Another Way to Help Your Heart

It has become nearly incontestable that lowering the blood levels of the amino acid homocysteine (Hcy) will greatly reduce the risk of cardiovascular disease, perhaps as much or even more so than by keeping cholesterol levels under control (see sidebar, "What is Homocysteine?"). So, how does one go about lowering Hcy? Almost unanimously, researchers and clinicians alike point to the benefits of consuming foods containing the B vitamins folic acid, B6, and B12, or, better yet, supplementing with relatively high amounts of these vitamins (see Vitamins - Our Bodies Cannot Get Enough From Food - Aug. 2000). What is not generally known, however, is that thyroid deficiency can be responsible for high levels of homocysteine, and supplementing with thyroid hormone can reduce these levels dramatically.

What is Homocysteine?

Homocysteine, an amino acid made in the body, is now recognized as an important risk factor for heart disease. Blood levels of homocysteine are thought to predict heart disease with equal or greater reliability than cholesterol does. The September 7, 1999 issue of Annals of Internal Medicine carried four studies on homocysteine and health.

The first study examined 1800 middle-aged Israelis from several ethnic groups over an 11-year period.4 The subjects with the highest homocysteine levels not only had more deaths from heart disease, but their death rate from all causes was significantly increased. The second study, on 8000 U.S. residents, found that homocysteine levels increased with age, and, very importantly, that two-thirds of the high homocysteine levels were associated with low levels of folic acid and vitamin B12.5 In the third study (described in the accompanying article), some patients with low thyroid function were found to have elevated homocysteine, and treatment with thyroid hormone brought the homocysteine levels back to normal.3 In the fourth study, on 2000 elderly people in Framingham, Massachusetts, it was found that high homocysteine levels predicted the occurrence of strokes.6

Research on homocysteine has had an arduous road - the first papers were written more than 20 years ago - but has finally been accepted by the mainstream of biomedical publications. And the consensus, at last, is that there are causal factors for heart disease beyond lifestyle choices, cholesterol, and genetics, involving a mechanism about which we can do something.

In Norway recently, it occurred to researchers that, while the condition called hypothyroidism (or low thyroid; see sidebar, "What is the Thyroid?") is associated with increased cardiovascular morbidity, this association cannot be fully explained on the basis of the atherosclerosis-causing lipids observed in such subjects.1 Noting that they had previously found elevated levels of serum total homocysteine, a cardiovascular risk factor, in hypothyroidism, they conducted a study on 17 patients who had undergone total thyroidectomy (surgical removal of the thyroid gland) because of thyroid cancer and who were being treated with the thyroid hormone thyroxine (T4).

What Is the Thyroid?

The thyroid is a small, butterfly-shaped gland just below the Adam's apple. This gland plays a central role in controlling the body's energy metabolism by producing four thyroid hormones that are carried throughout the body via the bloodstream. The way in which these hormones work can be likened to an air conditioner and the thermostat that regulates it. When there are sufficient thyroid hormones in the blood, the gland stops making them. This is the negative feedback principle of the air conditioner, which cycles off when the air is cool enough. Conversely, the thyroid turns up production when the need arises (when the air gets too warm).

In league with the thyroid is the pituitary gland, which works like the thermostat in your home. The pituitary tells the thyroid when to start and when to stop by sending thyroid-stimulating hormone to the thyroid.

It has been estimated that there are 20 million Americans who have some form of thyroid disease, much of which is undiagnosed or misdiagnosed. Although women are much more susceptible - thyroid deficiency may be as much as ten times more common in women than in men - no one of any age, race, sex, or economic status is immune. Age is definitely a factor in thyroid decline, which becomes ever more likely as we grow older.

Inadequate levels of thyroid hormones (hypothyroidism) is the most common problem, but some people have too much (hyperthyroidism). Other problems include inflammation of the thyroid gland (thyroiditis), enlargement (goiter), or the development of one or more lumps (nodules).

The therapeutic protocol required that the T4 treatment be discontinued for a period of four weeks. During that time, the subjects quickly attained a hypothyroid state, which was finally reversed by reinstating the T4. Periodic testing for Hcy, folic acid, vitamin B12, and cholesterol in the blood revealed a progressive and parallel increase in Hcy and cholesterol. However, these substances returned to their original levels within 4 to 6 weeks after reinstating the T4 therapy. Changes in folic acid and vitamin B12 were statistically insignificant. What is significant is that short-term thyroid deficiency resulted in elevated cholesterol and Hcy levels, both of which are cardiovascular risk factors.


