28 February 2009

Phasting versus dessert

When fasting (meaning, in this case, not eating any carbohydrates), the pancreas releases a polypeptide hormone, glucagon, that stimulates gluconeogenesis in the liver (1). Glucagon functions via a regulating bifunctional enzyme (1). The enzyme dephosphorylated acts as phophofructokinase-2 (PFK-2) and glucagon induces phosphorylation to produce fructose bisphosphatase-2 (FBPase-2) (1). The suppression of PFK-2 and increased activity of FBPase-2 reduces concentration of fructose 2,6-biphosphate (1).

Fructose 2,6-biphosphate’s presence regulates glycolysis and gluconeogenesis (1). It is the key positive modulator for glycolytic enzyme phophofructokinase (PFK) (not same as PFK-2), and PFK’s increased activity stimulates glycolysis by suppressing activity of fructose biphophatase (not same as FBase-2) (1). The reduced presence of fructose 2,6-biphosphate and, thus, increased activity of gluconeogenesis restores blood glucose levels successfully (1).

Phew! Now on to dessert.

In response to restored blood glucose levels from gluconeogenesis or when breaking a fast, the picture is reversed. The presence of glucose stimulates the pancreas to release insulin (1). Insulin reduces fructose 2,6-biphosphate via dephosphorylation of phosphofructokinase-2, and positively affects activity of glycogen synthase (also through dephosphorylation) stimulating glycogenesis (1).

So just remember, dessert equals dephosphorylation and phasting equals phosphorylation!

Reference List

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

22 February 2009

Why can't we convert fat to glucose?

As evident by many sugar-laden soda pop "potbellies" of North America, lipogenesis can obviously occur from drinking and eating too much sugar (1). Wouldn’t it be just grand to reverse the process and be able to lose all that fat via gluconeogenesis? Unfortunately mammals do not have the ability to synthesize glucose from fats (1).

The fact is that once glucose is converted to acetyl coA there is no method of getting back to glucose. The pyruvate dehydrogenase reaction that converts pyruvate to acetyl CoA is not reversible (1p252). Because lipid metabolism produces acetyl CoA via beta-oxidation, there can be no conversion to pyruvate or oxaloacetate that may have been used for gluconeogenesis (1p252). Further, the two carbons in the acetyl CoA molecule are lost upon entering the citric acid cycle (1p252). Thus, the acetyl CoA is used for energy (1p252).

There are some fatty acids that have an odd number of carbon atoms that can be converted to glucose, but these are not common in the diet (1p253). Maybe they should be made more common. Do they taste good?

Reference List

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

When to use a ketogenic diet

Normally what you need before you can start up aerobic respiration in the mitochondria is a multienzyme complex known as pyruvate dehydrogenase complex—of which the main enzyme is pyruvate decarboxylase. The complex acts on pyruvate, produced from glycolysis, in an oxidative decarboxylation reaction to produce acetyl-coA, which then enters the citric acid cycle (1).

What happens when pyruvate dehydrogenase is deficient? An actual genetic deficiency is rare, but it is the most common mitochondria-associated neurodegenerative disorder (2). When it does occur it significantly effects energy metabolism, poor use of glucose and build-up of lactic acid (2). Along with probable neurological impairments, too much glucose can exacerbate the problem leading to hyperglycemia and diabetes (2).

Diabetics , in essence, can also be described as a condition where pyruvate dehydrogenase complex activity is reduced(3-5). The lack of insulin to bring glucose into cells may be a factor, leading to little activity, or a nutritional deficiency of a vitamin such as thiamine (vitamin B-1) due to poor diet or starvation may lead to decreased production of the complex (3-5). In these cases, just as genetic deficiency, inefficient use of glucose results in hyperglycemia.

A ketogenic diet is used to manage the disease of pyruvate dehydrogenase deficiency (2). And it’s important to understand why this higher-fat, adequate protein, low-carb diet works for possible use with diabetes. It is because production of acetyl-coA can come from lipid metabolism via beta-oxidation as well as from amino acids isoleucine, lysine, phenylalanine, tyrosine and leucine (other amino acids are formed into pyruvate) (1p252).

There is plenty of research available showing that a ketogenic diet can help to control blood sugar (6-10). As a short-term therapy, the diet has had success even with children with Type II diabetes (11). But what of the side effects? As we know from critiques of the Atkin’s diet, a ketogenic diet produces fast weight loss through polyuria, but comes back with water retention from refeeding of carbohydrates (12) . The diet increases plasma cholesterol, uric acid, and may even cause hypokalemia (12). Further, you suffer nausea, fatigue, and hypotension (12). One must weigh the goods and bads of a ketogenic diet and make modifications as necessary.

Reference List

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

2. Henwood MJ, Thornton PS, Preis CM, Chee C, Grimberg A. Reconciling diabetes management and the ketogenic diet in a child with pyruvate dehydrogenase deficiency. J Child Neurol 2006;21:436-9.

3. Koivisto VA, Yki-Jarvinen H. Changes in muscle glucose metabolism in type 1 diabetes. Ann Med 1990;22:201-5.

4. Beltramo E, Berrone E, Tarallo S, Porta M. Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications. Acta Diabetol 2008;45:131-41.

5. Hutson NJ, Kerbey AL, Randle PJ, Sugden PH. Regulation of pyruvate dehydrogenase by insulin action. Prog Clin Biol Res 1979;31:707-19.

6. Westman EC, Yancy WS, Jr., Mavropoulos JC, Marquart M, McDuffie JR. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond) 2008;5:36.

7. Feinman RD, Makowske M. Metabolic syndrome and low-carbohydrate ketogenic diets in the medical school biochemistry curriculum. Metab Syndr Relat Disord 2003;1:189-97.

8. Nuttall FQ, Schweim K, Hoover H, Gannon MC. Effect of the LoBAG30 diet on blood glucose control in people with type 2 diabetes. Br J Nutr 2008;99:511-9.

9. Dashti HM, Mathew TC, Khadada M et al. Beneficial effects of ketogenic diet in obese diabetic subjects. Mol Cell Biochem 2007;302:249-56.

