Gene Heyden

Defending against Colon Cancer

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Aug 222017
 

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By Eugene L. Heyden, RN

Colon cancer scares me.  Actually, all cancers scare me.  But colon cancer scares me an awful lot.  I’ve seen the damage it can do.  Perhaps you should be afraid of it, too.

“Colorectal cancer remains the second leading cause of cancer mortality in the United States.”  (Orlich et al., 2015)

Combined with rectal cancer, cancers of the colon are diagnosed in over 135,000 individuals in the United States each year.  This year, 2017, it is anticipated that over 50,000 individuals in the United States will die from colorectal cancer.  And before they lose their life, it is safe to say that the majority will experience the nightmare of chemotherapy and surgery.  A lot of death.  A lot of suffering.  That’s what colorectal cancer is all about.

But there is some very good news to share.  With screening, typically by colonoscopy, we are finding precancerous lesions and early-stage cancers in the colon and rectum, removing them, and potentially saving a life in a matter of a few minutes . . . problem solved.  Unfortunately, even with colonoscopy, some pre-cancerous growths and relative large cancers are missed and trouble follows (Barclay et al., 2006).

Although we are talking colorectal cancer here, for sake of simplicity I will focus our attention on colon cancer.  Besides, for all practical purposes, the rectum is the terminal portion of the colon.  Indeed, although there are some genes more associated with colon cancer than with rectal cancer, and vice versa, “colon cancers and rectal cancers are typically considered to be essentially the same disease.”  (Hong et al., 2012)  And, when it comes to health and cancer prevention, it is safe to say, “What is good for the colon is good for the rectum.”  Now with that out of the way . . .

There are many, many things that promote colon health and prevent colon cancer.  Diet can do this, and I’ll get to that later.  But I can’t think of a better place to begin our discussion on colon cancer prevention than with vitamin D.

 

Vitamin D

“Several studies confirmed that increasing vitamin D3 lowers colon cancer risk, reduces polyp recurrence, and that sufficient levels of vitamin D are associated with better overall survival of colon cancer patients.

“Vitamin D3 has been estimated to lower the incidence of colorectal cancer by 50%, which is consistent with the inverse correlation between dietary vitamin D3 intake or sunlight exposure and colorectal cancer.  (Klampfer, 2014, emphasis added)

Vitamin D has a solid reputation when it comes to the prevention of a variety of cancers, colon cancer included.  How does it act to prevent colon cancer?  Let’s take a look.

First, vitamin D supports the overall health of the individual colon cell, promoting its orderly growth and regulating its cycle of life (Guraya, 2014).  It does this by regulating (activating or suppressing) genes involved in the control of cellular growth and function.  When vitamin D is in adequate supply, the colon cell has a better chance of functioning normally and can make important decisions with greater ease.  One important decision the colon cell almost always needs to make is what measures to initiate to address the threat of inflammation. Inflammation, inadequately addressed and left unrestrained, can lead to colon cancer.

Second, and speaking of inflammation, “Since inflammation plays [an] important role in cancer development, vitamin D exerts a strong anti-inflammatory role in delaying or preventing cancer development and/or progression.” (Guraya, 2014)  Not only does the colon cell need to respond to inflammation generated externally and posing a threat, the colon cell also needs to respond to inflammation generated by circumstances occurring within.  Vitamin D helps the colon cell defend itself against inflammation regardless of its origin, and does so by orchestrating a variety of anti-inflammatory responses.

Third, vitamin D helps protect against ordinary, yet harmful insults such as exposure to secondary bile acids, an “underrecognized cause of colon cancer.”  (Ajouz et al., 2014)  There is no escape from this threat.  We need fat in our diet; therefore, we need bile acids in our life—appropriately secreted by the liver into the small intestine, via the gallbladder, to aid in the digestion of fat (more fat in the diet, more bile acids . . . could be a problem).  Bile acids, although necessary, can pose a danger once they arrive in the colon.  We need to defend against this threat.

“Bile acids damage cell membranes, at least in part through an oxidative mechanism, provoking an inflammatory response and causing DNA damage.”  (Fedirko et al., 2010)

A bile acid is one thing; a secondary bile acid is quite another.  Bacteria in the colon act on bile acids and create a more intense threat, known as a secondary bile acid.  Fortunately, we have vitamin D.  To protect us from both primary and secondary bile acids, as well as other threats that cause oxidative stress and DNA damage, vitamin D increases the capacity of the colon cell to mount an aggressive antioxidant response (Fedirko et al., 2010).  Furthermore, vitamin D “promotes bile acid degradation,” secondary bile acids included.  (see Fedriko et al., 2010  Vitamin D plays a positive role in so many biological processes.  It should be in adequate supply.

Fourth, vitamin D stimulates genes involved in DNA repair (Fedirko et al., 2010; Guraya, 2014).  DNA damage occurs in each and every cell, day-in and day-out, and at a rate of 10,000 to 1,000,000 damaged regions per day!  (see Wikipedia, 2017)  For the colon cell, it is a way of life.  Bile acids cause DNA damage, as do many other threats (like that big, fat, juicy steak I saw you eating the other day, with no intention of sharing).  But, the cells of the colon are ready.  There are molecular machines positioned within each cell nucleus that tirelessly and continuously repair damaged DNA.  Cells make DNA repairs in astonishing numbers each day—thousands upon thousands (Wikipedia, 2017).  Why does the cell go to all this trouble?  It does this so it can function normally.  It does this hoping, above all hope, that it will not be transformed into a cancer cell, somehow knowing “DNA damage is an early step in the initiate of cancer.”  (Toden et al., 2006). A repaired segment of DNA is less likely to push a cell over to the dark side.

Fifth, vitamin D encourages the colon cell to die . . . and die right on time.  Believe it or not, the normal life cycle of a colon cell involves suicide.  The colon cell is literally programed to kill itself after only a short period of existence.  It has no other choice.  Its normal life span is 3–5 days.  After that, it must die.  “Why death at as such an early age,” you ask?  The colon cell lives in a crappy neighborhood (so true), and is so often damaged by the threats it encounters, that if it were to become elderly (say, 7 or 8 days old) the damage that has accrued increases the likelihood that it could be transformed into a cancer cell.  Pre-programmed, timely suicide solves this problem.  This whole scheme of things has a name.  It is called apoptosis.  And it’s important!  “Induction of apoptosis is directly linked with the anti-cancer action of vitamin D.”  (Guraya, 214)  Vitamin D, specifically its activated form (1,25(OH)2D), not only wants to encourage the death of the normal colon cell, it wants to encourage (as in, strongly encourage) the death of a colon cell that has been transformed into a cancer cell (Deeb et al., 2007).  Apoptosis kills a cancer, too, unless something is standing in the way.

Sixth, vitamin D silences specific genes involved in the proliferation of colon cancer cells (Klampfer, 2014).  Proliferation with respect to a cancer cell means unrestrained growth.  Proliferation allows a cancer cell to divide and divide and divide to form an expanding tumor.

I could go on and on about the various ways vitamin D acts to prevent colon cancer, but we need to move on to other important matters.  So, I’ll briefly mention one more anti-cancer benefit offered by vitamin D.

Seventh, should a colon cell be transformed into a cancer cell, and begin to proliferate, it will need to establish an impressive vascular system (angiogenesis).  You don’t want this.  Vitamin D may help in this regard. Vitamin D acts to inhibit angiogenesis (Deeb et al., 2006).  Clearly, vitamin D wants to save you from colon cancer, but if supplies are limited, all bets are off.

“Vitamin D supplementation has been shown to reduce CRC [colorectal cancer] related morality; thus reaffirming the significance of optimizing vitamin D concentrations for cancer prevention.”  (Guraya, 2017)

 

Dietary considerations

“Western dietary patterns—characterized by higher intake of red and processed meats, added sugar, and refined grains—have strongly linked with CLR [colorectal cancer] in numerous observational studies as well as in a systematic review and meta-analysis.”  (Mehta et al., 2017)

“It has been estimated that up to 25% of colorectal, 15% of breast and 10% of prostate, pancreas and endometrial cancers could be prevented by shifting to a healthy Mediterranean diet.”  (La Vecchia, 2004, emphasis added)

If you want to further reduce your colon cancer risk, look no further than the Mediterranean diet.  Actually, you can look a little further, as vegetarian and vegan diets also significantly reduce the risk of colon cancer (Orlich et al., 2015).  All three diets have several things in common.  And one thing in particular, they limit or entirely exclude the consumption of red meat.  I know you don’t want to hear any of this, but research has shown, without a doubt, that red meat—and most concerning, processed meat—promotes the development of colon cancer (Bastide at al., 2011).  The Mediterranean diet limits red meat as well as processed meats, and therefore, in addition to a plethora of good things tucked inside this diet, offers an exceptional degree of protection against colon cancer.  Since this diet allows you to still be a carnivore—allowing you to eat more chicken than you thought humanly possible—this diet may be more acceptable to you than a meatless, chickenless, vegetarian or vegan diet.

“A healthy diet model in European countries is the traditional Mediterranean diet, which is based on abundant and variable plant foods, high consumption of cereals, olive oil as the main (added) fat, low intake of (red) meat and moderate consumption of wine.”  (Giacosa et al., 2012)

Next, and with this little overview of the Mediterranean diet under our belt, let’s look more closely at how the Mediterranean diet acts to defend against colon cancer.

