Hyperkalemia is a result of potassium excess. It can be result of aldosterone deficiency causing potassium retention (too little excretion in the kidneys) (1p435). Also possible trauma that damages cells could cause released potassium to overload kidneys (1p435).
Reference List
1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
Although we may fight for it, in the end we just can’t stop people from naming their horses “Charlie”. But maybe we can help them with an involuntary contraction or spasm causing a muscle cramp, sometimes called a “charley horse”. Usually they occur due to an overused or injured muscle, but can also be caused by lack of minerals such as potassium (1). So, before and after exercise, eat your bananas.
Reference List
1. MedlinePlus. Charley Horse. Medline Encyclopedia. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/002066.htm
The symptoms of respiratory and metabolic acidosis are pretty similar. In both you see generalized weakness, fatigue, nausea, vomiting and CNS depression (1). How does a blood test distinguish from the two?
Respiratory acidosis differs from metabolic acidosis because it is a result of impaired pulmonary function causing a build-up of CO2 that lowers pH instead of one that is mainly caused by increased acid metabolic products (1). A blood test can indicate between the two by measuring pH, bicarbonate (HCO3-) and carbon dioxide (PCO2) (1).
If the test reveals acidic extracellular fluid (ECF) but normal CO2 indicating adequate respiratory function or low PCO2 indicating active ventilation response, then pH disruption has a metabolic source (1). An elevated PCO2 indicates inability to clear CO2 and the drop in pH is a result of carbonic acid formed (1).
Now if for any reason you accidentally swallow antifreeze, methanol or high doses of aspirin, you should know it can potentially cause either acidosis. To correct acidosis you use sodium bicarbonate (1). The same as baking soda.
Reference List
1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
Potassium, the main cation in the cells, is often lost through perspiration, feces and urine (1). A deficit of potassium is called hypokalemia (1). Hypokalemia may occur simply due to inadequate dietary potassium intake, although it is more likely due to a case where there is excessive loss of potassium (1).
Various reasons can cause excessive loss of potassium such as vomiting, heavy sweating or chronic diarrhea (1). It can often result of laxative abuse or drugs such as diuretics (1). It is possible to develop hypokalemia due to inappropriate IV fluid (1).The signs of hypokalemia are weakness, muscle twitching and depressed neuromuscular reflexes (1).
Reference List
1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
Saturated fats including trans fat can lead to a increased risk of cardiovascular disease mainly by raising cholesterol and causing a poor LDL:HDL ratio (1). Trans fat is thought to be more atherogenic because it has also been found to lower HDL cholesterol in studies (1-3).
But what about diabetes risk?
In 2006 a review on the literature of trans fats versus saturated fats in insulin resistance noted that while high intake of saturated fats may promote insulin resistance, it is too early to determine if trans fats create increased risk(3). However, a 2008 rat study published in Asia Pac J Clin Nutr (2) showed that rats fed a diet higher in saturated fats had decreased peripheral insulin sensitivity, but that if trans fat was included the effect was greater.
Biochemically the reason for the effects on insulin sensitivity from dietary trans fat may have to do with its potential interference with cell membrane functions and decreasing insulin concentration (3-5). Ultimately both saturated and trans fats decrease insulin concentration, but trans fat more so (3-5). Interestingly, a review in Atheroscler Suppl pointed out that conjugated trans fat appears to be the “most dramatic” of all fatty acids in impairing insulin sensitivity (5).
Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Ghafoorunissa G. Role of trans fatty acids in health and challenges to their reduction in Indian foods. Asia Pac J Clin Nutr 2008;17 Suppl 1:212-5.
3. Odegaard AO, Pereira MA. Trans fatty acids, insulin resistance, and type 2 diabetes. Nutr Rev 2006;64:364-72.
4. Bhathena SJ. Relationship between fatty acids and the endocrine and neuroendocrine system. Nutr Neurosci 2006;9:1-10.
5. Riserus U. Trans fatty acids and insulin resistance. Atheroscler Suppl 2006;7:37-9.
The presence of ovomucin, a natural trypsin inhibitor in eggs, can help block some of egg cholesterol absorption and bile acid reabsorption through enterohepatic circulation (1). Despite ovomucin, however, there does appear to be enough dietary cholesterol in eggs absorbed that can potentially cause increased cholesterol levels (2;3).
Reference List
1. Nagaoka S, Masaoka M, Zhang Q, Hasegawa M, Watanabe K. Egg ovomucin attenuates hypercholesterolemia in rats and inhibits cholesterol absorption in Caco-2 cells. Lipids 2002;37:267-72.