10. Henwood MJ, Thornton PS, Preis CM, Chee C, Grimberg A. Reconciling diabetes management and the ketogenic diet in a child with pyruvate dehydrogenase deficiency. J Child Neurol 2006;21:436-9.

11. Willi SM, Martin K, Datko FM, Brant BP. Treatment of type 2 diabetes in childhood using a very-low-calorie diet. Diabetes Care 2004;27:348-53.

12. Hirschel B. [Dr. Atkins' dietetic revolution: a critique]. Schweiz Med Wochenschr 1977;107:1017-25.

Focusing on the heart of the No. 1 and No. 3 killer

Almost half of us will die of a heart attack or stroke; in fact, it’s likely many of us have been developing a type of cardiovascular disease already (1). Just being male increases your risk, and if you happen to be a male, sedentary, obese smoker then you’re in real trouble (1). Adding these risk factors up doesn’t triple your chances, it multiplies them seven-fold (1)!

In light of American Heart Month, don’t forget to donate to cardiovascular disease research—spend with a clear conscience for clear arteries—but although the American Heart Association badly needs your funding, your cash is best suited for a pair of tennis shoes (1).

The conclusion on getting a heart attack is that the problem isn’t the heart, and in stroke, the brain isn’t at fault either (1). By far the greatest culprit is the accumulated thickening of thick sludge in scattered patches in your blood vessels that eventually merge to form large plaques (1). These atheromas represent atherosclerosis (1).

There’s no sign to us that plaque development is occurring (1). We feel no pain or any other symptoms (1). But our blood vessels are narrowing, called stenosis, more and more as they become hardened, due to calcification, and obstructed (1). The volume of blood delivered to tissues lessens (1). Eventually you might notice skin wounds heal slowly especially in the legs, and reduced blood flow to the brain is causing memory loss and confusion (1). The narrowing will sap your energy and ischemic heart disease results (1). Elevated blood pressure from hypertension worsens the problem and taxes the heart (1).

As blood swirls around plaque, splashing up against vessel walls, resulting endothelial damage might lead to a thromboembolic event (1). As platelets activate as well as a cascade of coagulation, an internal blood clot, or thrombus, can narrow the lumen further and consolidate the stenosis and ischemia (1). Another possibility is an aneurysm from blood flow pushing out a weakened vessel wall like a balloon (1). Usually thrombosis is the final case of fatal myocardial infarction (1).

Where hyperlipidemia, if you are obese, and hypercholesterolemia play roles are in contributing ingredients of plaque (1). LDL cholesterol makes multiple contributions to plaque development (1). When it is oxidized by free radicals and taken up by smooth muscle and macrophages, it leaves fats (intended to go to muscle and adipose tissue) to create foam cells that create thickening (1). The oxidized LDL then causes stimulation of plaque through growth factor production, promoting connective tissue desposition, and attracting monocytes that adhere to and modify endothelial surface (1). Further the LDL itself damages the endothelium causing inflammation (1).

In diabetes, sugars that circle LDL and bind to it in a process known as glycation then allows LDL to easily bind to endothelia (1). This in effect leads to more aggressive attraction of macrophages and promotion of connective tissue deposition enlarging the atheroma and inactivating nitric oxide, which is necessary for vasodilation (1).

When smoking, carbon monoxide that replaces oxygen in hemoglobin, causing hypoxia may also be atherogenic by promoting smooth muscle proliferation and LDL accumulation (1). Plus, the nicotine has vasoconstrictive effects, narrowing blood vessels further (1).

Reducing risk factors is the solution. In conclusion, by knowing more about how cardiovascular disease develops, we can help to prevent heart attacks and stroke. While lowering cholesterol is not justified by scientific research, reducing calories to avoid obesity is strongly supported, more so when saturated fat is reduced. Stopping the cigarette habit helps, and so does keeping blood pressure in check (1). Getting in shape, even with moderate exercise, by far can quickly yield results including a reduced heart rate of 10 beats a minute saving your heart more than 5 million beats a year that cause wear and tear (1). The goal is to avoid developing atherosclerosis further and leading a longer, healthier life.

Reference List

1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.

21 February 2009

Contraceptive use and increased risk of thrombosis?

It's interesting to note that contraceptives can increase risk of thrombosis. A report in 1980 showed that two women who died of myocardial infarction did not smoke or have hyperlipidemia, hypertension or atherosclerosis; the only connection was an oral contraceptive (1). I'd like to learn more about why this would happen.

1. Loire R, Touboul P, Gressard A, Rondepierre D, Tabib A. [Oral contraceptive and coronary thrombosis. Two clinicopathological cases]. Arch Mal Coeur Vaiss 1980;73:432-7.

Anticoagulants a factor for thrombosis?

Next time you're on a long car trip, check your legs to see if one is redder or warmer than the other. Or if your calf or thigh begins to ache. These could be symptoms of deep vein thrombosis, especially if you're genetically predisposed. Inactivity can cause the condition and blood thinners like heparin or warfarin are generally used as treatment (1).

But while we understand that hypercoagulation can be a factor for thrombosis, it’s important to note that anticoagulants can also potentially cause thrombosis. Oral anticoagulants can increase severity of bleeding, which can exacerbate intracerebral hemorrhage leading to significantly higher risk of a thromboembolic events (2).

Exercise and take your fish oil softgels!


1. WebMD. Deep vein thrombosis: Topic overview. Available at: http://www.webmd.com/heart-disease/tc/deep-vein-thrombosis-topic-overview.

2. Goldstein JN, Fazen LE, Wendell L et al. Risk of thromboembolism following acute intracerebral hemorrhage. Neurocrit Care 2009;10:28-34.

What are the factors leading up to thrombosis?

When a blood vessel is injured, a coagulation cascade is activated to form an organized clot to retain moisture and begin a healing process. Unlike a clot, a thrombus occurs in the blood vessel as a result of endothelial damage, altered blood flow or a hypercoagulation state that triggers platelet activation and a coagulation cascade (1). About one in 1,000 adults develop thrombosis annually (2).

