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Posts tagged ‘wellness’

Are You Angry? Consider Using Cod Liver Oil

January 22, 2019, 3:15 pm

Are You Angry? Consider Using Cod Liver Oil

Researchers conducted a study to examine the relationship of dietary intake of omega-3 and omega-6 fats with level of hostility. The study sampled 3,581 urban white and black young adults, half who consumed fish, which contains omega-3, and half who did not.

The outcome of this study suggests that high dietary intake of omega-3 fats may be related to lower odds of high hostility in young adulthood.

European Journal Clinical Nutrition January, 2004
Eur J Clin Nutr. 2004 Jan;58(1):24-31.

Dietary intake of n-3, n-6 fatty acids and fish: Relationship with hostility in young adults-the CARDIA study. Iribarren C, Markovitz JH, Jacobs DR, Schreiner PJ, Daviglus M, Hibbeln JR. 1Division of Research, Kaiser Permanente, Oakland, CA, USA.

BACKGROUND:: Hostility has been shown to predict both the development and manifestation of coronary disease. Examining the inter-relation of dietary intake of fish and of polyunsaturated (n-3 and n-6) essential fatty acids with hostility may provide additional insights into the cardioprotective effect of dietary fish and polyunsaturated fatty acids.

OBJECTIVE:: To examine the association of dietary n-3, n-6 fatty acids and fish with level of hostility in a sample of 3581 urban white and black young adults.

DESIGN:: Cross-sectional observational study as part of an ongoing cohort study. A dietary assessment in 1992-1993 and measurement of hostility and other covariates in 1990-1991 were used in the analysis.

RESULTS:: The multivariate odds ratios of scoring in the upper quartile of hostility (adjusting for age, sex, race, field center, educational attainment, marital status, body mass index, smoking, alcohol consumption and physical activity) associated with one standard deviation increase in docosahexaenoic acid (DHA, 22:6) intake was 0.90 (95% CI=0.82-0.98; P=0.02). Consumption of any fish rich in n-3 fatty acids, compared to no consumption, was also independently associated with lower odds of high hostility (OR=0.82; 95% CI=0.69-0.97; P=0.02).

CONCLUSIONS:: These results suggest that high dietary intake of DHA and consumption of fish rich in n-3 fatty acids may be related to lower likelihood of high hostility in young adulthood. The association between dietary n-3 fatty acids and hostile personality merits further research.European Journal of Clinical Nutrition (2004) 58, 24-31. doi:10.1038/sj.ejcn.1601739

New Findings About Omega-3 Fatty Acids and Depression

January 22, 2019, 3:08 pm

New Findings About Omega-3 Fatty Acids and Depression
By Alan C. Logan, ND, FRSH

Omega-3 fatty acids are polyunsaturated fatty acids that are considered essential because they cannot be synthesized by the human body. Dietary sources of omega-3 fatty acids include plants (particularly flax, canola, walnuts and hemp) and fish (particularly ocean fish such as sardines, anchovies, salmon and mackerel). Plants contain the parent omega-3, alpha-linolenic acid (ALA), which can be converted into eicosapentanoic acid (EPA) and docosahexanoic acid (DHA).1

Dietary fish and fish oil supplements are a direct source of EPA and DHA. The influence of ALA, EPA and DHA in human health has been the subject of intense research over the last three decades. Although best known for cardiovascular benefits, new findings indicate that the influence of omega-3 fatty acids in mental health, particularly EPA, may currently be underestimated. Epidemiological, experimental and new clinical studies have all shown a strong connection between omega-3 fatty acids, or a lack thereof, and major depression.

These exciting new findings are not entirely surprising when one considers that the brain itself is 60 percent fat and that one-third of all fatty acids are of the polyunsaturated variety.2,3 As discussed below, the current research highlights the critical role of these fatty acids in the central nervous system (CNS).

Omega-3 Intake Declines, Depression Rates Climb

There has been a significant drop-off in omega-3 fatty acid intake within Western countries over the last century. The opposite can be said of omega-6 intake. Although essential, omega-6-rich oils are found in abundance in the North American food supply. Currently these omega-6 oils (corn, safflower, sunflower, cottonseed, sesame) are outnumbering omega-3 fatty acids by a ratio of up to 20:1.4,5

This ratio is a long way off the close to 1:1 omega-6 to omega-3 ratio as recommended by the international panel of essential fatty acid experts in the Journal of the American College of Nutrition.6 The average daily intake of EPA/DHA combined is 130mg in North America, 520mg short of published recommendations and 870mg short of the 1000mg recommended by the American Heart Association in cases of heart disease.1

In direct contrast to the depletion of omega-3 fatty acids from the Western food supply, the rates of depression have dramatically increased in Western countries. In addition, depression is now occurring more commonly in younger persons. The average age of onset of depression has continued to dip over the last 100
years. Scientists investigating the change in rates of depression have made it clear that these findings cannot be explained away by changes in attitudes of health professionals or society, diagnostic criteria, reporting bias, institutional or other artifacts.7,8 Perhaps the inadequate omega-3 intake, the major deviations in fatty acids ratios and the quarter-century-old message that all fat is unhealthy has had an untold influence on rates of depression.

Fish Consumption and Depression

There have been a number of studies that have examined national and international fish consumption data and compared them to rates of depression. Dr. Joseph Hibbeln of the National Institutes of Health is a pioneer in this area. He, and his group, have shown that higher national consumption of fish for a nation equals lower rates of depression versus countries consuming the least amount of fish.9 He has also shown that higher fish consumption is correlated with lower risk of postpartum depression10 and seasonal affective disorder.11

Other researchers have shown that even within a nation, fish consumption is associated with lower risk of depression and higher mental health status.12,13 Finally, researches are now observing increasing rates of depression in regions of the world that are moving away from traditional omega-3-rich diets to typical Western foods.14

Laboratory Tests in Depression

The epidemiological studies clearly suggest that adequate omega-3 fatty acids may be an important protective factor in depression. Correlation, however, does not prove causation. To add to the strength of the epidemiological studies, scientists have examined the levels of omega-3 fatty acids in the blood cells and fat storage cells of those with major depression.

