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Abstract
Deep sea water (DSW), originally pumped from the Pacific Rim off the coast of Hualien County (Taiwan), and its mineral constituents, were concentrated by a low-temperature vacuum evaporation system to produce a hardness of approximately 400,000 mg/L of seawater mineral concentrate. The primary composition of this seawater mineral concentrate was ionic magnesium (Mg2+), which was approximately 96,000 mg/L. Referring to the human recommended daily allowance (RDA) of magnesium, we diluted the mineral concentrate to three different dosages: 0.1 × DSW (equivalent to 3.75 mg Mg2+/kg DSW); 1 × DSW (equivalent to 37.5 mg Mg2+/kg DSW); and 2 × DSW (equivalent to 75 mg Mg2+/kg DSW). Additionally, a magnesium chloride treatment was conducted for comparison with the DSW supplement. The study indicated that 0.1 × DSW, 1 × DSW and 2 × DSW decreased the systolic and diastolic pressures in spontaneous hypertensive rats in an eight-week experiment. DSW has been shown to reduce serum lipids and prevent atherogenesis in a hypercholesterolemic rabbit model. Our results demonstrated that 1 × DSW and 2 × DSW significantly suppressed the serum cholesterol levels, reduced the lipid accumulation in liver tissues, and limited aortic fatty streaks. These findings indicated that the antiatherogenic effects of DSW are associated with 5′-adenosine monophosphate-activated protein kinase (AMPK) stimulation and the consequent inhibition of phosphorylation of acetyl-CoA carboxylase (ACC) in atherosclerotic rabbits. We hypothesize that DSW could potentially be used as drinking water because it modulates blood pressure, reduces lipids, and prevents atherogenesis.
Highlights
50% of all deaths from cardiovascular diseases (CVD) in Western countries are due to coronary heart disease (CHD), and the primary cause of CHD is atherosclerosis
The body weights increased by approximately 189 g, 179 g, and 183 g after the administration with 0.1 ×Deep Sea Water (DSW), 1 ×DSW, and 2 ×DSW, respectively
Our results indicated that the plasma total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels were improved after eight weeks of a 0.5% cholesterol diet (Figure 1a–c)
Summary
50% of all deaths from cardiovascular diseases (CVD) in Western countries are due to coronary heart disease (CHD), and the primary cause of CHD is atherosclerosis. It is hypothesized that atherosclerosis begins when the endothelium becomes damaged, thereby allowing low-density lipoprotein cholesterol (LDL-C) to accumulate on the artery wall. Lipid accumulation, foam cell development, and vascular smooth muscle cell proliferation occur, and the arteries become narrowed and hardened [1]. Hypercholesterolemia and high levels of LDL cholesterol are two important stimuli that regulate the pathogenesis of atherosclerosis [1,2]. Steinberg et al demonstrated that oxidized LDL (oxLDL) is a key element involved in atherosclerotic plaque formation and atherogenicity [3]. When oxLDL is uptaken by vascular scavenger receptors, the transformation of macrophages into foam cells is triggered in atherosclerotic lesions [4]. A strong correlation between hypertension and CHD is widely under investigation. Several pathophysiologic mechanisms link both hypertension and CHD. Hypertension induces endothelial dysfunction, exacerbates the atherosclerotic process and contributes to make the atherosclerotic plaque more unstable [5]
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