First, by limiting red meat and processed meat, the Mediterranean diet limits the consumption of what is called heme.  Heme is a portion of the hemoglobin molecule.  Hemoglobin is the molecule within a red blood cell that carries oxygen throughout the bloodstream (sometime before the animal appears on the menu).  Heme holds an iron atom within, with iron adding yet another element of danger (more later).  The problem with heme is that heme damages cells along with its DNA (Toden et al., 2006).  This gives heme the ability to function as a true carcinogen (Oates and West, 2006).  There is a little heme in chicken and fish, but red meat has 10 times more!  (see Bastide et al., 2011; Sesink et al., 1999)  Reduced heme exposure is one of the main reasons why the Mediterranean diet protects against colon cancer.  Sorry folks, similar to beef, pork and lamb are rich in heme, and therefore pose a substantial colon cancer risk (Pericleous et al., 2013).

Second, the Mediterranean diet limits the consumption of dietary iron.  The foods you eat on this diet are typically made from scratch, not the factory-made, iron-fortified foods typical of the Western diet.  Importantly, by limiting red meat, the Mediterranean diet limits the iron held within heme.  There is a ton of iron in red meat.  Cut into a rare, juicy steak, and it will bleed.  Just to give you an idea of how much iron is involved, consider the fact that one red blood cell (so small it cannot be seen with the naked eye), may hold up to 1 billion iron atoms!  (see Casssat and Skaar, 2013)  Incredible!  That’s a lot of iron.  Enter the Mediterranean diet.  This is a diet that restricts the consumption of dietary iron.  No way does the average person need all the iron provided by the Western, red meat-based, iron-fortified diet.  And why is iron such a threat with respect to colon cancer?

“Iron is required for proliferation of normal and neoplastic [cancer] cells. The relationship between iron and cancer risk appears to be obvious in the colon due to its high concentrations of iron.”  (Cho et al., 2013) 

By limiting red meat, by limiting heme, the Mediterranean diet reduces the amount of iron available to threaten the colon cell.  “Iron can induce oxidative DNA damage.”  (Cross, et al., 2010)  In the colon, iron should be in short supply.  In the Western diet, it is in generous supply.

Third, the Mediterranean diet provides a whole host of things that help promote colon cell health and act to prevent colon cancer.  Case in point: The vegetable fibers you eat in abundance on this diet feed bacteria, and in turn, the bacteria produce metabolic by-products that feed the colon cell and act to prevent colon cancer in a variety of ways.  One such by-product is butyrate.

“Butyrate has a remarkable array of colonic health-promoting and antineoplastic properties: it is the preferred energy source for colonocytes, it maintains mucosal integrity and it suppresses inflammation and carcinogenesis through effects on immunity, gene expression and epigenetic modulation.  Protein residues and fat-stimulated bile acids are also metabolized by the microbiota to inflammatory and/or carcinogenic metabolites, which increase the risk of neoplastic [cancer] progression.”  (O’Keefe, 2016)

In addition to the abundance of fiber in the Mediterranean diet, this diet also includes generous amounts of vitamins such as folate, minerals such as calcium (often low in the Western diet), as well as a wide variety of bioactive substances that clearly provide health benefits and offer protection against colon cancer.  (see Fedirko et al., 2010)  The bioactive substances found in abundance in the plant-based, Mediterranean diet include chlorophyll from green vegetables, polyphenols, and quercetin—all offering positive health benefits and an impressive degree of protection against cancer of the colon and rectum (Oates and West, 2006; Bastide et al., 2011).  Clearly, the Mediterranean diet offers so many health benefits, it is regarded as a templet of what a good diet should look like when it comes to colorectal cancer prevention.  After all, diet is intimately associated with the development of cancers of both the colon and rectum.

“There is strong evidence that the risk of CRC [colorectal cancer] can be modified by lifestyle and environmental factors. It has been demonstrated that diet may account for or prevent as much as 80% of CRC incidence.”  (Nyström M, Mutanen, 2009, emphasis added)

Okay.  You really don’t want to give up or limit red meat entirely, at least anytime soon.  I understand.  Good news: You can block the negative effects of red meat by taking a page right out of the Mediterranean diet play book.  A diet high in calcium, or a diet high in vegetables (which is also high in calcium), both appear to offset the negative, carcinogenic effects of red meat consumption (Bastide et al, 2011; Oates and West, 2006)  Also, preparing red meat at lower temperatures reduces the amount of several cancer-causing chemicals that are generated when meat is cooked on at higher temperatures (Pericleous et al., 2013).  But just to be safe, I would still limit both red meat and processed meats in an effort to reduce the risk of colorectal cancer.

 

Alcohol restriction

“The Mediterranean diet also involves a ‘Mediterranean way of drinking’, that is, moderate consumption of red wine mainly with food.

. . . the risk of both colon and rectal cancer being about 50% increased with high levels of alcohol consumption.”  (Giacosa et al., 2012, emphasis added)

Mediterranean diet allows a little alcohol consumption, mainly red wine with meals, but not enough alcohol to make you an embarrassment to us all.  Limit the use of alcohol and you limit the risk of colon cancer, pure and simple.  I don’t make the rules; I just share them with you.  Make the prevention of colon cancer (and so many other problems associated with excess alcohol consumption) one great motivator to compel you to limit the intake of alcohol. “. . . comparing never drinkers, moderate drinkers who consume 2–3 drinks per day have a 21% increase CRC risk and heavy drinkers who have 4 or more per day have a 52% increased CRC risk.”  (Hou et al., 2013)
Smoking succession

“Up to 20% of current colorectal cancers in the United States may be due to tobacco smoke. Presumably tobacco smoke causes colon cancer due to the NDA damaging agents described for lung cancer. These agents may be taken up in the blood and carried to organs of the body.”  (Bernstein et al., 2013)

“Tobacco and excessive alcohol consumption cause about one-third of the total cancer burden, with precise figures varying from country to country.”  (Giacosa et al., 2012)

Need I say more?

 

Exercise as a defense

“Higher levels of physical activity have been reported to reduce the risk of [colorectal cancer] by up to 40% . . ..”  (Pericleous et al., 2013)

A sedentary lifestyle is a risk factor for colorectal cancer (Hou et al., 2013).  Obesity, as well.  Both can lead to another risk factor, type 2 diabetes (Pericleous et al., 2013).  The bottom line: Add increased physical activity and exercise to your plan to defend against colon cancer.  If you sit on your butt all day long, your risk of colorectal cancer is 20% higher than is you live an active lifestyle (Hou et al., 2013).

 

Green tea, anyone?

“Consumption of green tea has been associated with a 40% reduction in colorectal cancer risk in a cohort of 69,710 Chinese women.”  (Pericleous et al., 2013)

To reduce your risk of colorectal cancer, you may want to consider drinking green tea on a regular basis.  Or, you can get your green tea by supplementing daily with green tea extract.  A 40% reduction in the risk of colorectal cancer sounds nice to me.

 

Heredity as a threat

“Of common malignancies, colorectal cancer (CRC) has one of the largest proportions of familial cases. Kindred and twin studies estimated that approximately 30% of all CRC cases are an inherited form of the disease.”  (Jasperson et al., 2010)

“Even in the hereditary colon cancer syndromes, in which the susceptibility is inherited dominantly, cancer develops only as the result of progressive accumulation of genetic alterations.”  (Nyström M, Mutanen, 2009)

Most fortunately, genetics are not the final word.  Why is this important?  It gives the individual hope that should a close relative or identical twin contract colon or rectal cancer, it doesn’t mean they cannot take actions to substantially reduce their risk.  This entire article is all about what to do or what not do to reduce the risk of colorectal cancer.  Perhaps those who have a strong family history of this disease should pay very close attention to what we have discussed in this presentation.

To close this section on genetics, may I suggest: If the family ties to colorectal cancer are strong, an aggressive screening program is in order—particularly so if a close family member contracted colorectal cancer before age 50 (Mishra and Hall, 2012).  Under this circumstance, a once-every-5-year colonoscopy is simply not often enough.  In certain situations, a screening colonoscopy should be “initiated by “20–25 years of age and repeated every 1–2 years.”  (Jasperson et al., 2010)  Your physician will advise you.

 

Conclusion

It certainly looks like there is a lot we can do to prevent colon cancer.  I’ve changed my life after writing this article.  Hopefully, after reading it, you will change your life, too.  I’ve seen colon cancer.  I’ve seen the damage it can do.

 

Dedication

 

Highly Recommended (click on image to follow link)

 

 

 

References

Ajouz H, Mukherji D, Shamseddine A 2014 Secondary Bile Acids: An Underrecognized Cause of Colon Cancer. World Journal of Surgical Oncology. May 24; 12(1):164

Barclay RL, Vicari JJ, Doughty AS, Johanson JF, Greenlaw R 2006 Colonoscopic Withdrawal Times and Adenoma Detection During Screening Colonoscopy. New England Journal of Medicine. Dec 14; 355(24):2533–2541

Bastide NM, Pierre FH, Corpet DE 2011 Heme Iron from meat and Risk of Colorectal Cancer: A Meta-Analysis and a Review of the Mechanisms Involved. Cancer Prevention Research. Feb 1; 4(2):177–184

Bernstein C, Prasad AR, Nfonsam V, Bernstein H 2013 DNA Damage, DNA Repair and Cancer. In New Research Directions in DNA Repair. InTech, DOI: 10.5772/53919

Cassat JE, Skaar EP 2013 Iron in Infection and Immunity. Cell Host & Microbe. May 15; 13(5):509–519

Cho M, Eze OP, Xu R 2013 A Brief Review of the Controversial Role of Iron in Colorectal Carcinogenesis. J. Clin. Exp. Pathol. 3(137):2161–0681

Cross AJ, Ferrucci LM, Risch A, Graubard BI, Ward MH, Park Y, Hollenbeck AR, Schatzkin A, Sinha R 2010 A Large Prospective Study of Meat Consumption and Colorectal Cancer Risk: An Investigation of Potential Mechanisms Underlying This Association. Cancer Research. Mar 15; 70(6):2406–2414