Endothelial damage

Contributing to risk of thrombosis, endothelial damage can occur from hemodynamic stress (normal wear and tear). Hemodynamic stress is accentuated by conditions such as hypertension or infection (1). The stress eventually strips away endothelial cells exposing subendothelial collagen (1). This may occur, for example, on endocardial surface (1). The change can lead to platelet adherence, activation, aggregation and eventually a thrombus (1). Endothelial damage may occur from iatrogenic disease (a disease result of medical or surgical intervention) such as can be caused by an intravenous needle. Endothelial damage can also occur from trauma such as from an auto accident, a fall, or by radiation, high cholesterol or smoking (1).

Altered blood flow

The abnormal pattern of blood flow leads to thrombosis because it increases platelet contact with endothelium (1). It can occur from reduction in rate or turbulence, principally caused by cardiac damage or increased blood viscosity (1). At times, also, reduced venous blood flow is due to weakened vein walls, varicose veins, which disrupts functioning of leaflet valves (1). A malformed heart can cause blood flow turbulence that may create a thrombus in a cardiac chamber, called a mural thrombus (1). Lastly, a tumor causing inflammation or swelling can compress a vessel causing turbulence (1). Increased pressure from arterial pressure can eventually push out a weakened arterial wall causing a pouchlike bulge called an aneurysim (1). Blood swirls into the aneurism, platelets smash against the endothelium and thrombosis follows (1).

Blood Hypercoagulation

Hypercoagulation is suspected when turbulent blood flow or endothelial damage don’t appear the case in thrombosis (1). Genetic defects can lead to malfunction and overproduction of coagulation promoters or lack of coagulation inhibitors (1). A deficiency, for example of PG-I(2), a coagullaation inhibitor, leads to the liver overproducing clotting factors (1). Those with such “thrombophilic disorders” can applaud the discovery of factor V Leiden since its occurrence is most common in these disorders and subject to intense research (3).

Other Risk factors

Apart from genetic predisposition, thrombosis risk increases with advancing age, being male, being obese, after surgery, trauma, cancer, immobilization, pregnancy and exogenous hormones (2;4).


The sequela of thrombosis can resolve itself by being broken down or reduced, with the help of moderate exercise and cardiopulmonary fitness (1). A second consequence is organization where phagocytic digestion a couple or more days after the thrombus forms and with platelets and fibrin replaced by connective tissue; essentially the thrombus becomes part of the the vessel wall with endothelium formed over it and recanalization allows blood to flow through the thrombus (1). Propagation may occur when a thrombus enlarges, extends and continued coagulation produces a red cap that extends a significant distance (1). The major consequence is infarction, when ischemia forms a region of necrosis that completely occludes the lumen of a vessel (1). Infarction mainly can occur due to tissue vulnerability to hypoxia, pattern of vascular supply, capacity of oxygen delivery and the rate of occlusion (1).

Reference List

1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
2. Cushman M. Epidemiology and risk factors for venous thrombosis. Semin Hematol 2007;44:62-9.
3. Cushman M. Inherited risk factors for venous thrombosis. Hematology Am Soc Hematol Educ Program 2005;452-7.
4. Olson N, O'Meara ES, Jenny NS et al. Lipoprotein-associated phospholipase A2 and risk of venous thrombosis in older adults. Am J Hematol 2008;83:524-7.

15 February 2009

"Be careful reading health books. You may die of a misprint." - Mark Twain.

Unlike other nations where food and culture are intertwined and make up the diets of most people, here in the U.S. we have more diet books than we can read. Along with these come dietary philosophies that absolutely nothing to do with the exact science of true nutrition.

Obsession has a way of skewing fact and fiction merging them into a new viewpoint of the world that is borderline fantasy. A concern may be justified in some cases, but lack of education leads to a dangerous assumption.

Science must be first. And students must learn how to think critically. To eradicate the kind of illusion that somehow a philosophy of diet will povide one ability to ignore science, education is most important. Be very, very skeptical and only rely on scientifically trained individuals when it comes to your health.

There's so much misinformation out there. These are characterized by misunderstandings, lies, and even through indoctrinations. We've all been subjected to these. I think we all might have given up a food because someone told us it might cause "cancer" only to find it might actually prevent cancer.

Along with education, a lot of the time has to be dedicated to eradicating ideas that people think they already know. These come by browsing Internet sites, succumbing to ideas of those who may or may not have their best interest in mind, and even possibly forcing sellers of these ideas to take some responsibility for what they do.


Sickle cell anemia / malaria connection

Sickle cell anemia is a genetic blood disorder that occurs when production of red blood cells contain abnormally shaped hemoglobin that, in effect, also distort red blood cells making them look crescent-shaped or “sickle-like” (1). The hemolytic condition occurs because these cells have a lifespan of about 20 days versus the normal cell lifespan of 120 days; the marrow and spleen clear them out early leading to a low count in total red blood cells (1). Bone marrow is not able to replace the red blood cells fast enough (2).

About .2% of blacks of African origin are affected by sickle cell anemia as well as other groups (1). It affects millions worldwide and afflicts them with long-term pain and fatigue (2). Improved care is helping to keep patients alive into 40s and 50s (2). No cure is known, but bone marrow transplants are offering promising results (2).

The sickle cell trait is benign, passed by a defective gene (1). Two defective genes cause the blood disorder (1). Sickle cell genes are thought to have evolved as recently as 40,000 years ago as a defense against malaria in African populations (3). This hypothesis, tested in mice, is thought to be correct because of the anemia encourages rapid elimination of infected red blood cells by the liver and spleen, which may have led to increased survival against malaria (4-6).


1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
2. National Heart and Lung Institute. Sickle cell anemia. "What is sickle cell anemia?" Available at: http://www.nhlbi.nih.gov/health/dci/Diseases/Sca/SCA_WhatIs.html.
3. Boaz N. Evolving Health: The Origins of Illness and How the Modern World is Making us Sick. New York: John Wiley & Sons, 2009.
4. Min-Oo G, Fortin A, Tam MF, Gros P, Stevenson MM. Phenotypic expression of pyruvate kinase deficiency and protection against malaria in a mouse model. Genes Immun 2004;5:168-75.
5. Min-Oo G, Tam M, Stevenson MM, Gros P. Pyruvate kinase deficiency: correlation between enzyme activity, extent of hemolytic anemia and protection against malaria in independent mouse mutants. Blood Cells Mol Dis 2007;39:63-9.
6. Durand PM, Coetzer TL. Pyruvate kinase deficiency protects against malaria in humans. Haematologica 2008;93:939-40.