Four studies have shown that those with depression do indeed have lower levels of omega-3 fatty acids in the blood.15-18 One of the studies showed that the lower the level of EPA, the more severe the clinical depression.15 In addition, a recent study showed that the patients with depression have 35 percent less DHA in fat storage cells versus healthy controls.19

Experimental Studies

Over the last decade, neuroscientists have been examining the consequences of omega-3 deficiencies in the central nervous system. Alterations in serotonin and dopamine levels, as well as the functioning of these two important neurotransmitters is evident in an omega-3 deficiency. The changes observed in omega-3 deficiency in animals is strikingly similar to that found in autopsy studies of human depression.20

In addition to changing serotonin and dopamine levels and functioning, omega-3 deficiencies are known to compromise the blood-brain barrier, which normally protects the brain from unwanted matter gaining access.21 Omega-3 deficiency can also decrease normal blood flow to the brain,22,23 an interesting finding given the studies which show that patients with depression have compromised blood flow to a number of brain regions.24,25 Finally, omega-3 deficiency also causes a 35 percent reduction in brain phosphatidylserine (PS) levels.26 This is also of relevance when considering that PS has documented antidepressant activity in humans.27,28

Mechanisms of EPA/DHA Regulation of Mood

DHA is found in high levels in the cells of the central nervous system (neurons); here it acts as a form of scaffolding for structural support.29 When omega-3 intake is inadequate, the nerve cell becomes stiff as cholesterol and omega-6 fatty acids are substituted for omega-3.30 When a nerve cell becomes rigid, proper neurotransmission from cell to cell and within cells will be compromised.31

While DHA provides structure and helps to ensure normal neurotransmission, EPA may be more important in the signaling within nerve cells.32 Normalizing communications within nerve cells has been suggested to be an important factor in alleviating depressive symptoms.33 In addition, EPA can lower the levels of two important immune chemicals, tumour necrosis factor alpha (TNFa) and interleukin 1 beta (IL-1ß), as well as prostaglandin E2.34

All three of these chemicals are elevated in depression.35-38 In fact, higher levels of TNFa and IL-1ß are associated with severity of depression.39 Finally, EPA has been hypothesized to increase brain-derived neurotropic factor (BDNF), which is known to be lower in depressed patients.20 BDNF is neuroprotective, enhances neurotransmission, has antidepressant activity and supports normal brain structure. BDNF may prevent the death of nerve cells in depression.

Clinical Studies

There have been some published case reports indicating that flaxseed oil may be helpful in cases of bipolar depression and the anxiety disorder agoraphobia.40 The first controlled clinical trial indicating that omega-3 fatty acids may be of benefit in depression was published in 1999. In this case, 9:6 g of EPA/DHA versus placebo led to longer periods of remission and improvement in depressive symptoms in those with bipolar depression.41

Some researchers theorize that such high doses of EPA/DHA may not be necessary and that low levels of pure EPA may be of benefit.32 In a study published in the American Journal of Psychiatry, researchers showed that just 2g of pure EPA could improve the symptoms of treatment-resistant depression. The
researchers found that the EPA (versus placebo), when added to an ineffective antidepressant for one month, significantly improved depressive symptoms.42

A larger study published in Archives of General Psychiatry replicated these findings, however, this time various doses of EPA were examined. Those on ineffective antidepressants were given 1g, 2g or 4g of pure EPA or a placebo in addition to the medication. Interestingly, the 1g daily dose of EPA led to the most significant improvements over the three-month study; it appeared that less was more. There were significant improvements in depressive symptoms, sleep, anxiety, lassitude, libido and thoughts of suicide.43

Researchers from Taiwan Medical University published a recent study in which they found that a 4.4g EPA and 2.2g DHA mix could alleviate depression versus placebo in those with treatment-resistant depression. This was a two-month study involving patients who were on antidepressants that were not working. As with the other omega-3 studies discussed, the fish oil was well tolerated and no adverse events were reported.44

There is also evidence that omega-3 oils may be of benefit in treating depressive symptoms outside of major depressive disorder. Canadian researchers showed that Antarctic krill oil (400mg EPA, 240mg DHA) could improve depressive symptoms associated with premenstrual syndrome.45 Harvard researchers have also shown that just 1g of pure EPA is beneficial in the treatment of borderline personality disorder. This personality disorder, which is particularly difficult to treat, is characterized by both depressive and aggressive symptoms. This was a two-month placebo-controlled study and the results showed that EPA has a mood-regulating effect, improving both depression and aggression versus placebo.46

To date, with one exception, all studies conducted on omega-3 fatty acids and mood have had a positive outcome. The singular negative study examined pure DHA in patients with depression. The results in the case showed that DHA alone was no better than placebo in alleviating depressive symptoms.47


Although an influence of EPA and DHA on brain physiology and structure is apparent, the precise mechanisms whereby omega-3 fatty acids may alleviate depression remain unknown. The results of the clinical trials reinforce the epidemiological and experimental studies, underscoring the importance of adequate omega-3 intake in those with depression.

The long-term studies of fish oil supplements in the area of cardiovascular health, some spanning three-plus years, have shown that they are safe and well tolerated.48,49 Patients with depression or depressive symptoms should discuss omega-3 fatty acids with their health care providers. While scientists continue to unravel the neuropsychological influences of omega-3 fatty acids, it should be recognized that they are not a substitute for appropriate mental health evaluation and care.