Deeb KK, Trump DL, Johnson CS 2007 Vitamin D Signalling Pathways in Cancer: Potential for Anticancer Therapeutics. Nature Reviews. Cancer. Sep 1; 7(9):684

Fedirko V, Bostick RM, Long Q, Flanders WD, McCullough ML, Sidelnikov E, Daniel CR, Rutherford RE, Shaukat A 2010 Effects of Supplemental Vitamin D and Calcium on Oxidative DNA Damage Marker in Normal Colorectal Mucosa: A Randomized Clinical Trial. Cancer Epidemiology and Prevention Biomarkers. Jan 1; 19(1):280–291

Giacosa A, Barale R, Bavaresco L, Gatenby P, Gerbi V, Janssens J, Johnston B, Kas K, La Vecchia C, Mainguet P, Morazzoni P 2012 Cancer Prevention in Europe: The Mediterranean Diet as a Protective Choice. European Journal of Cancer Prevention. Jan 1; 22(1):90–95

Guraya SY 2014 Chemopreventive Role of Vitamin D in Colorectal Carcinoma. Journal of Microscopy and Ultrastructure. Mar 31; 2(1):1–6

Guraya SY 2017 The Association of Vitamin D Deficiency with Colorectal Cancer: A Wake-Up Call for Physicians and Health Authorities. Middle East Journal of Cancer April; 8(2):65–68

Hong TS, Clark JW, Haigis KM 2012 Cancers of the Colon and Rectum: Identical or Fraternal Twins? February; 2(2):117–121

Hou N, Huo D, Dignam JJ 2013 Prevention of Colorectal Cancer and Dietary Management. Chinese Clinical Oncology. Jun; 2(2):13

Jasperson KW, Tuohy TM, Neklason DW, Burt RW 2010 Hereditary and Familial Colon Cancer. Gastroenterology. May 31; 138(6):2044–2058

Klampfer L 2014 Vitamin D and Colon Cancer. World Journal of Gastrointestinal Oncology. 14 Nov 15; 6(11):430–437
La Vecchia C 2004 Mediterranean Diet and Cancer. Public Health Nutrition. Oct; 7(7):965–968

Mehta RS, Song M, Nishihara R, Drew DA, Wu K, Qian ZR, Fung TT, Hamada T, Masugi Y, da Silva A, Shi Y 2017 Dietary Patterns and Risk of Colorectal Cancer: Analysis by Tumor Location and Molecular Subtypes. Gastroenterology. Jun 30; 152(8):1944–1953

Mishra N, Hall J 2012 Identification of Patients at Risk for Hereditary Colorectal Cancer. Clinics in Colon and Rectal Surgery. Jun; 25(02):67–82

Nyström M, Mutanen M 2009 Diet and Epigenetics in Colon Cancer. World Journal of Gastroenterology. Jan 21;15(3):257

Oates PS, West AR 2006 Heme in Intestinal Epithelial Cell Turnover, Differentiation, Detoxification, Inflammation, Carcinogenesis, Absorption and Motility. World Journal of Gastroenterology. Jul 21; 12(27):4281

O’Keefe SJ 2016 Diet, Microorganisms and Their Metabolites, and Colon Cancer. Nat Rev Gastroenterol Hepatol. Dec 1; 13(12):691–706

Orlich MJ, Singh PN, Sabaté J, Fan J, Sveen L, Bennett H, Knutsen SF, Beeson WL, Jaceldo-Siegl K, Butler TL, Herring RP 2015 Vegetarian Dietary Patterns and the Risk of Colorectal Cancers. JAMA Internal Medicine. May 1; 175(5):767–776

Pericleous M, Mandair D, Caplin ME 2013 Diet and Supplements and Their Impact on Colorectal Cancer. Journal of Gastrointestinal Oncology. Dec; 4(4):409

Sesink AL, Termont DS, Kleibeuker JH, Van der Meer R 1999 Red Meat and Colon Cancer. Cancer Research. Nov 15; 59(22):5704–5709

Toden S, Bird AR, Topping DL, Conlon MA 2006 Resistant Starch Prevents Colonic DNA Damage Induced by High Dietary Cooked Red Meat or Casein in Rats. Cancer Biology & Therapy. 2006 Mar 1;5(3):267–272

Wikipedia 2017 DNA Repair. https://en.wikipedia.org/wiki/DNA_repair July 21

 

Disclaimer: This article is presented solely for informational purposes.  The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care.  It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein.  The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy.  This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician.  The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the resources that are herein recommended.
Copyright © 2017 Eugene L. Heyden, RN
All Rights Reserved

 

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Protecting the Heart: A Role for Vitamin D

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Jul 102017
 

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By Eugene L. Heyden, RN

Vitamin D protects against Cancer.  Vitamin D protects against autoimmune disease.  Vitamin D protects against Alzheimer’s disease, against Parkinson’s disease, and against multiple sclerosis.  It protects against so many diseases.  So, why would it not protect against heart disease?  The answer is “it does.”

“In the Health Professionals Follow-up Study, men with a high circulating level of vitamin D had half the risk of myocardial infarction as men with vitamin D insufficiency.”  (Kilkkinen et al., 2009, emphasis added)

Heart disease, more formally referred to as cardiac disease, falls under the umbrella term cardiovascular disease (CVD).  Cardiac disease just happens to be our No. 1 killer.  And this killer will destroy approximately one out of three of us living here on planet Earth (Aleksova et al., 2015).  And yes, I’ve seen this killer in action.

In my nursing career, I have spent nearly a quarter of a century in the trenches battling this killer—taking care of acute heart attack victims, patients with various degrees of heart failure, individuals recovering from open heart surgery, and those recovering from heart transplantation.  So unexpectedly, this killer preys on those who are vitamin D deficient, which is why I am writing to warn you of the danger.  It is quite likely you are among those who are at great risk.

“In the United States and Europe, > 40% of the adult population has low vitamin D levels.”  (Milazzo et al., 2017)

Surprisingly (but not to me), one study “found a high (96%) prevalence of vitamin D deficiency in patients with acute myocardial infarction.”  (De Metrio et al, 2015)  Apparently, vitamin D deficiency is something to avoid if you want to live a healthier life and a longer life, a life not inviting an early death to sweep you away.

A myocardial infarction (MI) is a fancy word for heart attack.  A heart attack is typically caused by a blood clot that forms in a narrowing in an artery, in this case a coronary artery, one that feeds a significant portion of the heart.  Given time, given circumstances, a blood clot will form in the narrowing and create a sudden blockage of blood flow, initiating the MI.  Unless resolved, death of the affected portion of the heart will occur.  Often the death of an entire person will occur.  Nearly 50% of MI sufferers die before they arrive at the hospital to receive life-saving care—all due to a coronary artery narrowing and the formation of a silly little blood clot.  One can see a narrowed coronary artery, as well as the occlusion, when coronary angiography is performed.  So now you know the basics as well as a medical term or two, and should readily appreciate the following:

“In more than 3000 subjects undergoing coronary angiography, severe vitamin D deficiency (25(OH)D <10 ng/mL) had 3 to 5 times risk of dying from sudden cardiac death or heart failure during a 7-year follow-up period compared with optimal levels of vitamin D (25(OH)D >30 ng/mL).”  (Judd and Tangpricha, 2009, emphasis added)

Unfortunately, there are so many individuals with vitamin D deficiency, even severe vitamin D deficiency, that given enough time, the commonplace yet the unthinkable can occur.  According to the Center for Disease Control and Prevention (CDC) (2015), coronary artery disease kills 370,000 Americans each year.  It looks like we could substantially reduce the number, perhaps by half, simply by solving the problem of vitamin D deficiency in our population.  But we’re not even close to thinking about doing this.  Instead, we think about other things and we allow vitamin D deficiency to persist.

At this point in our conversation I should probably tell you how vitamin D protects against heart disease.

To begin with, vitamin D restrains both systemic and vascular inflammation, protecting against the development of vascular disease.  Conversely, “Vitamin D deficiency stimulates systemic and vascular inflammation, enabling atherogenesis.”  (Mozos and Marginean, 2015)  Things just don’t happen out of the blue.  Apparently, inflammation occurring in coronary arteries is a pivotal step that leads to atherogenesis.  Atherogenesis is the disease process that damages the coronary artery, allows the damaged portion to narrow, and sets the stage for coronary artery occlusion.  And should an occlusion occur, the result is an MI . . . and people die.  Vitamin D acts to prevent this process, at the very beginning and at several key steps along the way.  But it must be in adequate supply.

In the disease process that leads to an MI, an abnormal uptake of both calcium and cholesterol progressively occurs within the wall of an injured, diseased portion of a coronary artery.  Vitamin D acts to prevent both calcification of a coronary artery and the accumulation of cholesterol within a compromised portion of a coronary artery.  (Mozos and Marginean, 2015)  Perhaps surprising to you (but not to me), cholesterol can accumulate in a coronary artery even when blood cholesterol levels are normal, as approximately 75% of heart attack victims have normal cholesterol levels (Champeau, 2015).  On the other hand, studies have shown that almost everyone who has a heart attack has a low vitamin D level.  So, it sounds like more attention should be paid to vitamin D levels than to cholesterol levels in our battle against coronary artery disease.  And why not? Vitamin D has so much to offer!

Among other things, vitamin D helps prevent abnormal clotting from occurring in a narrowed coronary artery.  (see Mozos and Marginean, 2015)  So at the very least, vitamin D may postpone (perhaps forever) what may have become an inevitable MI.

But there is more . . .

