5-HTP
Not Only for Depression
But for Heart Disease Too?

By Dr. Gail Valentine

en who suffer bouts of clinical depression are more than twice as likely to develop heart disease compared with men who have not experienced a history of depression.1 If you are a long-term reader of this publication, then you've read about the preliminary findings regarding the connection between depression and heart disease first announced in Life Enhancement's April 1997 issue [Depression and Heart Disease: The Serotonin Connection - Apr. 1997 ]. However, even more current findings, published recently in the Archives of Internal Medicine and conducted by researchers at Johns Hopkins University,2 go to an entirely new level. They indicate that depression is an accomplice to heart disease and may be far more widespread than previously reported. Further, the results represent the first clear confirmation that depression is one of the instrumental reasons why some people get cardiovascular disease and others do not.

When last we heard from this ongoing study in 1996, the report was that if you're a man and if you've ever suffered through a major depressive episode or had a history of two weeks or greater of dysphoria (profound sadness), your odds of having a subsequent heart attack are more than four times higher than if you have no history of serious depression. This risk was independent of other typical risk factors for heart disease (blood pressure, cholesterol, cigarette smoking, physical activity, obesity or family history of coronary artery disease). This finding was bad news when reported back in 1996, because dysphoria was not that common, therefore, the findings didn't affect as many people so it didn't ring home until now.


The results represent the first clear
confirmation that depression is
one of the instrumental reasons why
some people get cardiovascular
disease and others do not.

By following 1,190 male students for a period of four decades, the recent study found that 132, or approximately 12 percent, of those enrolled in the study had suffered one or more episodes of clinical depression, and that this subgroup was more than two times (2.12) as likely to develop heart disease as those who were free of depression. Researchers found on average that the symptoms of coronary artery disease surfaced in the students about 15 years after their initial bout of depression. Heart disease affected as many as several hundred of the entire group (who were medical students when the study began in 1948). Of all the students in the study, 153 in total died and of those, 34 died from cardiovascular disease.

While the men suffering depression drank more coffee than those without it, the two groups did not differ significantly in respective levels of blood pressure, cholesterol, cigarette smoking, physical activity, obesity or family history of coronary artery disease. The researchers also said depression was linked to a greater overall risk of death, although it was not found to be associated with a higher risk of stroke.


Study author Daniel Ford speculated
that one way to further explore
the link will be to examine how
the dramatic increase in the use
of antidepressants affects
heart disease rates.

ANTIDEPRESSANTS FOR THE PREVENTION OF DEPRESSION AND HEART DISEASE
The significant outcropping of this heart disease research will be to open the gates to investigate whether there is something that can be done about the causality. Study author Daniel Ford speculated that one way to further explore the link will be to examine how the dramatic increase in the use of antidepressants affects heart disease rates. Exactly. If antidepressants are found to be effective heart disease medications, then we must entertain questions concerning the age-related serotonin decline and its association with depression.

There is currently a burgeoning of literature on the relationship between mood disorders and heart disease.3 This is because the symptoms of depression are frequently under-diagnosed and under-treated in many patients, including those with cardiovascular disease. Thus, those who might profit most from antidepressants may never get them, or get them too late. But there's something further here. What about those who don't need antidepressants now, but will need them at some future date, but won't get them? Will future practices deal only with antidepressants for active depression or antidepressants for the prevention of depression and/or the prevention of heart disease?


If antidepressants can be viewed as
heart disease medications, then we
must entertain questions concerning
the age-related serotonin decline
and age-related depression.

Unfortunately, the common medical view about antidepressants is that they generally are not for "garden variety" or everyday types of depression or, even more so, they are not for use if one does not have depression but merely anticipates it. For example, if you are going through a career change, bearing up to the loss of a loved one or any one (or more!) of another seriously stressful event, the likelihood of the event precipitating depression is great. From the perspective of traditional medicine, use of an antidepressant under these circumstances is unwarranted. Considering the long treatment duration of antidepressants and given the side effects and others risks associated with these and many drugs, this position makes sense. However, this has not prevented some of the drug companies from putting forth the argument that anticholesterol drugs such as the statins, may be useful in preventing a semi-active or even totally inactive condition from becoming active and endangering cardiovascular health.

