McCarty Mark F
NutriGuard Research, 1051 Hermes Avenue, Encinitas, CA 92024, USA.
Med Hypotheses. 2005;64(5):1015-21. doi: 10.1016/j.mehy.2003.12.054.
Recent studies demonstrate low serum levels of 25-hydroxyvitamin D in patients with congestive heart failure (CHF). Although this may in part reflect reduced capacity for outdoor exercise, the possibility that poor vitamin D status increases risk for left ventricular hypertrophy (LVH), and its common sequel CHF, merits consideration. In cardiomyocytes, hormones which activate protein kinase C (PKC) -- including norepinephrine, angiotensin II, and endostatin, implicated in the pathogenesis of LVH -- induce a hypertrophic response analogous to that seen in LVH. Transgenic mice overexpressing PKC-beta2 or its upstream activator Galphaq in cardiac myofibers develop a syndrome similar to LVH. Parathyroid hormone (PTH) also activates Galphaq and PKC in cardiomyocytes, and provokes the expected hypertrophic response. Both primary and secondary hyperparathyroidism are associated with high risk for LVH. Moreover, in uncomplicated essential hypertension, left ventricular mass index has been shown to correlate very tightly with serum PTH levels, independent of blood pressure. This latter finding suggests that variations of PTH within the normal range can influence induction of LVH in at-risk subjects. If so, nutritional and lifestyle measures which modulate PTH secretion may have an impact on LVH risk. PTH secretion should be down-regulated by good vitamin D status -- achieved through supplementation or regular uv exposure -- and by vegan diets moderately low in bioavailable phosphate. Although high calcium intakes can likewise suppress PTH, they also boost renin secretion, which could have a countervailing effect on risk for LVH. Whether these nutritional measures do indeed influence LVH risk could be examined in prospective studies targeting patients at high risk, such as hypertensives.
近期研究表明，充血性心力衰竭（CHF）患者血清25-羟基维生素D水平较低。尽管这可能部分反映了户外运动能力下降，但维生素D状态不佳会增加左心室肥厚（LVH）及其常见后果CHF的风险，这一可能性值得考虑。在心肌细胞中，激活蛋白激酶C（PKC）的激素——包括去甲肾上腺素、血管紧张素II和内皮抑素，它们与LVH的发病机制有关——会诱导出类似于LVH中所见的肥厚反应。在心肌纤维中过表达PKC-β2或其上游激活剂Gαq的转基因小鼠会出现类似于LVH的综合征。甲状旁腺激素（PTH）也会在心肌细胞中激活Gαq和PKC，并引发预期的肥厚反应。原发性和继发性甲状旁腺功能亢进均与LVH的高风险相关。此外，在无并发症的原发性高血压中，左心室质量指数已被证明与血清PTH水平密切相关，与血压无关。后一项发现表明，正常范围内PTH的变化可影响高危人群LVH的诱导。如果是这样，调节PTH分泌的营养和生活方式措施可能会对LVH风险产生影响。良好的维生素D状态——通过补充或定期紫外线照射实现——以及生物可利用磷含量适度较低的纯素饮食应能下调PTH分泌。虽然高钙摄入量同样可以抑制PTH，但它们也会促进肾素分泌，这可能会对LVH风险产生抵消作用。这些营养措施是否确实会影响LVH风险，可以在前瞻性研究中针对高危患者，如高血压患者进行检验。