One response the heart mounts when experiencing a progressive narrowing of a coronary artery is to create what are called collaterals.  A collateral is a new vessel, created by the heart to perform a little bypass operation on itself.  A collateral will allow blood to flow around the narrowing in a coronary artery to supply blood to a threatened portion of the heart.  A network of collateral arteries can save you in the event of a sudden coronary occlusion.  Guess what?  Vitamin D stimulates the formation of collateral circulation.  It does this by stimulating growth factors and the like (Lima Jr. and Kunadian, 2015).  Less collateral circulation develops in the context of vitamin D deficiency.  Hence, “vitamin D levels were found to be an independent predictor of coronary collaterals development.”  (Lima Jr. and Kunadian, 2015)  Which is probably why one study found, “vitamin D deficiency was more common among patients in the poor-collateralization group compared to patients in the well-collateralization group.”  (Hossein-Nezhad et al., 2015)  So, it should be of no surprise that the authors reporting on this study make the following statement:

“Maintaining a normal vitamin D status should be a high priority in the general population. Likewise, vitamin D supplementation may be beneficial in the prevention of CAD [coronary artery disease] in patients with an increased risk for CAD.”  (Hossein-Nezhad et al., 2015)

Since the subject was brought up, perhaps now would be a great time to discuss vitamin D supplementation.  Simply put, we need to supplement because diet won’t cut it.  We know this because all those individuals, with those low vitamin D levels, those who have all those MI’s, are eaters.  Diet offered them little or no protection against vitamin D deficiency and little or no protection from coronary artery disease.  Of course, anyone can generate thousands of units of vitamin D each day by relevant sunlight exposure—but only during late-morning to mid-afternoon, and between March through September, leaving approximately 5 months of the year when no vitamin D can be made no matter how hard you try.

So, as you can see, vitamin D supplementation is clearly the answer, but not the only answer.  Vitamin D testing is in order.  “Zittermann et al. found a vitamin D level of 30–35 ng/L. as the best choice for risk reduction in cardiovascular mortality.”  (Mozos and Marginean, 2015)  Combining testing to see where you are at, supplementing with vitamin D as indicated—and repeat testing to determine if a therapeutic goal has been achieved and is maintained—is clearly the best approach to substantially reduce your risk of drawing the attention of our No. 1 killer.

On, no!  You’ve gone and done it.  You have had an MI.  Since you are reading this, it is safe to say you did not die.  But be aware, those who do not die from their MI, have a list of threats lying in wait, problems also related to an individual’s vitamin D status.

“Vitamin D status is prognostic for major postinfarction adverse events, such as heart failure hospitalizations, recurrent acute myocardial infarction, death, or restenosis [reocclusion] after percutaneous coronary intervention. A significant, moderate association was found between circulating vitamin D concentration and the risk of all-cause mortality, especially deaths due to coronary disease.”  (Mozos and Mardinean, 2015, emphasis added)

I think I’ve made things abundantly clear.  Vitamin D can protect you from experiencing an MI, death from an MI, and experiencing the adverse consequences of an MI.  But you can ignore all this if you want to (at your peril).  Or, you can take the steps necessary to become vitamin D sufficient and a lot less invisible to our No. 1 killer.

 

Highly recommended

Diet Guidelines to Improving Heart Health

 

References

Aleksova A, Belfiore R, Carriere C, Kassem S, La Carrubba S, Barbati G, Sinagra G 2015 Vitamin D Deficiency in Patients with Acute Myocardial Infarction: An Italian Single-Center Study. Int J Vitam Nutr Res. Jan 1; 85:23–30

Centers for Disease Control and Prevention 2015 Heart Disease Facts. Retrieved from https://www.cdc.gov/heartdisease/facts.htm

De Metrio M, Milazzo V, Rubino M, Cabiati A, Moltrasio M, Marana I, Campodonico J, Cosentino N, Veglia F, Bonomi A, Camera M 2015 Vitamin D Plasma Levels and In-Hospital and 1-Year Outcomes in Acute Coronary Syndromes: A Prospective Study. Medicine. May 1; 94(19):e857

Dogan Y, Sarli B, Baktir AO, Kurtul S, Akpek M, Sahin O, Odabas H, Dondurmacı E, Ugurlu M, Ozkan E 2015 25-Hydroxy-Vitamin D Level May Predict Presence of Coronary Collaterals in Patients with Chronic Coronary Total Occlusion. Postępy w Kardiologii Interwencyjnej= Advances in Interventional Cardiology. 11(3):191

Judd SE, Tangpricha V 2009 Vitamin D Deficiency and Risk for Cardiovascular Disease. The American Journal of the Medical Sciences. Jul; 338(1):40–44

Hossein-Nezhad A, Eshaghi SM, Maghbooli Z, Mirzaei K, Shirzad M, Curletto B, Chen TC 2014 The Role of Vitamin D Deficiency and Vitamin D Receptor Genotypes on the Degree of Collateralization in Patients with Suspected Coronary Artery Disease. BioMed Research International. Mar 6;2014

Kilkkinen A, Knekt P, Aro A, Rissanen H, Marniemi J, Heliövaara M, Impivaara O, Reunanen A 2009 Vitamin D Status and the Risk of Cardiovascular Disease Death. American Journal of Epidemiology. Oct 15; 170(8):1032–9

Milazzo V, De Metrio M, Cosentino N, Marenzi G, Tremoli E 2017 Vitamin D and Acute Myocardial Infarction. World Journal of Cardiology. Jan 26; 9(1):14

Mozos I, Marginean O 2015 Links between Vitamin D Deficiency and Cardiovascular Diseases. BioMed Research International. Apr 27; 2015

Lima Jr J, Kunadian V 2015 Vitamin D: Evidence for an Association with Coronary Collateral Circulation Development? Postępy w Kardiologii Interwencyjnej= Advances in Interventional Cardiology. 11(3):174

Champeau R 2009 Most Heart Attack Patients’ Cholesterol Levels Did Not Indicate Cardiac Risk [Press release]. http://newsroom.ucla.edu/releases/majority-of-hospitalized-heart-75668

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and not to be substituted for professional judgment and guidance or to provide a reason to neglect or delay appropriate medical care. It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein. The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy. This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician. The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the resources that are herein recommended.

 

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved

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Ulcerative Colitis: Diet for Success

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Jun 092017
 

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By Eugene L. Heyden, RN

I can’t imagine living a life like this.  But perhaps you can.  I don’t have ulcerative colitis, but perhaps you do.  I think I heard someone say, “This is getting old.”  I think it was you.  Let’s see if we can help you out a little in your struggle against this disease.

To sufficiently motivate you, the ulcerative colitis (UC) patient, I’ll need to start out a little on the negative side.  You’re not going to like this:

Modern-day therapeutics for IBD have limited efficacy and are not without their danger.  (Weinstock and Elliott, 2009, emphasis added)

“The current mainstays of IBD treatment are expensive anti-inflammatory and immunosuppressive drugs. Among those who can afford to be on treatment, approximately 40% are either unresponsive to any of the available drugs or cannot tolerate them. The chances that an IBD patient responds to medications and remains flare-up-free after 1 year on even the most potent medications, such as TNF inhibitors, is as low as 20–25%. Furthermore, medical therapy of IBD carries significant risks, among which are life-threatening infections, cancers (especially lymphoma) and neurological complications, such as demyelinating disease.”  (Mutlu and Gor, 2008)

Sounds a lot like current therapy for ulcerative colitis is not without considerable risk.  There is an alternative.  Diet is an alternative.  There is a lot of promise here.

“By comparison, diet therapy [for inflammatory bowel disease] has the potential to be safe, lifelong and relatively cheap.”   (Mutlu and Gor, 2008)

Don’t get me wrong, medications—although admittedly dangerous, unbelievably expensive, and too often unable to meet their objective—are necessary in the battle against ulcerative colitis.  Skillful use is required.  But drug therapy is not the only game in town.  Diet, if done right, can be a very effective therapy for ulcerative colitis.  And there is a plus: diet can easily fit in with current therapy.  Adding diet to your physician’s game plan may hasten remission and may eventually allow the discontinuation of drug therapy.  It may also help to maintain remission, once achieved.

Here, we will focus on several dietary approaches for the management of ulcerative colitis, all blended into a diet plan I believe will offer the most promise in achieving and maintaining remission.  You may have tried diet in the past with the hope of achieving remission, and failed.  It may be that some important considerations were not addressed by the diet you chose.  Mistakes may have been made.  A diet designed for ulcerative colitis should probably include the following features . . .

Sulfur restriction

“Dietary factors such as red and processed meat, protein, and alcohol, as well as sulfur and sulfate intake were positively associated with relapses in ulcerative colitis.”  (Tilg and Kaser, 2004)

“Foods rich in sulphur compounds have been associated with UC disease symptoms.  In addition, dietary sulphur can increase the likelihood of subsequent UC relapse.”  (Khalil et al., 2014)

“A high sulphur diet, either from sulphur amino acids or sulphate additives, results in the generation of hydrogen sulphide and mucosal damage in the colon.”  (Jowett et al., 2004)

When I became sufficiently aware of the harm a diet high in sulfur can cause the patient with ulcerative colitis, I literally said to myself, “Then, let’s do something about this.”  This is what you need to know.

Dietary sulfur (also spelled sulphur), in excessive amounts, creates havoc in the large bowel.  It often arrives as a component of non-digested protein that has escaped digestion elsewhere, with meat protein perhaps the most insidious.  Bacteria act on the undigested protein.  They have nothing better to do.  Besides, I’m sure they are after something they desperately need.  As a result of the increased availability of sulfur compounds, a class of bacteria known as sulfate-reducing bacteria—overgrow and crowd out other bacteria, many of which are beneficial and act to maintain bowel health and defend against disease.  Believe it or not, good bacteria promote healing, should healing be in order (Ouwehand et al., 2003).  On the other hand, sulfate-reducing bacteria are not all that into healing.  When in abundance, they are into mischief.