Alan C. Logan is a naturopathic physician licensed in Connecticut. Valedictorian of the Canadian College of Naturopathic Medicine, class of 2001, his recent medline-indexed article “Neurobehavioral Aspects of Omega-3 Fatty Acids: Possible Mechanisms and Therapeutic Value in Major Depression” is available to medical professionals by writing to Dr. Logan at aclnd@cfs-fm.org.

1. Holub BJ. Clinical Nutrition: 4. Omega-3 fatty acids in cardiovascular care. CMAJ 2002; 166: 608-15.
2. Bourre JM, Dumont O, Piciotti M, Clement M, et al. Essentiality of n-3 fatty acids for brain structure and function. World Rev Nutr Diet 1991; 66: 103-17.
3. Yehyda S, Rabinovitz S, Mostofsky DI. Essential fatty acids are mediators of brain biochemistry and cognitive functions. J Neurosci Res 1999; 56: 565-70.
4. Simopoulos AP. Evolutionary aspects of diet and essential fatty acids. World Rev Nutr Diet 2001; 88: 18-27.
5. Simopoulos AP. Overview of the evolutionary aspects of n-3 fatty acids in the diet. World Rev Nutr Diet 1998; 83: 1-11.
6. Simopoulos AP, Leaf A, Salem N. Workshop on the essentiality of and recommended dietary intakes for omega-6 and omega-3 fatty acids. J Am Coll Nutr 1999; 18: 487-9.
7. Klerman GL. The current age of youthful melancholia. Evidence for incrase in depression among adolescents and young adults. Br J Psychiatry 1998; 152: 4-14.
8. Klerman GL, Weissman MM. Increasing rates of depression. JAMA 1989; 261: 2229-35.
9. Hibbeln JR. Fish consumption and major depression. Lancet 1998; 351: 1213.
10. Hibbeln JR. Seafood consumption, the DHA content of mothers milk and prevalence rates of postpartum depression: a cross-national, ecological analysis. J Affect Disord 2002; 69: 15-29.
11. Cott J, Hibbeln JR. Lack of seasonal mood change in Icelanders. Am J Psychiatry 2001;158:328.
12. Tanskanen A, Hibbeln JR, Hintikka J, Haatainen K, Honkalampi K, Viinamaki H. Fish consumption, depression, and suicidality in a general population. Arch Gen Psychiatry 2001; 58: 512-513.
13. Silvers KM, Scott KM. Fish consumption and self reported physical and mental health status. Public Health Nutr 2002; 5: 427-31.
14. McGrath-Hanna NK, Greene DM, Tavernier RJ, Bult-Ito A. Diet and mental health status in the Arctic: is diet an important risk factor for mental health in circumpolar peoples? Int J Circumpolar Health 2003;62:228-41.
15. Adams PB, Lawson S, Sanigorski A, Sinclair AJ. Arachidonic acid to eicosapentanoic acid ratio in blood correlates positively with clinical symptoms of depression. Lipids 1996; 31: S157-S161.
16. Peet M, Murphy B, Shay J, Horrobin D. Depletion of omega-3 fatty acid levels in red blood cell membranes of depressive patients. Biol Psychiatry 1998; 43: 315-19.
17. Maes M, Christophe A, Delanghe J, Altamura C, Neels H, Meltzer HY. Lowered
n-3 polyunsaturated fatty acids in the serum phospholipids and cholesterol esters of depressed patients. Psychiatry Res 1999; 85: 275-291.
18. Tiemeier H, van Tuijl HR, Hofman A, et al. Plasma fatty acid composition and depression are associated in the elderly: the Rotterdam study. Am J Clin Nutr 2003;78:40-46.
19.Mamalakis G, Tornaritis M, Kafatos A. Depression and adipose essential polyunsaturated fatty acids. Prostaglandins Leukot Essent Fatty Acids 2002; 67: 311-18.
20. Logan AC. Neurobehavioral aspects of omega-3 fatty acids:possible mechanisms and therapeutic value in major depression. Altern Med Rev 2003;8:410-425.
21. Ziylan ZY, Bernard GC, LeFamconnier JM, Durand GA, Bourre JM. Effect of dietary n-3 fatty acid deficiency on blood-to-brain transfer of sucrose, alpha-aminoisobutyrie acid and phenylalamine in the rat. Neurosci Lett 1992; 137: 9-13.
22. Ito H, Kawashima R, Awata S, Ono S, et al. Hypoperfusion in the limbic system and prefrontal cortex in depression: SPECT with anatomic standardization technique. J Nucl Med 1996; 37: 410-4.
23. Kimbrell TA, Ketter TA, George MS, Little JT, et al. Regional cerebral glucose utilization in patients with a range of severities in unipolar depression. Biol Psychiatry 2002; 51: 237-52.
24. Ellis EF, Police RJ, Dodson LY, McKinney JS, Holt SA. Effect of dietary n-3 fatty acids on cerebral microcirculation. Am J Physiol 1992; 262: H1379-H1386.
25. de Wilde MC, Farkas E, Gerritis M, Kiliaan AJ, Luiten PGM. The effect of n-3 polyunsaturated fatty acid-rich diets on cognitive and cerebrovascular parameters in chronic cerebral hypoperfusion. Bran Res 2002; 947: 166-73.
