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Archive for January 2019

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.

Lack of stomach acid can cause many problems

January 18, 2019, 8:12 pm

Hypochlorhydria, or lack of stomach acid can cause lots of problems
From DoctorMyhill

Hypochlorhydria arises when the stomach is unable to produce hydrochloric acid. It is a greatly overlooked cause of problems.

Acid environment in the stomach 

The stomach requires an acid environment for several reasons.
1. acid is required for the digestion of protein,
2. acid is required for the stomach to empty correctly and failure to do so results in gastrooesophageal reflux disease (see Heartburn),
3. acid is required to sterilise the stomach and kill bacteria and yeast that may be ingested

4.an acid environment is required for the absorption of certain micronutrients, in particular divalent and trivalent cations such as calcium, magnesium, zinc, copper, iron, selenium, boron and so on.

As we age, our ability to produce stomach acid declines, but some people are simply not very good at producing stomach acid, sometimes because of pathology in the stomach (such as an allergic gastritis secondary to food intolerance), but sometimes for reasons unknown.

Problems arising from hypochlorhydria

There are many possible problems that could arise from hypochlorhydria:

1. Failure to digest foods properly. This will result in a general malabsorption of proteins. Indeed, hypochlorhydria as induced by antacids and H2 blockers and protein pump inhibitors substantially increases one’s risk of osteoporosis because the body simply does not have the raw material to replace bone. Many degenerative
conditions will be associated, therefore, with hypochlorhydria.
2. Failure to absorb trace elements. Trace elements are essential for normal body functioning. If these are not present then the biochemistry of the body will go slow, organs will go slow and this will accelerate the ageing process. Therefore, one would expect to see people getting diseases, such as cancer, heart disease and neurodegenerative conditions, before their time.
3. Failure to sterilise the stomach contents. This will make individuals more susceptible to gut infections such as gastroenteritis and possibly enteroviruses such as EpsteinBarr
virus, Coxsackie virus, Echovirus and so on. Gastric acid is an essential part of normal defences against disease. Gastric acid is also essential for getting rid of undesirable bacteria and yeast that appear in the diet. Particularly virulent strains, of course, may cause simple food poisoning. However, if there is an overgrowth of bacteria and yeast in the stomach, then foods will get fermented instead of being digested. This produces wind and gas resulting in bloating and alcohols, which may or may not be useful to the body.
4. Allergy to gut microbes. The idea here is that gut microbes are miniscule compared with human cells and all too easily spill over into the bloodstream with the potential to cause allergic or inflammatory reactions at distal sites. Irritable bladder or interstitial cystitis is an obvious case. But I suspect many other pathologies such as arthritis, venous ulcers, rosacea, “intrinsic” asthma, mesenteric adenitis, rheumatic fever, polymyalgia rheumatica and other such can be explained by this mechanism.
5. Fermenting brain. Nishihara has shown that fermenting gut may result in fermenting brain low levels of microbes in the brain may ferment neurotransmitters into LSD and amphetamine like substances (to cause hyperactivity, psychosis and other such) or ferment out serotonin, acetylcholine, GABA to cause low mood and depression. If this is correct then this explains a whole range of psychiatric conditions and establishes the mechanism of the widely observed foodmood connection. See Nishihara’s work at 1] (http://www.drmyhill.co.uk/drmyhill/images/d/dc/NISHIHARA.pdf) ]
6. Increased risk of stomach cancer. Having the wrong bacteria and yeast in the stomach will irritate the lining of the stomach and increase one’s risk of stomach cancer.
7. Malabsorption of vitamin B12. It is well known that the stomach must be acid in order to absorb B12. Indeed, using a proton pump inhibitor such as Omeprazole, will reduce absorption of vitamin B12 to less than 1% of expected. Many people already suffer from borderline B12 deficiency this is a difficult vitamin for the body to assimilate, but essential for normal biochemistry.
8. Risk factor for cancer. I suspect many bowel tumours are driven by microbes in the upper fermenting gut. Indeed we know that helicobacter pylori infection is a risk factor for stomach cancer. In Japan, where hypochlorhydria is very common, stomach cancer is a major killer.

Symptoms of hypochlorhydria

When any of the above problems go wrong, it can result in symptoms.
1. Accelerated ageing because of malabsorption.
2. Wind, gas and bloating as foods are fermented instead of being digested, i.e. irritable bowel syndrome.
3. A tendency to allergies the reason for this is that if foods are poorly digested, then large antigenically
interesting molecules get into the lower gut, where if the immune system reacts against them, that can switch on allergy.
4. Gastrooesophageal reflux disease
5. Iron deficiency Anaemia
6. B12 deficiency
7. A tendency to candida dysbiosis or bacterial dysbiosis.

Cause of hypochlorhydria

The stomach is lined with cells that are proton pumps that is to say they pump hydrogen ions from the blood stream into the lumen of the stomach. Stomach acid is simply concentrated hydrogen ions. There is a natural tendency for these hydrogen ions to diffuse back from where they came but this is prevented by very tight junctions between stomach wall cells. However, if the gut becomes inflamed for whatever reason, there is leaky gut and hydrogen ions leak back out. A common cause of inflammation and leaky gut is allergy. See Allergy to Foods, Inhalants & Chemicals, signs and symptoms of.