“The increased number of sulfate-reducing bacteria and intense process of dissimilatory sulfate reduction in the gut can cause inflammatory bowel diseases of humans and animals.”  (Kushkevych, 2014)

And not surprisingly, “The increased number of sulfate-reducing bacteria was found in feces from people with ulcerative colitis compared with healthy individuals.”  (Kushkevych, 2014)  We should not be feeding these guys.  Meat, and other foods rich in sulfur, like milk and eggs, will need to be restricted in a diet plan structured to defeat ulcerative colitis.  The following websites will be of great help in formulating a diet low in sulfur:

http://www.livestrong.com/article/441718-a-list-of-low-sulfur-foods/

http://livewell.jillianmichaels.com/lowsulfur-diets-5231.html

http://www.sulfites.org/sulfite-foods/

http://www.nutrientsreview.com/minerals/sulfur.html

The hazards posed by sulfur-fed, sulfate-reducing bacteria are largely due to the creation of a cell-toxic byproduct, namely hydrogen sulfide—a gas that readily diffuses into the cells that line the colon and blocks the utilization of butyrate, the primary fuel source for this cell type (Khalil et al., 2014; Kushkevych, 2014).  A poisoned cell is a dysfunctional cell.  A starving cell is a dysfunctional cell.  Under these conditions, the cells that line the colon are unable to maintain barrier integrity and are hampered in their ability to effectively defend against bacteria.  Excessive inflammation follows.  Say “Hello” to a disease that never goes away.  Say “Hello” to drugs and even more drugs, prescribed in a concerted effort to control all the madness.

Before we move on, please watch the following two videos.  (I give you no other choice.)  They do an outstanding job in warning you of the dangers and pointing you in the right direction.  Sulfur restriction has its rewards.  How does remission sound?

https://nutritionfacts.org/video/bowel-wars-hydrogen-sulfide-vs-butyrate/

https://nutritionfacts.org/video/treating-ulcerative-colitis-with-diet/

Now that you have visited the websites and watched the videos, I’m sure you will be able to, with your physician’s guidance and approval, put together a dietary plan to reduce the sulfur compounds in your life.  Now, you don’t need to avoid all dietary sulfur.  (Actually, you can’t.)  It looks like there is an intake threshold that can be well tolerated.  The threshold of dietary sulfur is reported to be a little less than ½ the intake usual to the Western diet (Pitcher and Cummings, 1969).  One last thing: A medication commonly used in ulcerative colitis, mesalazine (Azacol, Pentasa), acts to “inhibit sulfide formation by colonic bacteria.”  (Baumgart, 2017)  The take away: Drug therapy can assist you in your quest to reduce the damage caused by sulfur-containing compounds.

Let’s move on.  I see trouble ahead.  Big trouble.

 

Dietary iron restriction

“Accumulating evidence indicates that excess of unabsorbed iron that enters the colon lumen causes unwanted side effects at the intestinal host-microbiota interface.

“Besides the effects of iron on the gut microbiota, which may cause a shift towards a more pathogenic profile and an increase in virulence of enteric pathogens, iron may also directly exert unfavorable effects on the gut epithelium most likely by the promotion of redox stress.”  (Kortman et al., 2014)

This subject—dietary iron restriction—receives less attention in the clinical setting than other dietary strategies.  Actually, it is largely being ignored.  But we don’t have to.  Surprisingly, iron, a much-needed commodity for both you and bacteria bent on evil, can be a problem.  Ulcerative colitis is a problem.  Excessive exposure to iron may set the stage for the disease itself.  Listen up!

“The authors [investigating the association between iron in municipal water supplies and the incidence of IBD] found that [the] risk of developing inflammatory bowel disease was associated with high iron content.  The relative risk of developing inflammatory bowel disease, including ulcerative colitis and Crohn’s disease increased by 21% . . . when the iron content in drinking water increased by 0.1 mg/l.”  (Aamodt et al., 2008, emphasis added)

The quotations chosen for this section tell a real story, and should serve as a warning.  Iron, in excess of individual need, accumulates in the colon and produces two unwanted effects.  It harms the cells that line the colon.  It also feeds pathogenic bacteria that live in the bowel, colon included, and gives them a selective advantage.  So, in view of the research, a diet plan for ulcerative colitis should, in my opinion, limit the dietary intake of iron.  Let’s throw in another quotation just to underscore the seriousness of excessive iron exposure.

“Oral iron supplementation renders high fecal iron concentrations.  Since only a fraction of supplemented iron will be absorbed, virtually the entire dose winds up in the distal parts of the bowel.  In an already inflamed bowel, this may reinforce the inflammation by catalyzing production of ROS [reactive oxygen species] . . . .”  (Erichsen et al., 2003, emphasis added)

Since you seem to be no stranger to trouble, unfortunately, your ulcerative colitis may be complicate by anemia.  Anemia in this situation is not likely due to limited intake of dietary iron; rather, it is likely due to blood loss combined by an effort of the body to put the brakes on the uptake of iron.  The body, in its wisdom, generates a protein, hepcidin, sent forth (from the liver) to block the uptake of dietary iron from the upper small intestine.  It does this to limit iron availability for bacteria that may be poised to invade or have already invaded.  Eventually, anemia from iron deficiency may develop.  Iron replacement may become necessary.  If intravenous iron replacement is not offered or is not an option, there is a strategy for oral iron supplementation that may limit the damage to the colon caused by iron.  Here it is:

“Although conventional wisdom dictates administration of 200 mg elemental iron daily for correction of IDA [iron deficiency anemia], there is no rationale for using such a high dose of oral iron.  Iron absorption from the GI tract is highly efficient but saturable.  Accordingly, Rimon et al demonstrated that oral iron preparations at doses as low as 15 mg/d could be used to correct iron deficiency.”  (Bayraktar UD, Bayraktar S, 2010, emphasis added)

The low-dose iron replacement strategy exists for good reason:

“In this respect, a single tablet of . . . ferrous sulfate . . . provides more iron than what the intestine is able to absorb in 1 day.  On the other hand, nonabsorbed iron salts can be toxic to the intestinal mucosa, and perhaps, could activate the disease.  High doses of iron may cause diarrhea, which in turn not only impair the quality of life but may also make it difficult to differentiate from IBD relapse.”  (Gisbert and Gomollón, 2008, emphasis added)

So, a low-dose option for iron replacement to correct iron deficiency anemia appears to be in order.  And it may be that one should only supplement with iron once every 3 days.  There is what I call The 3-Day Rule.  I discuss this in my book, More to Consider in the Battle Against Crohn’s, as follows:

“The 3-day rule.  If oral iron is prescribed, perhaps the best strategy is outlined in Uritski et al., 2004.  They recommend, in a strategy aimed at limiting damage to the colon, taking low-dose iron, rather than normal- or high-dose iron, on an every-third-day schedule.  Taking supplementary iron every 3 days will coincide with the ordinary 3-day intestinal epithelial cell turnover rate.  This will minimize exposure to iron by each new generation of epithelial cells.”  (Heyden, 2016)

One positive thing to keep in mind: If you limit meat in your quest to limit dietary sulfur, you are substantially limiting iron for bacterial acquisition and limiting the exposure of iron (and sulfates) to the cells that line the colon.  Less damage can be inflicted.

Iron restriction—limiting iron in excess of one’s need—is clearly an important consideration in ulcerative colitis.  When in excess, iron can harm the cells that line the colon and strengthen the numbers and virulence of pathogenic bacteria.  You need to put the feasibility of dietary and supplemental iron restriction on your list of topics to discuss with your physician.  Limiting your exposure to iron may give you an edge in your battle against ulcerative colitis.  In my view, it is time (past time) to employ iron restriction as a strategy in the battle against this disease.

“Previous studies have shown that a reduction of intestinal iron sulfate content ameliorates the inflammatory activity in the gut lumen and that modification of iron homeostasis exerts anti-inflammatory effects by reducing local radical formation.”  (Weiss, 2013)

 

Omega 6 PUF (Poly Unsaturated Fat) restriction

“At least one study, in a Danish population, found that excessive consumption of omega-6 PUFA increases ulcerative colitis risk by 30%; whereas consumption of docosahexaenoic acid, an omega-3 PUFA, reduced the disease burden by 77%.”  (Brown et al., 2012, emphasis added)

“An increase in IBD [Crohn’s and ulcerative colitis] has been associated with increased dietary intake of omega-6 fatty acids in humans, while IBD patients remain in remission longer when dietary intake of omega-3 fatty acids increases.”  (Ghosh et al., 2013)

Omega-6 polyunsaturated fatty acids (PUFAs), abundant in red meat, almost all cooking oils and margarines, become incorporated in the wall of the cells that line the colon (IBD in EPIC Study Investigators, 2009).  Apparently, from this reservoir, they eventually leave the cell wall, migrate into the interior of the cell, and readily promote the generation of pro-inflammatory molecules with names such as prostaglandins, leukotrienes, and thromboxanes.  Yikes!  (At least it sounds bad.)  The net result is the creation of a chronic pro-inflammatory state in the lining of the colon, believed to contribute to the incidence of ulcerative colitis.  When this issue was carefully studied, the investigators issued the following statement:

“The main finding of this study was more than a doubling of the risk of ulcerative colitis with the highest intake of the dietary omega-6 PUFA, linoleic acid. ” (IBD in EPIC Study Investigators, 2009, emphasis added)    

So, as you can see, a diet formulated to defeat ulcerative colitis should probably be low in the omega-6s.  Accordingly, a drastic decrease in the use of the seed oils (corn, soy, peanut, safflower, cotton seed, sunflower, canola) will be necessary.  Well, there goes margarine, mayo, and most prepared entrees!  (At least in generous amounts.)  Look for foods prepared with olive oil (good luck with that).  The reward: Less inflammation in the cells that line the colon.  But that’s not the only reward.