26. Zimmer L, Vancassel S, Cantagrel S, Breton, et al. The dopamine mesocorticolimbic pathway is affected by deficiency in n-3 polyunsaturated fatty acids. Am J Clin Nutr 2002; 75: 662-7.
27. Brambilla F, Maggioni M. Blood levels of cytokines in elderly patients with major depressive disorder. Acta Psychiatr Scand 1998; 97: 309-13.
28.Maggioni M, Picotti GB, Bondiolotti GP, Panerai A, Cenacchi T, Nobile P, Brambilla F. Effects of phosphatidylserine therapy in geriatric patients with depressive disorders. Acta Psychiatr Scand 1990; 81: 265-70.
29. Bourre JM, Bonneil M, Clement M, Dumont O, et al. Function of dietary polyunsaturated fatty acids in the nervous system. Prostaglandins Leukot Essent Fatty Acids 1993; 48: 5-15.
30. Yehuda S, Rabinovitz S, Mostofsky DI. Modulation of learning and neuronal membrane composition in the rat by essential fatty acid preparation: time course analysis. Neurochem Res 1998; 23: 627-34.
31. Heron DS, Shinitzky M, Hershkowitz M, Samuel D. Lipid fluidity markedly modulates the binding of serotonin to mouse brain membranes. Proc Natl Acad Sci 1980; 77: 7463-67.
32. Horrobin DF. A new category of psychotropic drugs: neuroactive lipids as exemplified by ethyl eicosapentaenoate (E-E). Prog Drug Res 2002;59:171-99.
33. Stoll AL, Locke CA, Marangell LB, Severus WE. Omega-3 fatty acids and bipolar disorder: a review. Prostaglandins Leukot Essent Fatty Acids 1999; 60: 329-37.
34. James MJ, Cleland LG. Dietary n-3 fatty acids and therapy for rheumatoid arthritis. Semin Arthritis Rheum 1997;27:85-97.
35. Lieb J, Karmali R, Horrobin D. Elevated levels of prostaglandin E2 and
thromboxane B2 in depression. Prostaglandins Leukot Med 1983; 10: 361-7.
36.Ohishi K, Ueno R, Nishino S, Sakai T, Hayaishi O. Increased level of salivary prostaglandins in patients with major depression. Biol Psychiatry 1988; 23: 326-34.
37.Nishino S, Ueno R, Ohishi K, Sakai T, Hayaishi O. Salivary prostaglandin concentrations: possible state indicators for major depression. Am J Psychiatry 1989; 146: 365-8.
38.Maes M, Smith RS. Fatty acids, cytokines, and major depression. Biol Psychiatry 1998;43:313-14.
39.Shimizu E, Hashimoto K, Okamura N, et al. Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants. Biol Psychiatry 2003;54:70-75.
40. Rudin DO. The major psychoses and neuroses as omega-3 essential fatty acid deficiency syndrome: substrate pellagra. Biol Psychiatry 1981; 16: 837-850.
41. Stoll AL, Severus E, Freeman MP, Rueter S, et al. Omega-3 fatty acids in bipolar disorder. A preliminary double-blind, placebo-controlled trial. Arch Gen Psychiatry 1999; 56: 407-12.
42. Nemets B, Stahl Z, Belmaker RH. Addition of omega-3 fatty acid to maintenance medication treatment for recurrent unipolar depressive disorder. Am J Psychiatry 2002; 159: 477-9.
43. Peet M, Horrobin DF. A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite adequate treatment with standard drugs. Arch Gen Psychiatry 2002; 59: 913-19.
44. Su KP, Huang SY, Chiu CC, Shen WW. Omega-3 fatty acids in major depressive disorder. A preliminary double-blind, placebo controlled trial. Eur Neuropsychopharmacol 2003;13:267-71.
45. Sampalis F, Bunea R, Pelland MF, et al. Evaluation of the effects of Neptune krill oil on the management of premenstrual syndrome and dysmenorrheal. Altern Med Rev 2003;8:171-79.
46. Zanarini MC, Frankenburg FR. Omega-3 fatty acid treatment of women with borderline personality disorder: a double-blind, placebo-controlled pilot study. Am J Psychiatry 2003; 160: 167-69.
47. Marangell LB, Martinez JM, Zboyan HA, et al. A double-blind, placebo-controled study of the omega-3 fatty acid docosahexaenoic acid in the treatment of major depression. Am J Psychiatry 2003;160:996-98.
48.Marchioli R, Schweiger C, Tavazzi L, Valagussa F. Efficacy of n-3 polyunsaturated fatty acids after myocardial infarction: results of GISSI-prevenzione trial. Gruppo Italiano per lo studio della sopravvivenza nell’infarto miocardio. Lipids 2001; 36 Suppl: S119-26.
49. Marchioli R, Barzi F, Bomba E, Chieffo C, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time course analysis of the results of the Gruppo Italiano per lo studio della sopravvivenza nell’infarto myocardio (GISSI) – prevenzione. Circulation 2002; 105: 1897-903.