Treatment of hypochlorhydria

The treatment in the short term is to take acid supplements. Indeed, this may explain why cider vinegar is such a popular treatment for many problems the vinegar acidifies the stomach and improves the digestion of food. Clearly, this has the potential to affect a wide range of conditions. The problem with cider vinegar is that it contains yeast and would therefore not be tolerated by many people.

A second possibility is to take high dose ascorbic acid at mealtimes. Indeed, my standard recommendations for nutritional supplements suggest combining my Mineral Mix with ascorbic acid to be taken at mealtimes. Ascorbic acid, combined with the minerals, most of which are in the chloride form, reacts to form a combination of mineral ascorbates and hydrochloric acid. This is the perfect mixture to optimise absorption because it mildly acidifies the stomach and puts the minerals into the best available form to be absorbed, i.e. the ascorbate, and, of course, an acid environment.

The third approach is to take betaine hydrochloride. This is available in capsules, which need to be taken with food and the dose adjusted according to the response. I suggest that people start off with one capsule initially and build up to, maybe, four or five capsules depending on the size of the meal and the response to treatment. Often in the longer term with the correct diet (low glycaemic index, low allergy potential, smaller meals), getting rid of helicobacter pylori, and correct gut flora this cures the chronic gastritis and the stomach is again able to produce acid normally.

Some interesting clinical observations

It has been well known now for many decades that childhood asthma is associated with hypochlorhydria. Asthma in children tends to be caused by allergy to foods. If these foods are poorly digested, then they will be very much more antigenic and therefore very much more likely to switch on allergies and, therefore, asthma. Indeed, a study done in the 1930s showed that 80% of children with asthma also have hypochlorhydria. The two conditions are undoubtedly related. As the child’s stomach matures and acid eventually is produced, then the asthma disappears. What often occurs with hypochlorhydric children is that they malabsorb their food and therefore tend to be underweight. So clinically it is unusual to see overweight kids with asthma almost invariably they are thin children who wheeze. The treatment is as above, as well as trying to identify provoking foods. The commonest allergy food, of course, are dairy products.

A test for hypochlorhydria… Salivary VEGF

Dr John McLaren-Howard has again come up with a brilliant suggestion for a simple test to identify hypochlorhydria. The idea here is that it is very difficult for the stomach to produce stomach acid. The normal acidity of blood is about pH7, but the acidity of stomach acid can be as low as pH1 that means that hydrogen ions (which create acidity) are a million times more concentrated in the stomach than in the bloodstream. So the stomach wall has a very difficult job to do. The gastric parietal cells need quite a bit of energy from ATP to pump hydrogen ions from the inside of the parietal cell into the lumen of the stomach. The difficult bit is stopping these hydrogen ions leaking back again. This is achieved because the gastric parietal cells form a protective barrier between each other at the cell membrane tight junction to stop hydrogen ions leaking back. Because this is extremely hard work and the body does not want to waste energy, the main regulator for the cell membrane tight junction is vascular endothelial growth factor (VEGF).

What this means is that the more stomach acid is produced, the more VEGF is necessary to keep the glue going between gastric parietal cells. Therefore, one would expect salivary VEGF levels to be proportionate to the amount of stomach acid. And indeed this is the case. There is a huge amount of research that has been done with respect to VEGF, most of which is to do with high levels. However, the reverse is also true and low levels of VEGF would be a pointer towards hypochlorhydria.

This test would be invalidated by taking proton pump inhibitors and possibly other acid blockers, so for the best chance of an accurate result, really these drugs need to be stopped for four days prior to doing the test.

VEGF….test the practicalities

Saliva for VEGF tests should be unstimulated. That is: a sample is given at least one hour after a meal and at least 15 minutes after drinking soft drinks, tea or coffee. A break of 24 hours after alcohol ingestion is needed AND a similar break after any protonpumpinhibitor drugs are used and ideally any drug that interferes with stomach acidity. Put 12ml of saliva into the blue topped trace element free tube supplied and post to Acumen to arrive on a working day.

Bicarbonate burp test

This may give a rough guide the idea here is that sodium bicarbonate, when swallowed, reacts with stomach acid to make carbon dioxide which is subsequently burped up. The timing of the burp gives a clue as to how acid the stomach is. It is at least cheap and DIY. See [[[2] (https://healthesolutions.com/healthetipthebakingsodastomachacidtest/) ]]

Related Tests
Vascular endothelial growth factor (VEGF)salivary test for hypochlorhydria

Related Articles
Fermentation in the gut and CFS

External links
Hydrochloric acid production (http://highered.mcgrawhill.
com/sites/0072943696/student_view0/chapter16/animation__hydrochloric_acid_production____of_the_stomach.html) This is an interesting animation showing how hydrochloric acid is produced in the stomach.

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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!