Is your pernicious anemia due to lack of or mutated intrinsic factor?

Do you feel tired and weak all the time? You should find out if you have pernicious anemia. The blood disorder occures when you can't make enough red blood cells to take oxygen to your cells due to lacking B12.

Lack of B12 in the diet may be due to lack of intrinsic factor. To understand how this might happen, it’s important to understand just how cobalamin is absorbed. Cobalamin (B12) is taken up by R-binder, found in the saliva, after its released in the stomach from meat and dairy products that you eat (1). The bound complex then gets to the intestine where the cobalamin is released and binds to intrinsic factor (1). Cobalamin needs intrinsic factor to be absorbed because absorption only occurs when intrinsic factor binds to receptors of the distal ileum. Then cobalamin is released and taken up by a transport protein called transcobalamin II (1).

The lack of intrinsic factor can be caused by an autoimmune attack on intrinsic factor and the parietal cells producing it (1). Or it may be due to a possible mutation of intrinsic factor caused by mutation of intrinsic factor gene(2). In either case, dietary B12 from meat and dairy is unlikely to help with the anemia (1). B12 injections or sublingual dosages are necessary.


1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.

2. Remacha AF, Del RE, Sarda MP, Canals C, Simo M, Baiget M. Role of (Glu --> Arg, Q5R) mutation of the intrinsic factor in pernicious anemia and other causes of low vitamin B12. Ann Hematol 2008;87:599-600.

14 February 2009

How my wife's father died

The last time my wife saw her father, she was nine years old. He left  to the hospital to have some general blood tests done. His doc had told him he had symptoms of a blood disorder: pale skin, frequent nose bleeds and bleeding gums, frequent infections, weight loss, fever, poor appetite and extreme fatigue.

To rule out leukemia, a full blood count was used to determine how many cell types were in circulation. A differential blood count determined the proportion of blood cells by type and a hematocrit assay determined how many red blood cells were in the blood. 

Finally, a bone marrow sample confirmed leukemia, but my wife's father never knew. Due to low red blood cell count he was given a blood transfusion. The transfusion failed and he had died immediately after. My wife never had a chance to say goodbye.

Leukemia is a cancer of related cancers stemming from production of abnormal white blood cells and their proliferation throughout the body. Its cause is unknown and its prevention is unknown to be possible. However, those who smoke, who are exposed to benzene, or who have been through chemotherapy and radiation therapy for other cancers appear to be at higher risk.


08 February 2009

Iodine and The Origins of Human Diet and Brain

In his thorough review of the Paleolithic origins of the human diet, Cordain et al may have missed iodine and its role, according to Stephen Cunnane (1;2). Cunnane writes that “1 of the 2 nutrients (the other is iron)” that modern humans most often find themselves deficient in is iodine.

Human brain development, Cunnane explains, is heavily affected by sufficient iodine intake; inland populations of developed countries have avoided brain impairment only through intake of iodized table salt (2).

Cunnane suggests that shore-based food may have been part of the diet of early humans because otherwise iodine and other “brain-selective nutrients” such as docosahexaenoic acid and iron may not have allowed the human brain to evolve at all (2).

Anthropologists appear to be in agreement with Cunnane that the coastline may have been a critical point in the human story. One of the oldest-known human stone tool sites, in fact, was found in what would have been a coastal environment 125,000 years ago in eastern Africa (3).

Reference List

1. Cordain L, Eaton SB, Sebastian A et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.
2. Cunnane SC. Origins and evolution of the Western diet: implications of iodine and seafood intakes for the human brain. Am J Clin Nutr 2005;82:483-4.
3. University Of Toronto (2000, June 1). Stone Tools Reveal Ancient Seafood Diet. ScienceDaily. Retrieved September 11, 2009, from http://www.sciencedaily.com/releases/2000/05/000531070849.htm 


If you‘ve had children, chances are you’ve heard of a hemangioma. The fancy name may have sounded scary, but then you might have felt better knowing it was simply a common, benign, vascular tumor otherwise known as a birthmark (1).

Birthmarks affect less than 20 percent of infants and usually to pre-term birth white females born to women who are older in maternal age (1). The tumors grow for about a year and almost never cause complications (1). They later tend to disappear (1).

In rare cases, a birthmark may appear in the subglttic larynx (2). It won't be noted at birth, but as it enlarges a crouplike illness can develop and treatment may be needed to avoid obstruction of the airway from occurring (2). Usually this is not serious (2).


1. Bukowinski AT, Ryan MA, Slymen DJ, Sevick CJ, Alcaraz JE, Smith TC. Haemangiomas and associated congenital malformations in a large population-based sample of infants. Paediatr Perinat Epidemiol 2008;22:520-9.
2. Kontzoglou G, Triaridis S, Noussios G, Valeri R, Nanas C. Subglottic hemangioma treated with interferon alpha 2A. Acta Otorhinolaryngol Belg 2002;56:83-5.


What conventional cancer treatment has fewer side effects, is less expensive, and requires a shorter recovery time?

Cryosurgery, or cryotherapy, is the use of liquid nitrogen to destroy cancer by applying directly to affected cells with cotton or a spary and freezing them (1). The frozen tissue then thaws and is absorbed by the body or dissolves and forms a scab (1). There is only limited damage to other cells (1) unlike chemotherapy, and there is less irritative and obstructive voiding symptoms in comparison to brachytherapy (2).

The treatment is used in several cancers including liver cancers that have not spread, bone tumors, retinoblastoma, early-stage skin cancers and precancerous skin growths and conditions of the cervix (1). Its currently being evaluated for breast, colon and kidney cancers (1). And it may be useful in conjunction with other treatments (1).

1. National Cancer Institute. Available at: http://www.cancer.gov/cancertopics/factsheet/Therapy/cryosurgery.
2. Hubosky SG, Fabrizio MD, Schellhammer PF, Barone BB, Tepera CM, Given RW. Single center experience with third-generation cryosurgery for management of organ-confined prostate cancer: critical evaluation of short-term outcomes, complications, and patient quality of life. J Endourol 2007;21:1521-31.