2. Levy Y, Maor I, Presser D, Aviram M. Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation. Ann Nutr Metab 1996;40:243-51.
3. Applebaum-Bowden D, Hazzard WR, Cain J, Cheung MC, Kushwaha RS, Albers JJ. Short-term egg yolk feeding in humans. Increase in apolipoprotein B and low density lipoprotein cholesterol. Atherosclerosis 1979;33:385-96.
Raw egg white contains avidin. As dietary protein is digested, the presence of avidin can bind to biotin tightly preventing its absorption into the body (1). Because biotin is used as a prosthetic group in acetyl CoA carboxylase, a biotin deficiency can then inhibit the carboxylation reaction catalyzed by acetyl CoA carboxylase that converts malonyl CoA from acetyl CoA and CO2 (2). The conversion to malonyl CoA is ultimately the reaction by which carbons of a fatty acid are contributed to by acetyl CoA (2). Cooking destroys the avidin, which is a good thing.
But wait, an article in the latest Journal of Nutrition explains that Maillard reaction products (result of heating proteins and sugars) may alter amino acid availability and reduce digestibility of certain proteins (3). It would lead to believe that you’d want your protein raw or microfiltered versus fried or treated with ultra-high temperatures. Sure enough, you’ll get more protein from a raw egg, plus enzymes and vitamins.
In the end, if you’re going to eat eggs at all (see next post on cholesterol), it’s probably best to cook the egg minimally and take a quality multi-vitamin and an enzymes supplement. That way you don’t accidentally get salmonella.
Reference List
1. Brody T. Nutritional Biochemistry. San Diego: Academic Press, 1999.
2. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
3. Lacroix M, Bon C, Bos C et al. Ultra high temperature treatment, but not pasteurization, affects the postprandial kinetics of milk proteins in humans. J Nutr 2008;138:2342-7.
Along with the recommendation of exercise and a healthy diet (including a bit of red wine daily), both lovastatin and cholestyramine can be used in the treatment of familial hypercholesterolemia (1;2).
While lovastatin works as a HMG CoA reductase inhibitor to reduce cholesterol synthesis in the liver, cholestyramine acts as a bile acid-binding resin that increases fecal removal of cholesterol (1p152;3-4).
Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Netdoctor.co.uk. Familial hypercholesterolemia. Available at: http://www.netdoctor.co.uk/diseases/facts/familialhypercholesterolaemia.htm.
3. Netdoctor.co.uk. Questran (colestyramine). Available at: http://www.netdoctor.co.uk/medicines/100002209.html.
4. Medicine.net. Lovastatin (oral). Available at: http://www.medicinenet.com/lovastatin-oral/article.htm.
Without acyl CoA dehydrogenase to initiate the first step of mitochondrial beta-oxidation, your ability to metabolize fats is inhibited (1). That is, the enzyme—one of four depending on fatty acid chain lengths—catalyzes the formation of the double bond between alpha- and beta-carbons, which then are degraded to two-carbon acetyl CoA units (1p159).
Because the body relies on the production of acetyl CoA from its storage of fat for energy, the lack of acetyl CoA dehydrogenase and in its capacity to produce beta-oxidation causes the body to end up in a hypoglycemic (no glucose) and hypoketotic state (no ketones from oxidation of fatty acids) (1p159;2-3).
Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. PerkinElmer Genetics. Multiple Acyl-CoA Dehydrogenase Deficiency. Available at: http://www.perkinelmergenetics.com/MultipleAcylCoADehydrogenaseDeficiency.htm.
3. STAR-G. Genetic Fact Sheet for Parents: Fatty Acid Oxidation Disorders. Available at: http://www.newbornscreening.info/Parents/fattyaciddisorders/VLCADD.html.
We know that antioxidants such as vitamin E may slow development of atherosclerosis by reducing oxidation of LDL (1). So I bring to your attention a just-released study of note on antioxidant procyanidins of grape seed extract (2). The study was proposes a “corrective role” of the procyanidins on foam cells because of results in vitro that suggest the antioxidant effects reduce cholesterol and lipid accumulation as well as modulate expression of genes that play a role in inflammation (2).
Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009. 2. Terra X, Fernandez-Larrea J, Pujadas G et al. Inhibitory effects of grape seed procyanidins on foam cell formation in vitro. J Agric Food Chem 2009;57:2588-94.
Evolving Health 