Chiropractic and Exercise: Research says it is Better than Drugs

January 21, 2019, 4:16 pm

Chiropractors and Exercise Are Better than Drugs, says Research…whiplash, woman in pain holding neck

If you visit a conventional physician for pain, there’s a very good chance you’ll leave with a prescription for a medication, such as nonsteroidal anti-inflammatory drugs (NSAIDs like Ibuprofen), acetaminophen (Tylenol) and even opioids (OxyContin, Vicodin, etc.).  These are the go-to treatment for pain in the modern medical world.

However, there are better options than drugs for neck pain, not only in terms of pain relief, but also in helping to treat the underlying cause of the pain so that healing can truly occur. Wellness doctors such as chiropractors and osteopathic physicians (DOs) have helped millions of patients achieve pain relief without drugs.

Study Shows Exercises and Chiropractic Care Beat Drugs for Neck Pain

According to a study published in 2012 in the Annals of Internal Medicine and funded by the National Institutes of Health, medication is not the best option for treating neck pain.

After following 272 neck-pain patients for 12 weeks, those who used a chiropractor or exercise were more than twice as likely to be pain free compared to those who took medication.


  • 32 percent who received chiropractic care became pain free
  • 30 percent of those who exercised became pain free
  • 13 percent of those treated with medication became pain free

Researchers concluded:

“For participants with acute and subacute neck pain, SMT [spinal manipulation therapy] (in other words, a chiropractic adjustment) was more effective than medication in both the short and long term. However, a few instructional sessions of HEA [home exercise with advice] resulted in similar outcomes at most time points.”

In the case of neck pain, and many other kinds of pain, the underlying cause is often related to body mechanics (posture) or misalignments in your spine.  Addressing your posture, exercising, and chiropractic care is very effective at relieving the pain and addressing the underlying cause. If you have chronic pain of any kind, please understand that there are many safe and effective alternatives to prescription and over-the-counter painkillers.  These may require some patience as exercising, good posture habits, and chiropractic adjustments take time to help the body heal from a chronic problem that took months or even years to develop.

To see the full article containing information on this study and more about chiropractic care and specific exercises, please click HERE.

For more information on how chiropractic and wellness care can help you, please see our home page HERE.

Stomach Acid Drugs Increase Risk of Bacterial Infections, FDA Warns

January 19, 2019, 5:50 pm

Stomach Acid Drugs Increase Risk of Bacterial Infections, FDA Warns
by Live Science Staff | February 08, 2012 11:52am ET

The Food and Drug Administration is warning consumers today that certain stomach acid drugs may increase the risk of a serious intestinal bacteria infection.

The drugs, including Nexium, Prilosec, Prevacid, Zegerid and others, fall into a category called proton pump inhibitors (PPIs). They are prescribed to treat acid reflux, stomach ulcers and
other conditions, and work by reducing the amount of acid in the stomach.

The bacterial illness is called Clostridium difficile–associated diarrhea (CDAD), and its main symptom is diarrhea that does not improve , according to an FDA statement. The bacteria are
commonly referred to as “C. diff.”

Stomach acid is a very important defense mechanism against pathogens. It kills them,” said Dr. Edith R. Lederman, who authored a study published in October linking C. diff infections to stomach acid drugs, in an interview with MyHealthNewsDaily at the time.

Patients taking PPIs who develop diarrhea that does not improve may have CDAD, according to the FDA. The agency is working with manufacturers to include information in the drug labels about the increased risk with use of PPIs. PPIs are the third highest selling class of drugs in the U.S., according to 2010 findings from Consumer Reports.

Lederman’s study, published in the journal Clinical Infectious Diseases, showed nearly half of 485 patients hospitalized at a medical center over a four-year period who had C. difficile infections had previously been prescribed an acid suppressing drug, most of which were either proton-pump inhibitors (PPIs), such as Prilosec and Prevacid, or histamine2 antagonists, such as Tagamet and Zantac.

The FDA is also reviewing the risk of CDAD in users of histamine H2 receptor blockers.

The elderly , and people with certain medical problems, generally have the greatest chance of developing C. diff infections, according to the Centers for Disease Control and Prevention. The  infection can spread in hospitals because C. diff spores can live outside the human body for a very long time, and may be found on items such as bed linens, bed rails, bathroom fixtures and medical equipment.

There are antibiotics that can be used to treat C. diff, according to the CDC, but in some severe cases, surgery to remove the infected part of the intestines may be needed.

In Lederman’s study, 23 patients died from their C. diff infections; 19 of them had taken prescription acid suppressants during the 90 days before their hospital stay.

Hand washing, alcoholbased sanitizers, and taking only antibiotics that are prescribed by a doctor can lower a person’s risk of getting or spreading C. diff, according to the CDC.

Pass it on: People taking drugs that suppress stomach acid production may be at an increased risk for intestinal bacteria infections.

This story was provided by MyHealthNewsDaily, a sister site to LiveScience. Follow MyHealthNewsDaily on Twitter @MyHealth_MHND. Find us on Facebook.

Did you know? Calcium helps the body fight infection

January 18, 2019, 6:17 pm

Microbial Pathogenesis
Volume 24, Issue 5, May 1998, Pages 309-320

Roles of calcium and annexins in phagocytosis and elimination of an attenuated strain of Mycobacterium tuberculosisin human neutrophils

Meytham Majeed, Nasrin Perskvistf1, Joel D. Ernst, Kristina Orselius and Olle Stendahl Department of Medical Microbiology, Linköping University, Linköping, S-581 85,
Sweden Division of Infectious Diseases and Rosalind Russell Research Laboratory, University of California, San Francisco and San Francisco General Hospital, San Francisco, CA,
U.S.A. Received 2 October 1997; accepted 31 December 1997. Available online 9 April 2002.

The phagocytic function of neutrophils is a crucial element in the host defense against invading microorganisms. We investigated phagocytosis and intracellular killing of an
attenuated strain of Mycobacterium tuberculosis (H37Ra) by human neutrophils focusing on the role of the cytosolic free calcium concentration [Ca2+]I and certain cytosolic
calcium-dependent membrane-binding proteins annexins. Phagocytic uptake did not trigger a calcium rise and occurred independently of different calcium conditions, and in
a serum-dependent manner. Changes in the viability of H37Ra were determined by agar plate colony count and a radiometric assay. Neutrophils showed a capacity to kill ingested mycobacteria and this occurred without a rise in [Ca2+] i. The ability to kill H37Ra [Mycobacterium tuberculosis] decreased in the absence of extracellular calcium and when intra-extracellular calcium was reduced. Immunofluorescence staining revealed that during phagocytosis of H37Ra, annexins III, IV and VI translocated localization of annexin I and V remained unchanged. The translocation of annexin IV occurred even when Ca2+-depleted neutrophils ingested H37Ra in the absence of extracellular calcium. We concluded that neutrophil-mediated killing of mycobacteria is a Ca2+-dependent process. The fact that the association of certain annexins to the membrane vesicle containing H37Ra differ from other phagosomes
suggests a selective regulatory mechanism during phagocytosis of mycobacteria by neutrophils.