Treating cancer with IV-therapy vitamin C

Cancer treatment with vitamin C was first researched by Nobel-prize winner Linus Pauling in the 1970s. Massive oral doses, however, were not found to be effective according to Mayo Clinic. But researchers of the University of Puerto Rico are finding that intravenous (IV) massive doses just might be used as treatment (1-3).

The Bio-Communications Research Institute's RECNAC II project team led by Michael Gonzalez, Ph.D., has found that IV vitamin C is selectively toxic to cancerous tumor cells (1-3). The team hopes to someday establish that the treatment is an altertnative to highly toxic chemotherapy (4). Gonzalez hopes to have a book published soon about his experience (4).

Further research is needed to determine IV vitamin C-therapy's role in cancer treatment. It should not be considered an alternative cancer treatment.

1. Duconge J, Miranda-Massari JR, Gonzalez MJ, Jackson JA, Warnock W, Riordan NH. Pharmacokinetics of vitamin C: insights into the oral and intravenous administration of ascorbate. P R Health Sci J 2008;27:7-19.
2. Riordan HD, Casciari JJ, Gonzalez MJ et al. A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients. P R Health Sci J 2005;24:269-76.
3. Riordan HD, Riordan NH, Jackson JA et al. Intravenous vitamin C as a chemotherapy agent: a report on clinical cases. P R Health Sci J 2004;23:115-8.
4. Personal communication with Michael Gonzalez.

Another protein that could be targeted for breast cancer

Soon we may see a new way to treat breast cancer. Cyclophilin B is a protein that was just uncovered by Northwestern University researchers and was found to have an increased presence in metastases (1). The protein could be a target of drugs in the future (2).


1. Fang F, Flegler AJ, Du P, Lin S, Clevenger CV. Expression of cyclophilin B is associated with malignant progression and regulation of genes implicated in the pathogenesis of breast cancer. Am J Pathol 2009;174:297-308.

2. American Journal of Pathology (2009, January 12). Possible New Target For Treating Breast Cancer. ScienceDaily. Retrieved February 8, 2009, from http://www.sciencedaily.com­ /releases/2008/12/081230075154.htm

Hocus pocus cancer healing?

A review published in 2000 of four spontaneous cancer healing reports offered that the most likely event that occurred was immune modulation (1). Although mention was made of other factors such as "genetic therapy, withdrawal of carcinogens, infection, fever and vaccine roles, apoptosis, antibody, antiangiogenesis and maturation mechanisms, withdrawal of therapy, natural killer activity, endocrine, hormonal, and pregnancy factors, and prayers or psychoneuro-religious participation" (1).

Mind-body therapy has gained some interest as of late. At least a few doctors are discussing the idea that emotional and psychological support are harmless and may support treatment (2).


1. Chang WY. Complete spontaneous regression of cancer: four case reports, review of literature, and discussion of possible mechanisms involved. Hawaii Med J 2000;59:379-87.
2. Barasch MI. Remarkable recoveries: research and practice from a patient's perspective. Hematol Oncol Clin North Am 2008;22:755-66, x.

To reduce risk of colon cancer, head south

When you live in a sunny climate (like I do), your risk of colon cancer and other cancers drops. Scientists from Johns Hopkins University credit this phenomenon to possibility that greater serum levels of vitamin D is responsible. But don't start thinking of joining me in Arizona just yet. Skin cancer risk skyrockets here.


Mohr SB. A brief history of vitamin d and cancer prevention. Ann Epidemiol 2009;19:79-83.

Welcome home my gut-friendly little buddies!

Now that I'm off antibiotics it's time for probiotics. Considering that there are around 500 species of bacteria in our guts, it's worth noting that in the future we shouldn't question probiotic therapy, but should question which species to use.

The future of probiotic therapy may be in studies for selection of "disease-specific strains" that can be used in treatment in diseases such as Crohn's, ulcerative colitis, pancreatitis and even liver diseases (1). We also mustn't forget research into how certain prebiotics stimulate the ecology and growth of individual strains, a science some scientists are now calling "synbiotics" (2).

My outlook is a world of understanding our little friends the bacteria and living a full life enjoying wonderful food without fear of the aches and pains that come with gas, constipation and diarrhea.

1. Jonkers D, Stockbrugger R. Review article: Probiotics in gastrointestinal and liver diseases. Aliment Pharmacol Ther 2007;26 Suppl 2:133-48.
2. de VM, Schrezenmeir J. Probiotics, prebiotics, and synbiotics. Adv Biochem Eng Biotechnol 2008;111:1-66.

What happens when you don't chew your food

My mother always used to tell me to chew my food. Did she know that salivary alpha-amylase was hydrolyzing carbohydrates in my mouth? She probably had a good idea. Still, I swallow too quickly. So little gets digested and the food ends up in my stomach.

Alpha-amylase can't work in the stomach because the pH is too acidic (1p69). So digestion of carbohydrates finally continues when it enters the duodenum (1p69). Here stomach acid is neutralized (1p45) and alpha-amylase enters again secreted from the pancreas (1p69). Around half of carbohydrates are digested in the duodenum (1p48).

Although salivary amylase doesn't do much in our mouth, the reason it's there may give us clues in its role in evolution of human digestion. In fact, for breaking up starches quickly to obtain glucose, alpha-amylase is used for digestion by almost the entire animal kingdom, including amoebas and sponges (2). Biologists are now studying the how amylase genes are copied to find out more (3).


1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Da Lage JL, Danchin EG, Casane D. Where do animal alpha-amylases come from? An interkingdom trip. FEBS Lett 2007;581:3927-35.
3. Myers PZ. Amylase and human evolution. Pharyngula. Available at: http://scienceblogs.com/pharyngula/2008/12/amylase_and_human_evolution.php.

Bile, Bacteria and Bears

Enterohepatic circulation is the process of secretion and reabsorption of bile (1;2). When you eat a fatty meal, your gallbladder secretes bile to convert large fat globules to small droplets called micelles to be absorbed (1;2). Ninety percent of the bile is then reabsorbed via active transport or passive transport in the small intestine (1). In the colon, bacteria increase the recycled amount by deconjugating some non-absorbable primary bile acids to secondary acids, which are then absorbed passively (1). Along with bile and its component of cholesterol, other molecules may be circulated.

