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you gotta read this--hypertension and fructose, etc.

Posted by Chad on December 18, 2009 at 9:23 AM

I normally try to add my two cents when I read a post, then tag it onto my blog here.  In this case, there is nothing more to say.  Read, please:


Hypertension and the Metabolic Syndrome


 "I just came back from a Caribbean cruise. Let me tell you, there was plenty of obesity to be seen on a 24/7 floating super-buffet called a cruise ship. All of this had me thinking about the metabolic syndrome: Obesity, Type II Diabetes, High Uric Acid levels, Low HDL, high triglycerides and elevated small LDLHypertension.  For sometime now, the concept of hypertension in the metabolic syndrome was a puzzling factor in my mind. One can easily explain that high carbohydrate and fructose loads will exacerbate obesity, diabetes, uric acid levels and an abnormal lipid profile. But what about hypertension? 


Hypertension can be aggravated by decreased production of Nitric Oxide (NO).  Uric acid in high levels can chelate NO allowing for vasoconstriction.  Moreover, insulin resistance itself decreases NO production. Yet, I have many patients with hypertension and the metabolic syndrome who have normal uric acid levels. In addition, red wine increases NO levels but does not significantly lower blood pressure. So there must be more to the concept of hypertension and the metabolic syndrome.  And there is. The answer lays in our Paleolithic past and the kidneys.


As a Nephrologist, I have always been astounded by the multiple capacities of the kidneys. More so, the basic role of sodium regulation in the kidneys makes it obvious that life on Earth originated in the oceans.  Why? When blood flow arrives to the kidneys, the kidney filter dumps large amounts of electrolytes into its collecting system. After which the kidneys spend a large amount of energy reabsorbing the same electrolytes that it initially filtered through its collecting system.  From an energy economy standpoint, this never made sense to me.  Until...the idea of Darwin came into play. 



Life on planet Earth originated from the oceans – a sodium replete environment.  In thissetting, organisms needed to filter through large amounts of sodium and water in order to maintain a symbiotic relationship with their surroundings. Then life started to become land based. Survival on land meant that the kidneys needed to efficiently conserve water and sodium- the opposite of an oceanic environment. Sodium is important in not only blood pressure regulation but also normal cellular functioning.  But so is potassium. High potassium dietary intake lowers blood pressure. Normal potassium levels are also essential for cardiac electrical activity. But how much sodium and potassium do we need?  Normally functioning kidneys determine that. The dilemma is that our present diet is very high in sodium and low in potassium (vegetablesand fruits).


A comparison of sodium to potassium ratios really sets into place the importance of normally functioning kidneys. The Paleolithic man/women consumed a ratio of sodium to potassium of 1:16.  Modern man consumes a ratio of 3:1. This is almost a 50 times higher ratio for sodium to potassium. (1).  What does this have to do with the metabolic syndrome?  Everything...

 

The metabolic syndrome is an aberration of glucose metabolism through resistance of insulin. By definition, there must be a link between insulin resistance and hypertension. Considering that the kidneys are main regulators of sodium metabolism then insulin resistance and hypertension are connected through the kidneys. In fact, recent studies reveal this connection by means of a protein called serum- and glucocorticoid-inducible kinase 1 (SGK1). SGK1 increases sodium reabsorption and potassium excretion in the kidneys. Moreover, SGK1 is influenced by insulin. But it goes farther. SGK1 increases the glucose transporter activity of GLUT1 and GLUT4.


Insulin resistance leads to elevated insulin levels in order to try to compensate for the resistance itself. Higher plasma insulin levels would cause increased activity of SGK1 leading to elevated sodium reabsoprtion and aggravation of hypertension. Considering that the Paleolithic sodium to potassium ratio was 1:16, then sodium was a much more crucial electrolyte to conserve. And yet conservation is not our dilemma today but excretion of excessive sodium.  Furthermore, elevated insulin not only increases renal sodium retention (thus exacerbating hypertension) but also there would be increased absorption of intestinal glucose and cellular storage of glucose through the glucose transporters GLUT1 and GLUT4.  Such an increase of glucose storage would only lead to worsening obesity and diabetes in the metabolic syndrome.  This would have been perfect for the Paleo man/woman hunting and gathering for food in order to survive the winter.


This brings up the question. What if SGK1 was over stimulated like in a gene mutation? This would lead to increased obesity, diabetes and hypertension. According to a recent editorial, such a SGK1 variantmutation affects 3 to 5% of the Caucasian and approximately 10% of the African-American population(2).  Therefore, there is a segment of the population which is more prone to the metabolic syndrome.  I am sure that there are evolutionary advantages to expression of this mutation - just not for present man.


The activity of SGK1 is influenced by glucocorticoids (steroids), mineralocorticoids (like aldosterone), Vitamin D , progesterone, PPAR-gamma, Insulin,IGF-1 and others (1). It is inhibited by heparin. I have wondered why would insulin expression be linked to renal sodium reapsorption from an evolutionary prospective. Considering that sodium conservation was critical for survival for ancient man then the connection of sodium toinsulin may not be important. But recall that the Paleolithic sodium to potassium dietary ratio was 1:16. Thus potassium may have been the critical factor in this relationship to insulin. Potassium in the body is mainly an electrolyte found within the cells (referred to asintracellular). 98% is within the cells and 2% outside the cells.  Elevated serum potassium levels above 6.0 mEq/L can cause electrical disturbances on cardiac conduction. In the hospital setting, sugar in the form of dextrose and insulin are a quick way to lower serum potassium levels. Therefore, from an evolutionary standpoint, normal regulation of potassium in the blood stream was important as high potassium levels (hyperkalemia) would lower blood pressure and cause disturbances of normal cellular functioning. In contrast, sodium is the main electrolyte found outside the cells (extracellular).


So in summary, during the Paleolithic summer months, fruit and glucose intake was increased. Thus potassium intake was higher as well as insulin levels. The summer was hot and ancient humans lost sodium through sweat. To maintain a normal regulation of sodium and potassium, insulin signaled the kidneys to reabsorb sodium and excrete potassium through SGK1. SGK1 helped to promote intestinal glucose absorption ensuring survival for the winter.


As Billy Ealways tells me: "We got here some how." SGK1 is may be a reason why organisms have survived on land for billions of years.  A sodium topotassium ratio of 3:1 goes against who were are.  However, as Dr. Davis from the Heart Scan Blog points out, severe salt restriction may lead to iodine deficiency and low thyroid function.Therefore, iodine supplementation in the form of kelp tablets may help.


1) Palmer, B, Sterns, R: Fluid, Electrolytes, and Acid-Base Disturbances, NephSap. March 2009; Volume 8 (2): 61-65.


http://www.asn-online.org/education_and_meetings/nephsap/


2)Schwab M, Lupescu A, Mota M, Mota E, Frey A, Simon P, Mertens, PR,Floege J, Luft F, Asante-Poku S, Schaeffeler E, Lang F: Association ofSGK1 gene polymorphisms with type 2 diabetes. Cell Physiol Biochem 21:151–160, 2008"



Check out the blog below for more great information from a nephrologoist.


www.nephropal.blogspot.com




Categories: General Nutrition, Food politics, Weight Loss

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