DEPRESSION UNDETECTED OR DENIED
Other factors bring concern regarding the difficulty of diagnosing and treating depression. Often depression is silently fought by going undetected by the individual or the health care provider or being denied by the individual. Depressive symptoms may be so subtle, insidious and gradual as to go unrecognized. Those who are depressed may shrug it off by saying that this is not really happening to them. This process of denial itself is recognized as a symptom of depression. Consequently, many of those who need antidepressants will decline using them, perhaps until it is too late and cardiovascular disease has been initiated. On the other hand, if a person is aware of the early stages of depression, or perhaps affirms the possibility of depression in advance of any precipitating events or circumstances, and takes a serotonin precursor, the problems of depression and future heart disease are far less likely to arise, and without the side effects or risks of prescription antidepressants.


Higher brain levels of serotonin are
strongly associated with decreased
symptoms of depression, improved
memory function, better regulation of
appetite control and enhanced
mood functions.

AN OUNCE OF 5-HTP FOR PREVENTION
There is a multitude of scientific data substantiating the association between serotonin deficiency and depression. This has been demonstrated over the last decade with the successful use of Prozac, and other selective serotonin reuptake inhibitor (SSRI) drugs. SSRIs have been providing relief from depression and other mood disturbances, among other maladies. However, SSRIs are not without risks and side effects. Additionally, it has been scientifically established that the brain's serotonin system declines with age. [See The Sero-Less Gravity Club]. Combined with many findings associated with age-related depression, these conclusions provoke an intriguing way to think about depression.

There is that old adage about an ounce of prevention being worth a pound of cure. The serotonin precursor 5-HTP (5-hydroxytryptophan) may be used to help restore serotonin levels, to help prevent serotonin decline (whatever the cause) and without the concern of side effects. It is a natural substance and is safe for consumption within normal limits. For most individuals using 5-HTP as a dietary supplement, 50 to 100 mg per day, will give adequate replenishment. For some as little as 25 mg per day is effective. One ounce of 5-HTP equals 28,000 mg, or approximately 280 to 560 servings. This amounts to an ounce of prevention lasting for up to 3/4 to 1 1/2 years. One small ounce for a "pound" of benefits!

While it is unclear at this time whether antidepressants can provide a cure for heart disease, we do know that supplementing with a serotonin precursor like 5-HTP can assist in restoring brain serotonin levels. Higher brain levels of serotonin are strongly associated with improved memory function, better regulation of appetite control, decreased symptoms of depression and enhanced mood functions. Incidentally, there is some data to support the conclusion that maintaining normal levels of serotonin may help prevent age-associated immune function decline.4,5 Last but not least, since the scientific data is currently out on age-related serotonin decline, it makes good sense to apply the ounce of prevention theory to your anti-aging program. The principal goal of a well-designed supplement program is to be protective and preventative for all aspects of our health: physical, mental, and emotional. 

References

  1. Pratt LA, Ford DE, Crum RM, Armenian HK, Gallo JJ, Eaton WW. Depression, psychotropic medication, and risk of myocardial infarction. Prospective data from the Baltimore ECA follow-up. Circulation 1996 Dec 15;94(12):3123-3129.
  2. Ford DE, Mead LA, Chang PP, Cooper-Patrick L, Wang NY, Klag MJ. Depression is a risk factor for coronary artery disease in men: the precursors study. Arch Intern Med. 1998;158:1422-1426.
  3. Musselman DL, Evans DL, Nemeroff CB. The Relationship of Depression to cardiovascular Disease: Epidemiology, Biology, and Treatment. Arch Gen.Psychiatry 1998;55:580-592.
  4. 4. Bliznakov EG. Serotonin and its precursors as modulators of the immunological responsiveness in mice. J Med. 1980;11(2-3):81-105.
  5. Maes M, Verkerk R, Vandoolaeghe E, Van Hunsel F, Neels H, Wauters A, Demedts P, Scharpe S. Serotonin-immune interactions in major depression: lower serum tryptophan as a marker of an immune-inflammatory response. Eur Arch Psychiatry Clin Neurosci. 1997;247(3):154-161.

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