For this reason, it is important to understand how fiber and bacteria affects enterohepatic circulation. Guar gum, for example, is a soluble fiber that may prevent postprandial increase of conjugated bile acids (3). Other fibers are found to have the same effect (4;5). By absorbing cholesterol and keeping it from re-entering enterohepatic circulation, guar gum and pectin (just as phytostanols and phytosterols) both can be helpful in reducing blood cholesterol (1;6;7). Fiber’s impact also appears to affect enterohepatic circulation of estrogens (8;9).

Prebiotic fiber and probiotics may be useful for drug therapy. One such drug is the secondary bile acid ursodeoxycholic acid (USDA). USDA lowers cholesterol and treats cholestatic liver disease (10-14). But because of how expensive it is to synthesize, the ancient and now illegal practice of “milking” black bears for their bile (which contains USDA) continues in China (15). If prebiotic fiber and probiotics can help recirculate the drug through enterohepatic circulation, it may result in becoming cheaper to use.

On the other hand, the intestinal flora can be detrimental when taken with other drugs. Because of enterohepatic circulation, active promotion of bacteria in recycling drugs can overload the liver and cause damage to the body (16). In such a case, antibiotics may be necessary. Doctors must take this potential toxicity into consideration when helping patients (16).
Lastly, other exogenous or endogenous xenobiotics (toxins) might be recycled by probiotic or pathogenic bacteria through enterohepatic circulation (17). In effect, the liver is performing double duty in such cases by detoxifying and detoxifying again (17). Depending on the situation, antibiotic and probiotic therapy may be needed.

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
2. Roberts MS, Magnusson BM, Burczynski FJ, Weiss M. Enterohepatic circulation: physiological, pharmacokinetic and clinical implications. Clin Pharmacokinet 2002;41:751-90.
3. Hansen WE, Maurer H, Vollmar J, Brauning C. Guar gum and bile: effects on postprandial gallbladder contraction and on serum bile acids in man. Hepatogastroenterology 1983;30:131-3.
4. Kern F, Jr., Birkner HJ, Ostrower VS. Binding of bile acids by dietary fiber. Am J Clin Nutr 1978;31:S175-S179.
5. Eastwood MA. Fibre and enterohepatic circulation. Nutr Rev 1977;35:42-4.
6. Fernandez ML, Trejo A, McNamara DJ. Pectin isolated from prickly pear (Opuntia sp.) modifies low density lipoprotein metabolism in cholesterol-fed guinea pigs. J Nutr 1990;120:1283-90.
7. Ebihara K, Schneeman BO. Interaction of bile acids, phospholipids, cholesterol and triglyceride with dietary fibers in the small intestine of rats. J Nutr 1989;119:1100-6.
8. Gorbach SL, Goldin BR. Diet and the excretion and enterohepatic cycling of estrogens. Prev Med 1987;16:525-31.
9. Adlercreutz H, Fotsis T, Bannwart C, Hamalainen E, Bloigu S, Ollus A. Urinary estrogen profile determination in young Finnish vegetarian and omnivorous women. J Steroid Biochem 1986;24:289-96.
10. Maeda K, Kambara M, Tian Y, Hofmann AF, Sugiyama Y. Uptake of ursodeoxycholate and its conjugates by human hepatocytes: role of Na(+)-taurocholate cotransporting polypeptide (NTCP), organic anion transporting polypeptide (OATP) 1B1 (OATP-C), and oatp1B3 (OATP8). Mol Pharm 2006;3:70-7.
11. Angelin B, Eusufzai S. Effects of ursodeoxycholic acid on plasma lipids. Scand J Gastroenterol Suppl 1994;204:24-6.
12. Hofmann AF. Pharmacology of ursodeoxycholic acid, an enterohepatic drug. Scand J Gastroenterol Suppl 1994;204:1-15.
13. Rudolph G, Endele R, Senn M, Stiehl A. Effect of ursodeoxycholic acid on the kinetics of cholic acid and chenodeoxycholic acid in patients with primary sclerosing cholangitis. Hepatology 1993;17:1028-32.
14. Mazzella G, Parini P, Bazzoli F et al. Ursodeoxycholic acid administration on bile acid metabolism in patients with early stages of primary biliary cirrhosis. Dig Dis Sci 1993;38:896-902.
15. Feng Y, Siu K, Wang N et al. Bear bile: dilemma of traditional medicinal use and animal protection. J Ethnobiol Ethnomed 2009;5:2.
16. Mikov M. The metabolism of drugs by the gut flora. Eur J Drug Metab Pharmacokinet 1994;19:201-7.
17. Liska DJ. The detoxification enzyme systems. Altern Med Rev 1998;3:187-98.

07 February 2009

Why I'm lactose intolerant

I've always thought it a little disgusting to drink a liquid that squirts out from another animal's mammary gland, but research suggests my European ancestors have been doing so for centuries. The reason why so many of European heritage (like me) have lactose intolerance has to do with antibiotics. The guts of my ancestors (post-agriculture) evolved bacteria that helped them digest that lactose, which antibiotics eliminate.

There is strong evidence supporting probiotic therapy (1-4). In Japan, there are at least 20 probiotic foods that have health claims (1). And one of the key benefits of probiotics is alleviating symptoms of lactose intolerance (2-3). In fact, our efforts in leading people with lactose intolerance to avoid lactose might change in the future. At least one scientific article has suggested that lactose may have potential prebiotic effects, meaning it could be instrumental to grow probiotic bacteria and inhibit growth of pathogenic bacteria (4;5p54).


1. Farnworth ER. The evidence to support health claims for probiotics. J Nutr 2008;138:1250S-4S.

2. He T, Priebe MG, Zhong Y et al. Effects of yogurt and bifidobacteria supplementation on the colonic microbiota in lactose-intolerant subjects. J Appl Microbiol 2008;104:595-604.

3. Zhong Y, Huang CY, He T, Harmsen HM. [Effect of probiotics and yogurt on colonic microflora in subjects with lactose intolerance]. Wei Sheng Yan Jiu 2006;35:587-91.