One study found that omega-6 excess alters the nature of tissues and cells, and this alteration creates a specific host response that favors dysbiosis and allows pathogenic bacteria to thrive.  (Kaliannan et al., 2015)  I discuss this issue in a post entitled, Have You Fed Your Pathogens Today.  Be sure to check it out.

 

Note: In the quotations used in this section, I took the liberty of changing the terminology used in order to provide consistency and to use terms you are more likely to be familiar with.  Hence, if an author used n-6 or v-6 to refer to the omega-6 fatty acids, I inserted omega-6 in its place.

 

Plant-based, natural foods dieting

It should be clear by now that a plant-based, natural foods diet is the best approach for limiting sulfur, limiting iron availability, and limiting the omega-6 fatty acids in your life.  Get up to speed on vegetarianism!  Say your goodbyes to burgers and fries.  And to do things right, you will need to limit the omega-6-rich seed oils, often high in vegetarian foods.  Limiting factory-prepared foods will help in this regard.  Use olive oil or butter from grass-fed cows in your vegetarian entrée preparation.  Eat fresh fruit as tolerated.  Limit or eliminate dried fruit (and nuts) preserved with sulfites.  These are just a few of the things to keep in mind as you diet for success.   And on a natural foods diet, foods prepared by you or someone who loves you, will reduce your exposure to other evils found in the Western diet such as carrageenan (high in sulfur), other emulsifiers (that may degrade the lining of the bowel and increase concentrations of bad bacteria), and various additives like preservatives, microparticles, and artificial sweeteners—all known to be harmful to people like you and people like me.  (I’m dropping hints all over the place!)

I’ll be nice and let you eat a little meat from time to time, to satisfy the carnivore within.  A lot of vegetables, tolerable fruits and berries, and a little meat perhaps once a week—Hey, that sounds a lot like the most effective diet for IBD ever devised!  The diet in question is far more effective than drug therapy alone to induce and maintain remission (at least for Crohn’s).  It is called The Semi-Vegetarian Diet.  I cover it in a post entitled, Crohn’s Disease: Finding a Way Out Japanese Style.  (Chiba et al., 2010)  You, the ulcerative colitis patient, could certainly benefit from reading it.

Be aware, vegetables may be a problem for the ulcerative colitis patient.  The fiber and carbohydrates in vegetables may be problematic.  To work around these issues, an excellent protocol has been devised.  The diet is called The IBD Anti-Inflammatory Diet (IBD-AID).  On page 4 of the article featuring this diet, you will find a handy chart.  The chart with its dos and don’ts, as well as the tips scattered throughout the article, will help you deal with problems associated with vegetables.  Read this paper and print out the protocol.  Share it with your physician.  The link is built into the title below.

An Anti-Inflammatory Diet as Treatment for Inflammatory Bowel Disease:    A Case Series Report (Olemdzki et al., 2014)

I think I can bring this article to a close, now that you have watched the videos and read the above paper as well as the posts mentioned in this presentation.  And this I know: Diet for success is not easy.  It is work.  You may even need professional help pulling it off.  But it may have its rewards.  How does remission sound?

 

Related Posts

http://impactofvitamind.com/have-you-fed-your-pathogens-today2/

http://impactofvitamind.com/crohns-disease-finding-a-way-out-japanese-style/

 

References

Aamodt G, Bukholm G, Jahnsen J, Moum B, Vatn MH 2008 The Association Between Water Supply and Inflammatory Bowel Disease Based on a 1990–1993 Cohort Study in Southeastern Norway. Am J Epidemiol. 168:1065–1072

Baumgart DC, editor 2012 Crohn’s Disease and Ulcerative Colitis: From Epidemiology and Immunobiology to a Rational Diagnostic and Therapeutic Approach. Springer Science & Business Media. Feb 2

Baytraktar UD, Bayraktar S 2010 Treatment of Iron Deficiency Anemia Associated with Gastrointestinal Tract Diseases. World J Gastrointerol. June 14; 16(22):2720–2725

Brown K, DeCoff, D, Molcan E, Gibson DL 2012. Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Disease. Nutrients. Aug 21; 4(8):1095–1119

Chiba M, Abe T, Tsuda H, Sugawara T, Tsuda S, Tozawa H, Fujiwara K, Imai H 2010 Lifestyle-Related Disease in Crohn’s Disease: Relapse Prevention by a Semi-Vegetarian Diet. World J Gastroenterol. May 28; 16(20):2484–2495

Erichsen K, Hausken T, Ulavik RJ, Berstad A, Berge RK 2003 Ferrous Fumarate Deteriorated Plasma Antioxidant Status in Patients with Crohn Disease. Scand J Gastroenterol. 5:543–450

Gisbert JP, Gomollón F 2008 Common Misconceptions in the Diagnosis and Management of Anemia in Inflammatory Disease. American Journal of Gastroenterology. 103:1299–1307

Ghosh S, DeCoffe D, Brown K, Rajendiran E, Estaki M, Dai C, Yip A, Gibson DL 2013 Fish Oil Attenuates Omega-6 Polyunsaturated Fatty Acid-Induced Dysbiosis and Infectious Colitis but Impairs LPS Dephosphorylation Activity Causing Sepsis. PloS one. Feb 6; 8(2):e55468

IBD in EPIC Study Investigators 2009 Linoleic Acid, a Dietary n-6 Polyunsaturated Fatty Acid, and the Aetiology of Ulcerative Colitis: A Nested Case–Control Study within A European Prospective Cohort Study. Gut. Dec 1; 58(12):1606–1611

Jowett SL, Seal CJ, Pearce MS, Phillips E, Gregory W, Barton JR, Welfare MR 2004 Influence of Dietary Factors on the Clinical Course of Ulcerative Colitis: A Prospective Cohort Study. Oct 1; 53(10):1479–1484

Khalil NA, Walton GE, Gibson GR, Tuohy KM, Andrews SC 2014 In Vitro Batch Cultures of Gut Microbiota from Healthy and Ulcerative Colitis (UC) Subjects Suggest That Sulphate-Reducing Bacterial Levels Are Raised in UC and by a Protein-Rich Diet. International Journal of Food Sciences and Nutrition. Feb 1; 65(1):79–88

Kiliannan K, Wang B, Li XY, Kim KJ, Kang JX 2015. A Host-Microbiome Interaction Mediates the Opposing Effects of Omega-6 and Omega-3 Fatty Acids on Metabolic Endotoxemia. Scientific Reports. 5

Kortman G AM, Raffatellu M, Swinkels DW, Tjalsma H 2014 Nutritional Iron Turned Inside Out: Intestinal Stress from a Gut Microbial Perspective. FEMS Microbial Rev. 38:1202–1234

Kushkevych IV 2014 Etiological Role of Sulfate-Reducing Bacteria in the Development of Inflammatory Bowel Diseases and Ulcerative Colitis. American Journal of Infectious Diseases and Microbiology. Jan 23; 2(3):63–73

Kushkevych I, Kollar P, Suchy P, Parak T, Pauk K, Imramovsky A 2015 Activity of Selected Salicylamides against Intestinal Sulfate-Reducing Bacteria. Neuroendocrinology Letters. Jan 1; 36:106–113

Olendzki BC, Silverstein TD, Persuitte GM, Ma Y, Baldwin KR, Cave D 2014 An Anti-Inflammatory Diet as Treatment for Inflammatory Bowel Disease: A Case Series Report. Nutrition Journal. Jan 16; 13(1):5

Ouwehand AC, Salminen S, Roberts PJ, Ovaska J, Salminen E 2003 Disease-Dependent Adhesion of Lactic Acid Bacteria to the Human Intestinal Mucosa. Clinical and Diagnostic Laboratory Immunology. Jul 1; 10(4):643–646

Pitcher MC, Cummings JH 1996 Hydrogen Sulphide: A B  acterial Toxin in Ulcerative Colitis? Gut. Jul 1; 39(1):1–4

Uritski R, Barshack I, Bilkis I, Ghebremeskel K, Reifen R 2004 Dietary Iron Affects Inflammatory Status in a Rat Model of Colitis. J. Nutr. 134:2251–2255

Weiss G 2013 Intestinal Irony: How Probiotic Bacteria Outcompete Bad Bugs. Cell Host & Microbe. 14; July 17; 14:3–4

Heyden EL 2016 More to Consider in the Battle Against Crohn’s. Impact Health Publishing. Spokane, WA. USA

Mutlu EA, Gor N 2008 To Diet or Not If You Have Inflammatory Bowel Disease. Expert Review of Gastroenterology & Hepatology. Oct 1; 2(5):613–616

Tilg H, Kaser A 2004 Diet and Relapsing Ulcerative Colitis: Take Off the Meat? Gut. 53:1399–1404

Weinstock JV, Elliott DE 2008 Helminths and the IBD Hygiene Hypothesis. Inflammatory Bowel Diseases. 15(1):128–133

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care. It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein. The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy. This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician. The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the resources that are herein recommended.

 

 

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved

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So Tell Me . . . What Are You Doing to Prevent Breast Cancer?

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Jun 022017
 

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By Eugene L. Heyden, RN

This needs to end.  One in eight women will deal with breast cancer at least once in their lifetime.  And you never know, the incidence of breast cancer may be on the rise.  As a post-surgical recovery nurse, I see it almost every day in my nursing practice.  I wish so many did not have to be so brave.

In the earliest days of civilization, breast cancer was exceedingly rare.  In ancient Egypt, a mummy or two may have contracted the disease (before they became mummies), but that was about it.