In another study examining the connection between hypothyroidism and homocysteine, low thyroid was noted to decrease liver enzymes that play a role in breaking down serum total homocysteine.2 In patients recovering from thyroid cancer or autoimmune thyroiditis, high levels of thyroid-stimulating hormone (TSH) were associated with high levels of homocysteine.3 This is consistent with the correlation between low levels of T4 and high levels of Hcy, because T4 levels are low when TSH is elevated. In this study, analysis confirmed that TSH is the strongest predictor of Hcy, independent of age, folic acid, vitamin B12, and creatinine (a waste product of protein metabolism that is found in the urine), whose levels are also related (but inversely) to those of Hcy.

When T4 was given, Hcy went down. The authors concluded from this that homocysteine is elevated in hypothyroidism. Moreover, the association of this hyperhomocysteinemia (high Hcy) with lipid abnormalities occurring in hypothyroidism may represent an extreme atherogenic situation and cardiovascular compromise. Perhaps the best course of action to combat this condition, therefore, is to use a combination of thyroid hormone and the vitamins found to be beneficial for reducing Hcy, i.e., vitamins B6, B12, and folic acid.

To determine whether restoration of proper thyroid function by treatment with T4 would reduce or normalize plasma homocysteine levels, 14 patients were chosen to participate in a study.3 Of that number, ten were women and four were men (ages 25 to 77). Four were newly diagnosed with chronic hypothyroidism, and ten had been rendered acutely hypothyroid because of thyroidectomy necessitated by cancer. The patients' Hcy levels were measured at the beginning of the study and then again at 3 months and 9 months after receiving T4. When normal thyroid function was attained, it was found that all patients had reduced plasma homocysteine levels, with a median drop of 44%. The levels even returned to normal in seven of the eight patients with elevated pretreatment values. The message is clear: thyroid deficiency can be a significant cause of elevated homocysteine levels, which are an independent risk factor for the onset or acceleration of atherosclerosis.

It has become increasingly clear that maintaining proper hormone balance is essential for preserving our health. This is especially true as we age and our bodies become less efficient in producing the right biomolecules in the right amounts at the right times. Supplementing with a small amount of standardized whole thyroid, especially in conjunction with other glandular extracts, as well-known nutrition physician Dr. Jonathan Wright advocates, is a good way to help keep us healthy as we grow wiser with our additional years.


  1. Lien EA, Nedrebo BG, Varhaug JE, Nygard O, Aakvaag A, Ueland PM. Plasma total homocysteine levels during short-term iatrogenic hypothyroidism. J Clin Endocrinol Metab 2000 Mar;85(3):1049-53.
  2. Catargi B, Parrot-Roulaud F, Cochet C, Ducassou D, Roger P, Tabarin A. Homocysteine, hypothyroidism, and effect of thyroid hormone replacement. Thyroid 1999 Dec;9(12):1163-6.
  3. Hussein WI, Green R, Jacobsen DW, Faiman C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med 1999 Sep 7;131(5):348-51.
  4. Kark JD, Selhub J, Adler B, Gofin J, Abramson JH, Friedman G, Rosenberg IH. Nonfasting plasma total homocysteine level and mortality in middle-aged and elderly men and women in Jerusalem. Ann Intern Med 1999 Sep 7;131(5):321-30.
  5. Selhub J, Jacques PF, Rosenberg IH, Rogers G, Bowman BA, Gunter EW, Wright JD, Johnson CL. Serum total homocysteine concentrations in the third National Health and Nutrition Examination Survey (1991-1994): population reference ranges and contribution of vitamin status to high serum concentrations. Ann Intern Med 1999 Sep 7;131(5):331-9.
  6. Bostom AG, Rosenberg IH, Silbershatz H, Jacques PF, Selhub J, D'Agostino RB, Wilson PW, Wolf PA. Nonfasting plasma total homocysteine levels and stroke incidence in elderly persons: the Framingham Study. Ann Intern Med 1999 Sep 7;131(5):352-5.

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