Calcium spikes in activated macrophages during Fc receptor-mediated phagocytosis 

Jesse T. Myers and Joel A. Swanson Cellular and Molecular Biology Graduate Program and Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor Correspondence: Joel A. Swanson, Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109-0620. E-mail: jswan@umich.edu

Rises in intracellular-free calcium ([Ca2+]i) have been variously associated with Fc
receptor (FcR)-mediated phagocytosis in macrophages. We show here that
activation of murine bone marrow-derived macrophages increases calcium spiking
after FcR ligation. Ratiometric fluorescence microscopy was used to measure [Ca2+]i
during phagocytosis of immunoglobulin G (IgG)-opsonized erythrocytes. Whereas 13%
of nonactivated macrophages increased [Ca2+]i in the form of one or more spikes, 56% of
those activated with lipopolysaccharides (LPS; 18 h at 100 ng/ml) and interferon- (IFN-
; 100 U/ml) and 73% of macrophages activated with LPS, IFN- , interleukin (IL)-6 (5
ng/ml), and anti-IL-10 IgG (5 μg/ml) spiked calcium during phagocytosis. Calcium
spikes were inhibited by thapsigargin (Tg), indicating that they originated from
endoplasmic reticulum. The fact that activated macrophages showed a more dramatic
response suggested that calcium spikes during phagocytosis mediate or regulate
biochemical mechanisms for microbicidal activities. However, lowering [Ca2+]i with
ethyleneglycol-bis(ß-aminoethylether)-N,N’-tetraacetic acid or inhibiting calcium spikes
with Tg did not inhibit phagosome-lysosome fusion or the generation of reactive oxygen
or nitrogen species. Thus, the increased calcium spiking in activated macrophages was not
directly associated with the mechanism of phagocytosis or the increased antimicrobial
activities of activated macrophages.

Cell Calcium. 1990 Nov-Dec;11(10):655-63.

Oxidase activation in individual neutrophils is dependent on the onset and magnitude of the Ca2+ signal.
Hallett MB, Davies EV, Campbell AK. Department of Surgery, University of Wales College of Medicine, Cardiff, UK.

Using single-cell ratio imaging of Fura-2-loaded neutrophils, we demonstrate that
the heterogeneity and asynchrony of the oxidase response originates from
variability in the timing and magnitude of the cytosolic free Ca2+ signal. The
Ca2+ signals from individual cells could be classified into four types: (a) type 1, a
transient rise in Ca2+ occurring within 6 s; (b) type 2, an oscillating cytosolic free
Ca2+; (c) type 3, a latent Ca2+ transient significantly delayed (21-56 s); and (d)
type 4, no significant Ca2+ rise. These response types accounted for
approximately 41%, 15%, 26% and 18% of the population respectively for
stimulation with 1 microM f-met-leu-phe peptide (n = 27) and 52.5%, 15%,
11.5% and 21% respectively for 0.1 microM f-met-leu-phe peptide (n = 52). The
oxidase in neutrophils in which the cytosolic free Ca2+ concentration rose to
greater than 250 nM always became activated. In the presence of
extracellular Ca2+, cytosolic Ca2+ rose uniformly throughout the cell,
whereas in the absence of extracellular Ca2+, a localized Ca2+ ‘cloud’ was
observed in approximately 30% of cells. A localized activation of the oxidase
accompanied the presence of the Ca2+ ‘cloud’ when the 250 nM Ca2+
threshold was exceeded. The data presented here therefore demonstrate a
tight coupling in individual neutrophils between an elevation in cytosolic free
Ca2+ above a threshold of 250 nM and activation of the oxidase.

PMID: 1965710 [PubMed – indexed for MEDLINE] Science. 1986 Jun 20;232(4757):1554-6.

Calcium modulation activates Epstein-Barr virus genome in latently infected cells.
Faggioni A, Zompetta C, Grimaldi S, Barile G, Frati L, Lazdins J.

In many viral infections the host cell carries the viral genome without producing
viral particles, a phenomenon known as viral latency. The cellular mechanisms
by which viral latency is maintained or viral replication is induced are not
known. The modulation of intracellular calcium concentrations by calcium
ionophores induced Epstein-Barr viral antigens in lymphoblastoid cell lines
that carry the virus. When calcium ionophores were used in conjunction with
direct activators of protein kinase C (12-O-tetradecanoyl phorbol-13-acetate
and a synthetic diacylglycerol), a greater induction of viral antigens was
observed than with either agent alone. Activation of protein kinase C may be
required for the expression of the viral genome.

PMID: 3012779 [PubMed – indexed for MEDLINE] April 17, 2003

How do cells signal and attack foreign matter?
U-M Kellogg Eye Center researcher’s high-speed images show how cells mobilize for immune response
ANN ARBOR, MI – New high-speed imaging techniques are allowing scientists to show how a
single cell mobilizes its resources to activate its immune response, a news research study shows.
Howard R. Petty, Ph.D., professor and biophysicist at the University of Michigan Health System’s Kellogg Eye Center,
has dazzled his colleagues with movies of fluorescent-lit calcium waves that pulse through the cell, issuing an
intracellular call-to-arms to attack the pathogens within. He explains that these high-speed images provide
a level of detail about cell signaling that simply wasn’t possible just a few years ago.

