Ischemic heart disease as deficiency disease

Area of Science:

• Cardiovascular Medicine
• Nutritional Science
• Biochemistry

Background:

• The prevailing 20th-century paradigm for ischemic heart disease (IHD) focused on dietary fat intoxication.
• This lipid-centric view neglects crucial data and overlooks other contributing factors to IHD.
• IHD development involves complex mechanisms including arterial spasm, cardiac rhythm, and homocysteine metabolism, often independent of dietary fat.

Purpose of the Study:

• To challenge the overemphasis on lipid metabolism in IHD etiology.
• To propose a paradigm shift viewing IHD as a deficiency disorder.
• To highlight the role of homocysteine and its metabolic regulation in IHD.

Main Methods:

• Review of existing data on IHD risk factors and pathophysiology.
• Analysis of the role of homocysteine and its inhibitory effect on lysyl oxidase.
• Examination of nutrient supplementation's impact on homocysteine metabolism.

Main Results:

• Heart disease risk does not correlate with fat intake within nations.
• Homocysteine thiolactone inhibits lysyl oxidase, crucial for arterial integrity.
• Copper deficiency can impair paraoxonase activity, affecting homocysteine thiolactone hydrolysis.
• Nutrient supplementation (betaine, copper, folate, pyridoxine, vitamin B-12) can reduce plasma homocysteine.

Conclusions:

• Ischemic heart disease may be better understood as a deficiency disorder rather than solely an intoxication issue.
• Targeting homocysteine metabolism through nutrient supplementation offers a promising therapeutic and research avenue.
• Further research into IHD as a deficiency disease is warranted.