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.
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.
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).
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.
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.
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.
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.
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.
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.
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).
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.
No, aldosterone is not a new dietary supplement to pump you up the size of Arnold. It’s a hormone made up by your adrenal glands to help you hold onto sodium and rid off potassium whenever needed (1).
How is aldosterone released?
- Particularly it begins with the electrolyte-fluctuation-sensitive kidneys (1). They stimulate aldosterone production by secreting renin, a proteolytic enzyme (1). The secretion happens whenever there is decreased perfusion pressure that’s sensed by receptors in the kidneys’ juxtaglomerular apparatuses (“kidney brains” that tell the kidneys’ functional units, its nephrons, what to do) (1). The renin hydrolyzes angiosteninogen, a free-wheeling protein coming from the liver, to angiotensin I (1). Another enzyme, appropriately named angiotensin-converging enzyme (ACE), converts angiotensin I to angiotensin II. Angiotensin II interacts with adrenal cortical cell receptors and voila! aldosterone is released (1).
- Decreased atrial natriuretic peptide will stimulate release. This hormone from atrial cells ends up occurring if blood pressure elevates and, as opposed to aldosterone, causes excretion of sodium (1).
- Other possibilities for release are increased potassium concentration, increased ACTH, or decreased sodium (1).
Aldosterone and hypertension
High aldosterone levels are also a good indicator for transient ischemia attack and stroke (2-4). ACE inhibitors are a leading therapy (and subject to numerous new research papers) for intervening in the renin-angiotensin-aldosterone system along with angiotensin II type 1 receptor antagonists (2-4). The research on these are proving they are useful for those with hypertenstion and helping to prevent cardiac arrhythmias and sudden cardiac death (2-4).
Vitamin D appears to have association with aldosterone and hypertension. Just a few days ago a French study reported what many have suspected–that as the seasons change and the days become warmer, blood pressure begins to lower (5). And according to ScienceDaily, the study may be explained due to vitamin D deficiency (6).
The data is supported by the Framingham Heart Study and Nurses Health Study, which found vitamin D deficiency increased risk of hypertension, heart attack and stroke (6). A 1989 study that showed that long-term vitamin D supplementation lowered blood pressure in patients with essential hypertension (7).
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism, 5th ed. Belmont, CA: Thomson Wadsworth, 2009, p 553.
2. Ishiguro K, Hayashi K, Sasamura H, Sakamaki Y, Itoh H. “Pulse” treatment with high-dose angiotensin blocker reverses renal arteriolar hypertrophy and regresses hypertension. Hypertension 2009;53:83-9.2.
3. Makkar KM, Sanoski CA, Spinler SA. Role of Angiotensin-Converting Enzyme Inhibitors, Angiotensin II Receptor Blockers, and Aldosterone Antagonists in the Prevention of Atrial and Ventricular Arrhythmias. Pharmacotherapy 2009;29:31-48.3.
4. Qian C, Schoemaker RG, van Gilst WH, Roks AJ. The role of the renin-angiotensin-aldosterone system in cardiovascular progenitor cell function. Clin Sci (Lond) 2009;116:301-14.4. Vyssoulis GP, Karpanou EA, Tzamou VE et al. Aldosterone levels and stroke incidence in essential hypertensive patients. Int J Cardiol 2009.
5. Alperovitch A, Lacombe JM, Hanon O et al. Relationship between blood pressure and outdoor temperature in a large sample of elderly individuals: the Three-City study. Arch Intern Med 2009;169:75-80.
6. ScienceDaily. Blood Pressure Varies by the Season. 20 Jan 2009. Available at: http://www.sciencedaily.com/releases/2009/01/090116091523.htm
7. Lind L, Wengle B, Wide L, Ljunghall S. Reduction of blood pressure during long-term treatment with active vitamin D (alphacalcidol) is dependent on plasma renin activity and calcium status. A double-blind, placebo-controlled study. Am J Hypertens 1989;2:20-5.