With the passage of time, the incidence of breast cancer steadily increased.  Of course, until modern times, most people died well before their fifties and sixties, and seldom made it to their eighties or nineties.  And if they did make it that far, they had to cheat by skipping their seventies altogether.  But times they have changed.  Thankfully, we are now living longer.  The down side: longevity has emerged as a major risk factor in the development of breast cancer.

A review of the literature reveals a host of breast cancer risks, so many that it makes one wonder why breast cancer is not more common than it is.  Reproductive factors appear to be the most relevant.  “Epidemiological studies indicate sexual history as the most important risk factor for breast cancer.”  (Anguiano and Aceves, 2011)  More specifically,

“Established risk factors that increase the likelihood of developing breast cancer include age, family disposition, early menarche, late menopause, age at first childbirth, no breast feeding, benign mammary lesions, and hormone replacement therapy.”  (Gerber et al., 2003)  

The above quotation suggests that something you want, something you need, namely estrogen, is an important player in the development of breast cancer.  We will visit this association a time or two during the course of our conversation.

Obviously, most of the reproductive-related risk factors mentioned above are not subject to change.  But there are risks for developing breast cancer that are.  The modifiable risk factors include meat consumption, with a higher risk associated with meat prepared “well-done”—the byproducts created are carcinogenic.  Modifiable risk factors also include physical inactivity and obesity (Gerber et al., 2003).  With respect to physical activity, surprisingly . . .

“A retrospective study of 1945 physically active and 1995 physically inactive female college students revealed that, after 16 years, athletes had a 40% decrease in breast cancer risk, which increased to 80% by the age of 45, and this effect is still detectable in the postmenopause.”  (Gerber et al., 2003, emphasis added)   

Dietary factors identified to increase the risk of breast cancer include fried and grilled foods, due to the carcinogens produced.  There is more.  Excessive caloric consumption, and the excessive consumption of saturated fats, sugar, alcohol, “significantly correlated with an increased risk of developing breast cancer.”   (Gerber et al., 2003)

In view of the above, consider this:

“It is widely accepted that breast cancer development is a multifactorial process with very limited impact of isolated single factors.”  (Gerber et al., 2003)

The above statement clearly justifies a battle plan against breast cancer that includes reducing one’s exposure to as many risk factors as reasonably possible.  For you, certain life-style changes may be in order.

Before we move on, smoking needs to be addressed.  Exposure to the carcinogens found in tobacco smoke substantially increases an individual’s risk for contracting breast cancer.  “Tobacco smoke contains at least 20 chemical compounds that induce mammary cancers in rodents.”  (Gaudet et al., 2013)   Furthermore, “Women who smoke have detectable smoking metabolites in their breast fluid.”  (Gaudet et al., 2013).   It gets worse.  The carcinogens in cigarette smoke can bind with specific segments of DNA associated with breast cancer risk (Gaudet et al., 2013).  This is certainly not good news.  Add smoking to the habitual consumption of alcohol, and the risk of breast cancer is further elevated (Gerber et al., 2003; Reynolds et al., 2004).  Smoking.  Drinking.  Both can cause a lot of harm.  Best stay away.

We have briefly reviewed the breast cancer risk factors that perhaps receive the most attention.  We should certainly take notice—and concerted efforts to modify one’s lifestyle to reduce exposure to the various breast cancer risks is a wise course of action.  But we really need to get down to business.  There are breasts to save.  There are lives to save.  How does a 40%, 50%, or perhaps up to a 70% reduction in breast cancer risk sound?  Sounds good to me!  Sounds like we need to talk about vitamin D.

 

Vitamin D deficiency

“In the 1980s and 1990s, several observations suggested that living at higher latitudes increased the risk of developing and dying of colon, prostate, breast, and several other cancers.”  (Holick and Chen, 2008)

“Ecological studies have associated high levels of sunlight exposure with low breast cancer incidence and mortality rates.”  (Cui and Rohan, 2006)

Stemming from observations that breast cancer occurs more frequently in those who have limited exposure to the sun, a new branch of research emerged and has yielded some very important insights into the actions of vitamin D and its role in preventing breast cancer, as follows . . .

First, vitamin D is not a true vitamin.  It is a steroid hormone.  Once it is transformed by tissues and cells into its active form (1,25(OH)2D), vitamin D has something important to do.  Regulating genes is something important to do.

“The local production of 1,25(OH)2D in non-calcium regulating tissues such as the colon, prostate, and breast is thought to be for the purpose of regulating up to 200 genes, which helps to control cell growth and cellular differentiation and may be responsible for decreasing the risk of the cells being transformed into a malignant state.”  (Holick and Chen, 2008)

Second, vitamin D assists in the quiet disposal of aging, damaged breast cells, regulating the events that encourage them to commit suicide in a manner that renders them harmless and rapidly nonexistent.  (Shao et all., 2012)  Say goodbye to the cancerous and the precancerous breast cell.  You won’t miss them.

Third, vitamin D promotes DNA repair.  “Vitamin D enhances the expression of DNA repair genes . . . thereby promoting effective DNA double-strand break (DSB) repair, protecting cells from DNA damage and stress and consequently, carcinogenesis.”  (Kitagishi et al., 2013)  A cell with repaired DNA is less likely to become a cancer cell.

Fourth, vitamin D reduces local inflammation in the breast, simply because vitamin D deficiency increases local inflammation in the breast (Shao et all., 2012).  It’s that simple.  “Chronic inflammation is believed to contribute to the development and progression of breast cancer.”  (Pierce et al., 2009)

Fifth, vitamin D downregulates the estrogen receptor.  (Shao et al., 2012)  This is obviously good news.  The active form of vitamin D suppresses the estrogen pathway by reducing the expression of the gene coding aromatase, the enzyme that converts androgens to estrogens.”  (Shao et all., 2012, emphasis added)  More good news: Active vitamin D “downregulates estrogen receptor (ER)-α, the receptor that mediates the actions of estrogen.”  (Shao et al., 2012, emphasis added)

And finally, if the worst happens—a breast cell becomes transformed into a cancer cell—vitamin D inhibits the formation of a vascular supply that will allow the cancer cell to thrive and continually divide.  It also blocks the cellular events that allow a cancer cell to metastasize.  (see Shao et al., 2012)

With everything vitamin D has to offer in the battle against breast cancer, aren’t you at least a little surprised, possibly outraged, so little attention is paid to vitamin D in the battle against breast cancer?  Vitamin D wants to save you from this disease.  What is standing in the way?

Unfortunately, our society is standing in the way.  The knowledge we lack, the lifestyle we live, the actions we fail to take, the research we set aside, a medical profession seemingly unaware of the danger, allows vitamin D deficiency to exist and persist.  It is very wide spread.  It is an epidemic!  This unfortunate state of affairs places people like you and people like me at great risk of a variety of diseases, breast cancer included.  You are probably vitamin D deficient right now, and don’t even know it.

Here is a test:  Are you achieving a cumulative total of 1 to 2 hours of sun exposure each week, between 10 AM and 3PM (April through September), clothed just enough to be decent?  Yes/No?  Do you take a multivitamin containing vitamin D and do you drink 30 to 40 glasses of vitamin D-fortified milk per day?  Yes/No?  Do you take thousands of IUs of supplemental vitamin D per day (not hundreds, as is the current recommendation)?   Yes/No?  If you answered yes to any of the above, you are likely getting enough vitamin D and I can take you off my list of people to worry about.  Be aware, realistically, you can’t eat enough walrus blubber or sardines to achieve or maintain vitamin D sufficiency.  Believe me, I’ve tried!  So, forget diet as the path to vitamin D sufficiency.  It doesn’t work.  The amount of vitamin D we ordinarily obtain in our diet only helps us squeak by.  What, then, should you consider?

If you are serious about breast cancer prevention, ask your physician to check your vitamin D level.   Do not take “No” for an answer.  Pay for the blood test out of pocket, if need be.  (About 50 bucks, and well worth it.)  The results obtained will determine if you are vitamin D deficient, how deficient you are, and will help define the steps necessary to help you achieve and maintain a respectable degree of vitamin D sufficiency, and be better protected from breast cancer.  “So tell me,” you ask, “what does a ‘respectable degree of vitamin D sufficiency’ look like?”

In a study conducted in Italy, women with a vitamin D level greater than 40 ng/mL demonstrated a 40% reduction of breast cancer risk (Crew et al., 2011).

A study conducted in New York State demonstrated a 50% reduction in breast cancer risk in subjects who were post-menopausal and maintain a vitamin D level greater than 40 ng/mL (Crew et al., 2011).  Vitamin D is obviously powerful stuff, so it wouldn’t surprise me at all if a greater than 40% to 50% reduction in breast cancer risk can be achieved . . . somewhere.

A large population-based study in Germany found about a 70% reduction in breast cancer risk with a vitamin D level greater than 30 ng/mL in post-menopausal women (Crew et al., 2011).

One final study to add to the mix.  This one is based on a combined analysis of two separate studies.  The investigators report: “Women with 25(OH)D concentrations ≥ 40 ng/ml had a significantly lower risk of cancer (~70%) compared to women with concentrations <20 ng/mL.”  (McDonnell et al., 2016, emphasis added)

Are you getting the message?  Only a vitamin D level will tell you where you stand.  And it takes a vitamin D level of 30 ng/mL, 40 ng/mL, perhaps more, to achieve a robust level of breast cancer protection, the level of breast cancer protection you deserve.  This will not be accomplished by the little vitamin D found in diet, a little vitamin D tucked into a multivitamin, a little vitamin D found in a few glasses of milk per day, and the little vitamin D generated by casual sunlight exposure.  I will show you why.

