David S. Klein, M.D.

Nutritional Suggestions

Nutrient Protocols are underway.  Until then, I will list some of the more interesting abstracts for you to read.   dsk

NOTE: Interesting Article. Reason enough to take supplemental (high dose) folic acid. Basically, this demonstrates that Folic Acid (Folate) decreases 'hardening of the arteries' or atherosclerosis. Did somebody say 'anti-aging?' dsk.

Williams C, Kingwell BA, Burke K, McPherson J, Dart AM. Folic acid supplementation for 3 wk reduces pulse pressure and large artery stiffness independent of MTHFR genotype. Am J Clin Nutr. Jul 82(1):26-31, 2005.

BACKGROUND: Folic acid reduces plasma homocysteine and may be an important therapy for preventing cardiovascular disease. A key mechanism may be the reduction of arterial stiffness.
OBJECTIVE: The effect of folic acid supplementation on blood pressure and large artery stiffness was examined in relation to methylenetetrahydrofolate reductase (MTHFR) genotype.
DESIGN: Forty-one asymptomatic men with normal or high-normal ambulatory blood pressure (systolic: >130 to <145 mm Hg; diastolic: >80 to <90 mm Hg) participated. The study had a randomized, placebo-controlled, double-blind, crossover design that incorporated 3-wk treatments with 5 mg folic acid/d or matching placebo; each treatment was separated by a 4-wk washout phase.
RESULTS: Folic acid reduced brachial pulse pressure by 4.7 +/- 1.6 mm Hg (P < 0.05) without changing mean arterial pressure. Systemic arterial compliance increased by 0.15 +/- 0.03 mL/mm Hg (P < 0.05) after folic acid treatment but did not change after placebo treatment. These responses did not significantly correlate with either homocysteine or folate plasma concentrations. MTHFR genotype CC homozygotes (without the 677C-->T polymorphism) with normal blood pressure had a larger reduction in homocysteine concentrations in response to folic acid than did T allele carriers. Blood pressure and arterial stiffness responses were independent of MTHFR genotype.
CONCLUSION: Folic acid is a safe and effective supplement that targets large artery stiffness and may prevent isolated systolic hypertension.

Corrado E, Novo S. Role of inflammation and infection in vascular disease.Acta Chir Belg. 2005 Nov-Dec;105(6):567-79.

Relationship of infection, inflammation, and atherosclerosis has been a subject of intensive investigation in recent years. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. Chlamydia pneumoniae (Cp) infection in early life may accelerate atherosclerosis, leading to cardiovascular complications. Other infections, simultaneously occurring with Cp, may result in a synergistic effect to promote atherosclerosis. Chronic Helicobacter pylori infection is known to increase the pH level of the gastric juice and to decrease ascorbic acid levels, both of which will lead to a reduced folate absorption. Low folate hampers the methionine synthase reaction. This leads to an increased concentration of homocysteine in the blood, resulting in damage of endothelial cells. Cytomegalovirus (CMV) infection is associated with accelerated atherosclerosis following cardiac transplantation; several studies have found that patients with a previous CMV infection had a high independent risk of restenosis after coronary angiography. Inflammatory markers are independent predictors of cardiovascular and cerebrovascular events. Large population-based studies such as the study from the MONICA (MONItoring trends and determinants in Cardiovascular disease) Augsberg Center in Germany, the Atherosclerosis Risk in Communities Study, the Women's Health Study, the Honolulu Heart Study, have also suggested the relation between the levels of CRP and risk of coronary disease. Over the past decade also another marker of inflammation has been studied; fibrinogen has been identified as an independent risk factor for CAD in several large prospective studies. All these studies suggested a new, possible role of markers of infection and inflammation beyond traditional cardiovascular risk factors, in the development and progression of atherosclerosis. However, the clinical and therapeutic implications of these results remain to be evaluated. Although antibiotic treatment of infections in CAD patients had no impact on mortality in large prospective trials, promising data is coming from smaller studies and further studies are needed to investigate the possibility to submit this category of high-risk patients to therapeutical approaches of primary prevention.

The Role of Arginine in Cancer Prevention

D. Scott LindArginine and Cancer J. Nutr. 134:2837S-2841S, 2004.

" Arginine has numerous roles in cellular metabolism that may influence the multistep process that results in cancer. Arginine-derived NO has many overlapping and conflicting regulatory roles in tumor initiation, promotion, and progression. Further mechanistic studies are necessary to develop biologically based anti-neoplastic strategies targeted at arginine’s metabolic pathways. ^"

David S. Klein, MD, FACA, FACPM, FACMIMS
Director, Pain Center of Orlando
www.suffernomore.com