In the April 15 issue of the Proceedings of the National Academy of Sciences, Petty provides more detail on cell
signaling, depicting what he calls the “molecular machinery” underlying the immune response. He has identified a
sequence of amino acids (LTL) that controls the calcium wave pathway and, crucially, the ability
of immune cells to destroy targets. The findings are important because they could eventually lead scientists to design drugs based
on the amino acid motif. “Our clinical goal,” explains Petty, “is to characterize the
immune cell’s signaling function so that we can interrupt it or somehow intervene when it begins to misfire.” The process
has implications for treating autoimmune diseases such as arthritis, multiple sclerosis, and the eye disorder uveitis.

Through images of phagocytosis, the process by which a cell engulfs and then destroys its
target, Petty is able to track the movement of calcium waves as they send signals to key
players in the immune response. The “calcium wave” is a stream of calcium ions coming into the cell, which is detected by the fluorescence emission of a calcium-sensing dye.

As a cell membrane begins to surround its target, two calcium waves begin to circulate. When the target is completely surrounded, one wave traveling
In phagocytosis, a wave traveling around the cell’s perimeter splits in two, with the
second wave encircling the phagosome or sac-like compartment. This second wave
allows the digestive enzymes to enter the phagosome and destroy the target.

When a mutation is introduced, phagocytosis is not completed because the
calcium wave circles the cell and bypasses the phagosome altogether.
around the cell’s perimeter splits in two, with the second wave encircling
the phagosome or sac-like compartment. This second wave allows the
digestive enzymes to enter the phagosome and finally destroy the target.

When Petty introduced a mutation in the gene (FcyRIIA) that controls phagocytosis, he found that
the calcium wave simply circled the cell and bypassed the phagosome altogether. As a result, the
immune cell could engulf, but could not carry out the destruction of its target. This led him to
conclude that the LTL sequence orchestrates the cell signaling process.
The sequence may also have a role in directing other cell activities, for example signaling the
endoplasmic reticulum to form a spindle that connects the phagosome and the outer cell
membrane. “The spindle seems to act as an extension cord that signals the calcium wave into the
phagosome to finish the attack,” suggests Petty.
Petty explains that many of these findings are possible thanks to high-speed imaging techniques
that enable him to merge knowledge of physics with cell and molecular biology. He uses high
sensitivity fluorescence imaging with shutter speeds 600,000 times faster than video frames.
“Before the advent of high-speed imaging, you could not ask many of these questions because
we had no way to see the movement of calcium waves,” he says. “With conventional imaging you
ended up with a blur of calcium.” By contrast, Petty’s images resemble the movement of a comet
across the night sky.

In the study reported in PNAS, Petty used leucocytes as a model for the process. The amino acid
sequence is in the region of the gene FcyRIIA. He is currently studying the same phenomena in
the eye, where phagocytosis disposes of the regularly-shed remnants of photoreceptor cells.
The paper, Signal sequence within FcRIIA controls calcium wave propagation patterns: Apparent
role in phagolysosome fusion, also appears on the PNAS internet site at www.pnas.org.
In addition to Petty, authors on the paper include Randall G. Worth, Moo-Kyung Kim, Andrei L.
Kindzelskii, and Alan D. Schreiber.

Cellular and Molecular Life Sciences (CMLS)
Publisher: Birkhäuser Verlag AG ISSN: 1420-682X
Issue: Volume 58, Number 11/October 2001 Pages: 1727 – 1733

Role of serum components in the binding and phagocytosis of oxidatively damaged erythrocytes by autologous mouse macrophages
K Tanaka A1, Y Usui A1, S Kojo A1
A1 Department of Food Science and Nutrition, Nara Women’s University, Nara
630-8506 (Japan), Fax + 81 742 302459, e-mail: kojo@cc.nara-wu.ac.jp


Abstract. To investigate the role of autologous serum components in the
recognition of damaged cells by macrophages, we examined the binding and
phagocytosis of damage oxidatively damaged red blood cells with Cu2+ and
ascorbate (oxRBCs — oxidatively damaged red blood cells) by autologous resident
mouse peritoneal macrophages. The binding of oxRBCs by macrophages was
independent of the presence of serum. However, phagocytosis by macrophages
increased with serum concentration, and macrophages showed little ingestion of
oxRBCs in a serum-free medium. Macrophages neither bound nor appreciably
ingested native RBCs (before oxidation) in either the absence or presence of
autologous serum. Mouse macrophages ingested significantly more native as
well as oxRBCs in the presence of heat-inactivated fetal calf serum than in the
presence of heat-inactivated mouse serum. Pretreated oxRBCs with normal
serum were rarely ingested by macrophages in a serum-free medium.
Phagocytosis of oxRBCs was significantly inhibited by depletion
of IgG* or calcium from serum, by heat inactivation of
complement, or by antiserum against mouse C3. These results
demonstrate that serum components such as IgG, C3, and
calcium are involved in phagocytosis of oxRBCs by autologous

* IgG : A class of immunoglobulins that include the most common antibodies circulating in the
blood, that facilitate the phagocytic destruction of microorganisms foreign to the body, that bind to
and activate complement, and that are the only immunoglobulins to cross over the placenta.

Meet our Chiropractor, Dr. Trent Burrup

January 17, 2019, 9:16 pm

New to the Institute? Meet our chiropractor, Dr. Trent Burrup, by clicking the video below!



October 26, 2018, 3:07 pm

Chiropractic Care For Misaligned Ribs

Chiropractic, rib cage imageChiropractors can adjust misaligned ribs.  This can be a common problem, and there are many reasons a person may experience a rib “out of place”.