4. Szilagyi A. Review article: lactose--a potential prebiotic. Aliment Pharmacol Ther 2002;16:1591-602.

5. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

Can fish oil replace drugs to treat Crohn's?

It's too bad anti-inflammation drugs, cortisone, steroids and immune system suppressors have to be used with this disease.

Fish oil enjoys fame for helping to reduce inflammation in joints (1-2), which would suggest it might be helpful in Crohn's disease. But the fish oil hope for this inflammatory disease was extinguished last month; as study showed it caused no adverse effects, but had no beneficial effects either (3). Shucks.


1. Calder PC. Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on 'Nutrition and autoimmune disease' PUFA, inflammatory processes and rheumatoid arthritis. Proc Nutr Soc 2008;67:409-18.

2. Adam O, Beringer C, Kless T et al. Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Rheumatol Int 2003;23:27-36.

3. Turner D, Zlotkin SH, Shah PS, Griffiths AM. Omega 3 fatty acids (fish oil) for maintenance of remission in Crohn's disease. Cochrane Database Syst Rev 2009;CD006320.

Smoking improves ulcerative colitis?

You should quit smoking no matter what for all its ill effects, but according to a just-released report, smoking might actually help with symptoms of ulcerative colitis (1). In fact, patients that quit smoking might actually worsen ulcerative colitis (1).

Don't tell the tobacco companies!

The study also evaluated smoking on Crohn's and found that it aggravates the disease and is a risk factor (1).

Don't smoke!


1. van der Heide F, Dijkstra A, Weersma RK et al. Effects of active and passive smoking on disease course of Crohn's disease and ulcerative colitis. Inflamm Bowel Dis 2009.

What is Kapidex?

Kapidex is good news. FDA just approved it to help heal esophagaeal damage related to GERD (1). The drug features what scientists are calling "new-generation" acid-pump antagonists, which bind to proton pumps of the parietal cells by producing disulphide bonds (2).

These newer drugs (esomeprazole and rabeprazole) work faster than older ones, provide relief for more than 24 hours, and have a lower oxidative hepatic metabolism rate, which lessens possibility of interacting with other drugs (2).


1. Hitti M. "FDA OKs New GERD Drug Kapidex Once-Daily Formula Approved to Treat GERD and Erosive Esophagitis." WebMD Health News. Available at: http://www.webmd.com/heartburn-gerd/news/20090206/fda-oks-new-gerd-drug-kapidex.

2. de Korwin JD, Ducrotte P, Vallot T. [New-generation proton pump inhibitors: progress in the treatment of peptic acid diseases?]. Presse Med 2004;33:746-54.

How Can I Avoid a Toxic Gut?

Does passing gas embarrass me? Yes. But it happens to all of us. And I just blame it on my little friends (and sometimes not so friendly), bacteria (1). Abdominal pain and diarrhea? If it were continual I'd start to worry, but I'd rest assured I wasn't alone. One in five of us is suffering from an inflammatory bowel diseases (IBDs) such as ulcerative colitis or Crohn's (2). The pain and diarhea could also indicate Celiac disease or, if accompanied by nausea, pancreatits. Unfortunately if I had Celiac, it may be genetic, linked to leukocyte antigens (1). Pancreatis might mean gallstones, liver disease, or a viral infection (1). Mostly I worry about heartburn, which could become chronic and lead to gastroesophageal reflux disease (GERD), but I'm happy to hear FDA just approved Kapidex, a new proton-pump inhibitor that has already helped 6,000 patients with healing (3).

With a little luck and a well-planned diet, I think I can avoid most of these conditions of digestion (except the gas) in the future. That old Mexican doctor who saved my life when I was in Puebla would agree. After I tried to take advantage of a few too many delicious chile rellenos and ended up in his Urgent Care office suffering from the worst diarrhea and vomiting of my life, he told me, "Your stomach is so inflamed you might've died. No more spicy foods." Then he gave me a shot back in the you-know-what. My bland diet of the last few years has kept the epithelial lining of my gut mucosa pretty healthy so far, but I could do more.

If I expect this tube I call my GI tract (from my mouth to my anus) to digest and absorb nutrients until I'm ancient, then I've got to eat smaller, gut-manageable meals (1p60). I can also drink my water between meals, not during to keep the meals small (1p60). Also, I can balance the macronutrients in my meals. For example, by keeping each meal higher in protein and lower in fat, I'd be doing myself a favor. Too much fat can weaken gastroeseophageal sphincter pressure potentially leading to reflux, and the extra protein could increase pressure helping me to avoid reflux (1p59). I'd avoid excess protein and alcohol because both can overstimulate hydrochloric acid secretion (1p59).

Other good news of a diet higher in protein and low in fat is that if I happen to suffer from IBDs or pancreatitis. Both conditions affect fat digestion and absorption necessitating a lower-fat diet, and the extra protein can correct any protein loss due to malabsorption of amino acids (1p60-61).

Luckily (cross my fingers) my Argentine mother provided me with the genes to handle the gluten. Pasta and pizza are staples in Argentine culture. But if Celiac disease does turn out to be a problem for me, then wheat and barley are out. I can't have my small intestine inflamed or my lymphocytes and cytokines to destroying my enterocyte absorptive surface (1p60-61). I'd end up switching to rice-flour Argentine food.

1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.

2. Mayo Clinic. "Irritable Bowel Syndrome." Available at: http://www.mayoclinic.com/health/irritable-bowel-syndrome/DS00106.

3. Hitti M. "FDA OKs New GERD Drug Kapidex Once-Daily Formula Approved to Treat GERD and Erosive Esophagitis." WebMD Health News. Available at: http://www.webmd.com/heartburn-gerd/news/20090206/fda-oks-new-gerd-drug-kapidex.

05 February 2009

Evolutionary Discordance

There is a surging interest in perspectives of evolution to shed light on solutions for health—not at all discounted by this year’s Charles Darwin’s 200th birth anniversary. Many health-care professionals have even called for a return to a more primitive pattern of diet, environment and exercise that first made our ancient genome thrive (1-8).

