Joel Fuhrman - Eat To Live

152 Joel Fuhrman, M.D.

who provides sustained guidance and support. After spending ade-

quate time with a doctor reviewing all the risks of the conventional

approach and discussing how reversal is possible with aggressive nu-

tritional management, how many patients do you think would choose

to have their chests split open with bypass surgery?

Even if you are lucky enough to have no postoperative compli-

cations from bypass, some degree of brain injury occurs in almost

every patient from the time spent hooked up to the heart-lung ma-

chine. On neuropsychological testing six months later, about 20 per-

cent still show deterioration.^19 Brain injury can range from subtle

degrees of intellectual impairment or memory loss to personality

changes and permanent brain damage.^20

Even if you do fine after angioplasty, stent placement, or bypass,

atherosclerosis develops at a faster rate in those arteries that were

subject to bypass or angioplasty — the plaque grows faster after sur-

gery. Approximately one-third of arteries treated by angioplasty clog

up again within four to six months.^21 This is called restenosis.

Restenosis is an iatrogenic (physician-caused) disease. Because

restenosis involves scarring, it does not behave like native athero-

sclerosis and does not respond as favorably or as predictably to lifestyle

modifications later on. In other words, because of the changes made

to the atherosclerotic plaque by the angioplasty treatment, the block-

ages are less responsive to nutritional intervention when they re-

turn. Many patients are worse off after treatment, not better. If they

had followed my CAD (coronary artery disease) reversal plan instead,

they would be watching their heart get healthier each week.

Stenting attempts to reduce this high risk of restenosis but has

not solved the problem.^22 Stents are tiny wire-mesh tubes that are

laced in the narrowed segment of arteries that were stretched by bal-

loon angioplasty. The stent may also cause vascular instability or in-

flammation where the stent ends and the native plaque begins, thus

increasing the risk for coronary thrombosis.^23 It would be good to re-

mind patients that revascularization procedures do not influence the

underlying disease, because the rest of the coronary vasculature,

with diffuse, nonangiographical noticeable atherosclerosis, is still there

posing a risk for future cardiac events, whether the procedure i

done or not.

Heart attacks most commonly occur when plaque of a lipid-rich

segment ruptures. These vulnerable areas of plaque are not neces-

sarily those that are seen as significantly narrowed on catherization.