The ribs are attached to the thoracic spine, and their primary function is to protect internal organs, primarily the heart and lungs. Ribs constantly move while you breathe, allowing your chest to contract and expand.  Since your ribs are in constant motion, it doesn’t take much for a misalignment to occur. Usually a person will notice a pinching sensation in the front or back of the chest area if a rib is out of alignment.

Some common reasons for misaligned ribs include: Poor posture, Pregnancy, Yard work, Working out, Heavy Lifting, Extreme Coughing and Sneezing, and anything else that puts pressure on the rib cage.

Chiropractors are trained to know how to address misaligned ribs and put them back into place. Regular Chiropractic adjustments can also help prevent the misalignment of ribs. If you are constantly in pain from rib misalignment, there may be an underlying problem that needs to be addressed, warranting chiropractic care.

For more information on how chiropractic adjustments can help your misaligned ribs and other health problems, please see our home page at SuperDocDC.com.

The Institute of Chiropractic and Acupuncture Therapy provides chiropractic, acupuncture, and other wellness therapies to patients in West Jordan, and the Salt Lake City Metro Area.  Our chiropractor, Dr. Trent Burrup focuses on wellness through chiropractic adjustments, acupuncture treatments and numerous other holistic therapies. Come experience the difference at The Institute!

Image courtesy of freedigitalphotos.net


July 25, 2018, 5:17 pm

Chiropractors have tremendous success treating neck pain, back pain, and headaches. However, chiropractic can help many other health conditions not typically associated with chiropractic.

Many people come to The Institute of Chiropractic and Acupuncture Therapy because they have had little or no response to medical treatment or other chiropractic treatments.  Here are some common conditions we see in our clinic that have had successful outcomes with chiropractic treatments:

Headaches              Chiropractor Adjustment of Woman in White Shirt, Image         Chronic Fatigue Syndrome

Back and neck pain           Fibromyalgia

Auto injuries/whiplash       Hormone Imbalances

Sports Injuries                  Digestive issues

Depression                       Allergies


There are many different chiropractic techniques that can be used for adjustments.  At The Institute some of the specific chiropractic techniques and methods Dr. Burrup has been trained in include Gonstead, Activator, Diversified, Thompson, Toggle Recoil, Nimmo, sports injury and extremity adjustment.

The goal of our clinic is to help our patients become empowered with their health, achieving their optimal wellness goals.  If you are suffering needlessly from pain, have a condition that has not responded well to medical care or other chiropractic treatments, or are trying to achieve optimal wellness in your life, chiropractic can help you on the road back to better health!

Dr. Trent Burrup is a chiropractor who provides care in Salt Lake City and surrounding areas including Sandy, Draper, South Jordan, West Jordan, Murray, and all other Salt Lake Metro areas. Come experience the difference at The Institute!

Chiropractic and Your Feet…the Foundation of Your Body

July 2, 2018, 8:59 am

Have you ever had foot pain?  Watch our video below and see our chiropractor, Dr. Trent Burrup, explain how your FEET are the foundation of your whole body, how they affect the whole body, and a simple trick to keep your feet relaxed and feeling good!

For more information on chiropractic and how it can help you, please see our website at SuperDocDC.com.

Dr. Trent Burrup provides chiropractic, acupuncture, and other wellness therapies in Salt Lake City and surrounding areas.  We have patients that come from Utah County, Davis County, and as far north as Logan, even some from out of State!  Come experience the difference at the Institute! 

The Institute of Chiropractic is located in West Jordan.

3 Ways Chiropractic can Help Runners

June 14, 2018, 4:30 pm

3 Ways Chiropractic Can Help Runners

Chiropractor Trent Burrup runs St. George Marathon in 2014

Dr. Trent Burrup, Chiropractor, runs St. George Marathon in 2014

Running is a favorite form of exercise for many people.  Simply put, it is popular because it can be done almost anywhere, burns up lots of calories, and uses no special equipment.  Running is also great for your health! It helps decrease stress, control weight, increase stamina and energy, and is great for your heart.

The downside of the benefits is that running causes its share of injuries to the body.

Tendonitis, ankle sprains, shin splints, and knee strains are a few of the many injuries brought on or exacerbated by a regular running routine.

So what do you do? It’s important to take precautions to not get injured in the first place. Running in high quality shoes, stretching, and knowing your body’s limits are 3 ways to help reduce injuries.

Another great choice is getting regular chiropractic care. Runners can reap many positive benefits from visiting a chiropractor. Three big benefits chiropractic care offers to runners and other athletes are the following:

Increased Range of Motion: Loose and relaxed joints allow for greater flexibility and movement.  This will in turn benefit a runner’s gait and running time. Chiropractic care helps loosen joints and increase range of motion, which in turn helps a runner move more freely and better avoid running injuries.

Decreased Healing Time for Injuries: By using chiropractic adjustments, chiropractors can promote healing in the body as a whole, as well as treating specific injuries.  Specific treatments can include extremity adjustments and laser therapy to decrease pain and accelerate healing.  This allows runners to get back to running quicker and minimize time lost in improving times or preparing for races.

More Resistance to Becoming Injured: One common way runners get hurt is by one part of the body compensating for another. Chiropractic treatment helps to keep the spine and extremities in alignment, allowing all parts of the body to function properly, and reduces the negative impact of the jarring motion of running.

Running is a popular exercise routine for many, and has many positive benefits in a person’s health and well-being. By taking proper steps to minimize the chance of injury, runners can enjoy the benefits of running and minimize the risks.

Chiropractic care can be an effective part of making certain your body is in prime running condition and resistant to injury. If a person does get an injury, chiropractic care can help increase healing time and decrease time needed to recover.

Ready! Set! Run!

For more information on Chiropractic and how it can help you, please see our home page at SuperDocDC.com.