.

22. Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA. 2002 Dec 4;288(21):2709-16.

23. Mosca L, Grundy SM, Judelson D, et al. Guide to Preventive Cardiology for Women. AHA/ACC Scientific Statement Consensus panel statement. Circulation. 1999 May 11;99(18):2480-4.

24. Clarke R, Daly L, Robinson K, et al. Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med. 1991 Apr 25;324(17):1149-55.

25. Robinson K, Mayer E, Jacobsen DW. Homocysteine and coronary artery disease. Cleve Clin J Med. 1994 Nov;61(6):438-50.

26. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA. 1995 Oct 4;274(13):1049-57.

27. Mitra B, Panja M. High sensitive C-reactive protein: a novel biochemical markers and its role in coronary artery disease. J Assoc Physicians India. 2005 Jan;53:25-32.

28. Ridker PM, Morrow DA. C-reactive protein, inflammation, and coronary risk. Cardiol Clin. 2003 Aug;21(3):315-25.

29. Merriman S, Haw C, Kirk J, Stubbs J. Risk factors for coronary heart disease among inpatients who have mild intellectual disability and mental illness. J Intellect Disabil Res. 2005 May;49(Pt 5):309-16.

30. Gupta R, Sarna M, Thanvi J, et al. High prevalence of multiple coronary risk factors in Punjabi Bhatia community: Jaipur Heart Watch-3. Indian Heart J. 2004 Nov;56(6):646-52.

31. Cassidy AE, Bielak LF, Zhou Y, et al. Progression of subclinical coronary atherosclerosis: does obesity make a difference? Circulation. 2005 Apr 19;111(15):1877-82.

32. Bunker SJ, Colquhoun DM, Esler MD, et al. "Stress" and coronary heart disease: psychosocial risk factors. Med J Aust. 2003 Mar 17;178(6):272-6.

33. Banerjee A, Chisti Y, Banerjee UC. Streptokinase—a clinically useful thrombolytic agent. Biotechnol Adv. 2004 Feb;22(4):287-307.
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