Cordain et al (3) and others (1;4) make nothing short of an understatement in suggesting that contemporary chronic diseases and health issues are partially, if not largely, due to an evolutionary “clashing” (3;4) with new patterns introduced in our modern world.

Attempts of Cordain et al (3), however, of pointing out nutritional alterations since the agricultural revolution to reveal “evolutionary discordance” between Western diet and one in line with “genetically determined biology” can be considered far reaching.

An example is Cordain et al’s case that refined sugar consumption increased since 500 BC and high-fructose corn syrup since the 1970s may have caused discordance (3). Lacking evidence directly associated with hominin diets, it is left unknown how simple sugars may have actually shaped evolution of hominins.

The data, however, on ape diets suggests a fruitarian ancestry governed by plants (1). Although the sugars of these fruits are evidenced to have been accompanied by diverse dietary fiber sources (5), nutritional variations may have occurred not unlike refined sugars and large amounts of fructose. It is also unclear why fructose, heavily associated with diabetes (9-11), should be prevalent in the main foods of a hominin ancestral diet.

Science must ultimately make up perceptions on factual matter regarding nutrition and medicine where historical and archeological evidence fall short and can only present clues.

Double-blind, randomized cross-over designed trials on each discordance—cereals, refined sugars, refined vegetable oils, alcohol, salt, fatty domestic meats, etc.—and how differing amounts affect health must be researched for proper nutritional determinations.

For example, two interventions over a year’s time could be performed in which one group could be given wild-caught salmon and deer meat and the placebo group would receive farmed salmon and deer meat. Blood lipids and abdominal fat stores can be measured throughout the year.

Because of possible interplay from each discordance that should not be discounted, double-blind randomized cross-over trials should also include versions of whole, supposed Paleolithic diets.

Each study performed, in turn, may also offer revelations into evolutionary past. And perhaps, to make things more interesting, the studies should also be performed on bonobos and chimpanzees.

Reference List

1. Boaz N. Evolving Health: The Origins of Illness and How the Modern World is Making us Sick. New York: John Wiley & Sons, 2009.
2. Cordain L. The Paleo Diet. Hoboken, New Jersey: John Wiley & Sons, 2002.
3. Cordain L, Eaton SB, Sebastian A et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.
4. Gibson G. It Takes a Genome: How a Clash Between Our Genes and Modern Life is Making us Sick. Sydney, Australia: FT Press, 2009.
5. Leach JD. Evolutionary perspective on dietary intake of fibre and colorectal cancer. Eur J Clin Nutr 2007;61:140-2.
6. Marean CW, Bar-Matthews M, Bernatchez J et al. Early human use of marine resources and pigment in South Africa during the Middle Pleistocene. Nature 2007;449:905-8.
7. Nesse RM, Williams GC. Why We Get Sick: The New Science of Darwinian Medicine. New York: Vintage, 1996.
8. Wrangham R. Catching Fire: How Cooking Made Us Human. New York: Basic Books, 2009.
9. Sartorelli DS, Franco LJ, Gimeno SG, Ferreira SR, Cardoso MA. Dietary fructose, fruits, fruit juices and glucose tolerance status in Japanese-Brazilians. Nutr Metab Cardiovasc Dis 2009;19:77-83.
10. Ouyang X, Cirillo P, Sautin Y et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol 2008;48:993-9.
11. Basciano H, Federico L, Adeli K. Fructose, insulin resistance, and metabolic dyslipidemia. Nutr Metab (Lond) 2005;2:5.

01 February 2009

How to recognize diabetic ketoacidosis

Diabetic ketoacidosis occurs when glucose rises in the blood and there's too little insulin (1). The hyperglycemia is accompanied by breakdown of fats producing ketones (1).

Diabetics can quickly recognize the problem due to excessive thirst and frequent urination (2). The increased urine production can potentially cause electrolyte disturbances (1-3). High ketone levels in the urine will tell if diagnosis is correct (1-2).

It has to be treated right away with insulin administration and replacement of electrolytes and fluids (3).

1. Fleckman AM. Diabetic ketoacidosis. Endocrinol Metab Clin North Am 1993;22:181-207.

2. Israel RS. Diabetic ketoacidosis. Emerg Med Clin North Am 1989;7:859-71.

3. Bergenstal RM. Diabetic ketoacidosis. How to treat and, when possible, prevent. Postgrad Med 1985;77:151-7, 161.

"Hitting the wall" with low-carb

Along with potassium depletion, low-carb diets can cause fatigue to set in due to used up glycogen stores. A low-carb diet, for example, might cause a high-mileage runner to "hit the wall" (1). Generally endurance athletes practice carb loading simply to fill up those glycogen stores to ensure lasting energy (1).

1. http://www.faqs.org/sports-science/Je-Mo/Low-Carbohydrate-Diets-and-Athletic-Performance.html

Low-Carb Quick Weight Loss Doesn't Hold Water or Electrolytes

Alright, so you can lose weight fast with a low-carb diet. The lack of carbs will send the liver and muscles for their glycogen storage using up water and stimulating increased production of urine, or polyuria (1). Along with the osmotic diuresis, or increased urination, will be loss of sodium and potassium (1-2).

Couple that with a change of diet that eliminates water-retaining carbohydrates and foods high in potassium and water (such as fruits), and the diet could lead to dehydration and othostatic hypotension as well as potassium deficiency (1-2). Fatigue sets in due to used up glycogen stores (1). Exacerbating these potentials are appetite suppression and possible vomiting resulting from nausea, common in low-carb diets, which can lead to more depletion of electrolytes (1).

Even a moderate deficiency of potassium can increase calcium excretion, elevate blood pressure and cause abnormal bone turnover (2p455). If hypokalemia occurs from heavy loss of potassium (such as from vomiting), then there would be an increased risk of cardiac arrhythmia, muscle weakness, irritability, hypercalciuria, glucose intolerance and mental disorientation (2p455).

Potassium supplements can correct potassium deficiency, but too much can be toxic, producing hyperkalemia, which can lead to severe cardiac arrhythmias and cardiac arrest (2p455).


1. Hirschel B. [Dr. Atkins' dietetic revolution: a critique]. Schweiz Med Wochenschr 1977;107:1017-25.

2. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.