In earlier posts, I've stressed the fact that the vast majority (90-95%) of all cases of hypertension diagnosed are "essential hypertension"--that is, hypertension with no known cause.
Increasingly, however, it appears that many cases of hypertension may in fact be cases of high levels of inflammation in the body--in particular, cases of inflammation of the liver.
When large amounts of fat are stored in the liver, the liver becomes stressed. This raises the level of several liver enzymes, and has been strongly associated with hypertension.[1]
Metabolic Syndrome, or Syndrome X, commonly has has high blood pressure as a key marker. The early stages of Metabolic Syndrome are characterized by high blood levels of insulin. Insulin raises blood pressure, so the linkage between Metabolic Syndrome and hypertension might seem to be obvious; but as Metabolic Syndrome progresses into Type II diabetes, the pancreas becomes unable to provide insulin, and blood insulin levels plummet. If it were insulin levels alone causing the hypertension, we would expect that as people became diabetic, their blood pressure would fall--but instead, the opposite occurs, and blood pressure usually worsens with the onset of diabetes.
The real culprit may be fatty liver, which is common in Metabolic Syndrome and in Type II diabetes (indeed, some researchers now feel that fatty liver is one of the hallmarks of Metabolic Syndrome). The mechanism by which fatty liver causes increases in blod pressure has only recently been discovered. As fat accumulates in the liver, the liver becomes inflammed. In response, it releases C-Reactive Protein (CRP). CRP is one of the classic markers of inflammation; for example, it rises sharply when the body is fighting an infection. CRP's role in cardiovascular disease is controversial, and CRP testing has been shown to be a poor predictor of heart disease or stroke. [2]
CRP is, however, intimately involved in hypertension, and recent research shows how CRP circulating in the bloodstream acts upon the arteries to raise blood pressure. [3]
Fatty liver disease is traditionally divided into two flavors--Alcoholic Fatty Liver Disease (AFLD), and Non-Alcoholic Fatty Liver Disease (NAFLD). The only difference between the two, however, is that NAFLD is not attributed to overconsumption of alcohol; the condition of the liver is indistinguishable in the two diseases. When the liver becomes highly inflamed, AFLD is called alcoholic hepatitis, while NAFLD progresses into Non-Alcoholic Steatohepatitis (NASH). NAFLD was only recently recognized as a specific disease, but it is widespread: in one major study, one-third of adults were discovered to have fatty livers (defined as a liver-fat content of 5.5% or more), although the prevalence varied considerably by ethnic group. [4]
NAFLD is considered by some to be mainly a metabolic disease--part of Metabolic Syndrome--while others consider it to be simply a disease of obesity. Since obesity is one of the hallmarks of Metabolic Syndrome, this may be a moot distinction.
Almost everyone is now familiar with the fact that those who accumulate fat around their stomachs are at greater risk for heart disease than those who accumulate fat around their hips--the so-called "apple" and "pear" patterns of fat storage. This turns out not to be quite accurate. Samuel Klein, a leading researcher on the connection between liver problems and cardivascular disease, says, "Abdominal fat is not the best marker for risk. It appears liver fat is the real marker. Abdominal fat probably has been cited in the past because it tends to track so closely with liver fat. But if you look at people where the two don't correspond — with excess fat in the liver but not in the abdomen and vice versa — the only thing that consistently predicts metabolic derangements is fat in the liver." [5]
Klein goes on to say, ""Fatty liver disease is completely reversible. If you lose weight, you quickly eliminate fat in your liver. As little as two days of calorie restriction can improve the situation dramatically, and as fat in the liver is reduced, insulin sensitivity and metabolic problems improve."
The linkage between fatty liver and hypertension is an important research result, because most cases of fatty liver can be cured--by the patient, without medication or medical intervention. Weight loss of five percent of body weight shows quick improvement in liver fat accumulation and insulin resistance, while a loss of nine percent of body weight or more appears to reverse liver damage. [6,7].
Even moderate levels of exercise also have a powerful and rapid effect on reversing fatty liver, even without substantial weight loss. [8,9].
I'll have more on this topic in my next post.
[1] Stranges, Saverio, et al. Body Fat Distribution, Liver Enzymes, and Risk of Hypertension. Hypertension. 2005;46;1186-1193.
[2] Baker, S.L.. C-Reactive Protein Test for Heart Disease Found Useless. Natural News, Aug. 4, 2009.
[3] CRP Liver Protein Induces Hypertension. Medical News Today (medicalnewstoday.com ). Feb. 22, 2007.
[4] Prevalence of Non-alcoholic Fatty Liver Disease Varies by Ethnicity. Medical News Today (medicalnewstoday.com ). Dec. 8, 2004.
[5] Dryden, Jim. Apple or pear shape is not main culprit to heart woes — it's liver fat. Washington University St. Louis School of Medicine, Public Affairs News Release. Dec 3. 2008.
[6] Harrison, Stephen A., et al. Orlistat for overweight subjects with nonalcoholic steatohepatitis: A randomized, prospective trial. Hepatology. 2009: 49(1); 80-86.
[7] Weight loss reverses fatty liver disease. Indo-Asian News Service. Feb 20, 2009.
[8] Exercise Helps Patients With Non-Alcoholic Fatty Liver Disease. Medical News Today (medicalnewstoday.com ). Jul. 3, 2009.
[9] Moderate exercise can reduce fatty livers in diabetics. Indo-Asian News Service. Sep. 20, 2008.
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Fatty Liver, Inflammation, and Hypertension
Monday, August 17, 2009
Fatty Liver, Inflammation, and Hypertension
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