In general, for every 100 IU of vitamin D, the serum 25OHD2 level increases by ~ 1.0 mg/mL.”  (Shao et al., 2012)  To put things into perspective, a multivitamin tablet containing 600 IU vitamin D, will create or support a vitamin D level of 6 ng/mL.  Add three glasses of milk per day (100 IU/glass) and now you’re up to 9 ng/mL.  I’ll be generous and allow you causal sunlight exposure.  If you’re lucky, the vitamin D created by casual sunlight exposure during the right time of day and season of the year will add perhaps 10 ng/mL to your vitamin D level.  Now you’re up to about 20 ng/mL.  Congratulations!  You are vitamin D deficient, and not well protected against breast cancer.

Vitamin D levels >20ng/mL but <30ng/mL are considered insufficient.  Data from observational studies have suggested that the optimal level of 25(OH)D for breast cancer prevention is probably 40–60 ng/mL.”  (Shao et al., 2012, emphasis added)

I guess you have something important to do.  Promptly have your vitamin D level checked.  Follow up by taking the steps necessary to achieve and maintain a “respectable” degree of vitamin D sufficiency.  This will take regular sunlight exposure and/or substantial vitamin D supplementation.  Dietary sources of vitamin D and casual sunlight exposure are helpful but just not enough.  For me, it takes 8,000 IU of vitamin D/day to keep my vitamin D level in the 40–60 ng/mL range.   You may not need this level of supplementation.  You may need 2,000 IU/day, 4,000 IU/day, or perhaps 6,000 IU/day to maintain a vitamin D level in the 40–60 ng/mL range.  If you are significantly overweight, you may need more, a lot more—due to the fact that the more fat you have, the more vitamin D you place in storage.  A physician can easily sort this all out and get you (and keep you) on the right track.

Since I spent so much time on vitamin D in this article, I will need to be brief as we continue.  Next, we will discuss iodine deficiency.  There is danger here.

 

Iodine deficiency

“It has been demonstrated that iodine contributes to the maintenance of the normal integrity of the mammary gland.”  (Aceves et al., 2005)

“Iodine plays a role in the development and maintenance of healthy breast tissue (expanding after puberty) and in breast remodeling during lactation, and pregnancy.”  (Rappaport, 2017)

“Experimental findings showing the ability of iodine or iodine-rich seaweed to inhibit breast tumor development is supported by the relatively low rate of breast cancer in Japanese women who consume a diet containing iodine-rich seaweed.”  (Smyth, 2003)

A Japanese woman, eating the traditional Japanese diet, maintains an “exceptionally low” risk of developing breast cancer (Rappaport, 2007).  The reason?  Her diet includes generous amounts of iodine due to the consumption of seaweed, which on average supplies 5,280 µg of iodine per day (Anguiano and Aceves, 2011).  Take the same Japanese woman and move her to the USA, allow her to adopt the Western diet, and her iodine intake dramatically drops to approximately 200 µg per day (Anguiano and Aceves, 2011).  As a result, her “exceptionally low” breast cancer risk vanishes into thin air (Anguiano and Aceves, 2011).  She could easily find herself among the one in eight.

Unfortunately, we have not come to terms with the fact that we, in the USA, are generally iodine deficient.  This causes a lot of harm—including pregnancy loss, neurological damage to our offspring, and, of all things, a greater risk of breast cancer.  And there are many reasons why we are deficient in iodine.   I only have time to mention one.

One reason why iodine deficiency is prevalent in the USA is that we allow bromine, “a suspected carcinogen,” to be added to certain beverages and commercial bakery products.  (This additive has been banned in many countries due to a variety of health concerns.)  Bromine is evil because it interferes with the uptake of iodine in the thyroid gland and probably in the breast. (see Rappaport, 2017)

One team of investigators, studying the role iodine deficiency plays in the development of breast cancer, demonstrated in laboratory animals “a potent protective effect (70%)” on breast cancer following exposure to a potent carcinogen (Aceves et al., 2005, emphasis added).

Another piece of evidence that iodine has a protective effect against cancer development, is as follows:

“Iodine deficiency is associated with fibrocystic breast disease, which can be effectively treated or prevented with iodine supplementation. Fibrocystic breast disease affects at least 50% of women of child-bearing age and is associated with an increased risk of developing breast cancer.  (Rappaport, 2017)

Clearly, iodine sufficiency should be part of your personal strategy to prevent breast cancer.  There is no reliable laboratory test available to determine if you are iodine deficient, so if you follow the Western diet or if you are a vegetarian or vegan, assume that your iodine status is marginal at best.  To become iodine sufficient, the recommendation of the experts is to include more iodine-rich foods in your diet and/or to supplement responsibly.  Your physician can advise.

I should point out that supplementing with iodine is not without some risk.   Occasionally, iodine supplementation can unmask an underlying thyroid hormone abnormality, creating symptoms that should promptly be reported (Teng et al., 2011; Pearce et al., 2013).   That being said, it certainly appears that the benefits of iodine supplementation far outweigh the risks.  Please consider placing iodine supplementation on your list of things to strongly consider in your quest to lower your breast cancer risk.  The evidence for a protective effect is very strong.

One more topic to discuss (briefly), then I’ll let you go.

 

Iron excess

“Iron overload, which was previously uncommon, has become more common in the United States than iron deficiency.”  (Moore et al., 2009)

“In humans, elevated body iron storage has been shown to increase the risk of several cancers including breast cancer.”  (Liehr and Jones, 2003)

“Both estrogen and iron are considered cancer promoters.”  (Jian et al., 2011)

When it comes to breast cancer, excess dietary iron intake is not good news.  “In humans, elevated body iron storage has been shown to increase the risk of several cancers including breast cancer.”  (Liehr and Jones, 2001)  Surprisingly, estrogen does not act alone, it works hand in hand with iron in the development of breast cancer (Jian et al., 2011; Liehr and Jones, 2001).  And it certainly appears that the more iron accumulation that occurs within the breast, over time, the greater challenges the breast cells face, which leads to a greater breast cancer risk.  No one else is telling you this, so I guess it’s up to me.

Our society is making one big mistake, and has for quite some time.  We expose ourselves to iron in amounts far greater than our need.  Sure, an individual can be low in iron, but not our population as a whole.   So, to lend a helping hand to the children who may need extra iron to meet growth needs, or to help out those who need to replace iron due to iron loss during menstruation, we supplement and we fortify.  But this is not without risk.

“Iron supplements are ingested by a sizable portion of the population in the Unites States along with their daily vitamin pills or as a medication for real or suspected iron deficiency states. In addition, many foods are enriched with iron, including bread, cereal, other flour products and baby formulas.  This iron supplementation is ingested in addition to the high consumption of red meat in the United States and other Western societies, which already provides a high basal level of dietary iron.  In this way, the average American diet provides a positive daily iron balance.”  (Liehr and Jones, 2003)

So, in a well-thought-out strategy to lower your breast cancer risk, it may be wise to limit dietary intake of foods high in iron, avoid taking supplements that contain iron (unless specifically directed by your physician), and donate blood on a regular basis.  Donate blood?!!  Yes.  This is the best method available to reduce tissue iron stores, particularly suitable to address the problem of iron accumulation that normally occurs postmenopausal.  (Before then, you donated blood on a monthly basis, if you will recall . . . all the misery.)  There is not a lot in the literature that supports blood donation as a strategy for breast cancer prevention, but it can only help.  And even if it doesn’t make that big of a difference in reducing your risk of breast cancer, look at all the people you will be helping.  With regular blood donation, you might even lower your risk of cardiovascular disease, neurodegenerative disease, and other forms of cancer.  One more thing to mention along these lines . . .

Antioxidant supplementation have been shown to help reduce the risk of breast cancer associated with elevated iron intake.  According to one study, “a direct association between processed meat intake (rich in heme iron) and breast cancer risk, and this association was no longer significant in the group supplemented with antioxidants.”  (Diallo et al., 2016)

 

Conclusion 

Before you read this article, you may have thought that little if anything could be done to lower your breast cancer risk.  Perhaps now you know differently, and realize that by taking a few simple steps you can substantially reduce your risk of one of the greatest evils of our time.  Don’t be found among the one in eight.

 

Related Post

What Is This?  (It Might Have Something to Do with Vitamin D)

 

Highly recommended

Everything You Need to Know About Your Breasts Before and After Pregnancy

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care. It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein. The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy. This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician. The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the resources that are herein recommended.

 

References

Aceves C, Anguiano B, Delgado G 2005 Is Iodine a Gatekeeper of the Integrity of the Mammary Gland? Journal of Mammary Gland Biology and Neoplasia. Apr 1; 10(2):189–196

Anguiano B, Aceves C 2011 Iodine in Mammary and Prostate Pathologies. Current Chemical Biology. Sep 1; 5(3):177–182

Crew KD, Gammon MD, Steck SE, Hershman DL, Cremers S, Dworakowski E, Shane E, Terry MB, Desai M, Teitelbaum SL, Neugut AI 2009 Association Between Plasma 25-Hydroxyvitamin D and Breast Cancer Risk. Cancer Prevention Research. Jun 1; 2(6):598–604

Cui Y, Rohan TE 2006 Vitamin D, Calcium, and Breast Cancer Risk: A Review. Cancer Epidemiol Biomarkers Prev 15(18):1427–1437

Diallo A, Deschasaux M, Partula V, Latino-Martel P, Srour B, Hercberg S, Galan P, Fassier P, Guéraud F, Pierre FH, Touvier M 2016 Dietary iron intake and breast cancer risk: modulation by an antioxidant supplementation. Oncotarget. Oct 12; 7(48):79008–79016

Gaudet MM, Gapstur SM, Sun J, Diver WR, Hannan LM, Thun MJ 2013 Active Smoking and Breast Cancer Risk: Original Cohort Data and Meta-Analysis. Journal of the National Cancer Institute. Feb 28: djt023

Gerber B, Müller H, Reimer T, Krause A, Friese K 2003 Nutrition and Lifestyle Factors on the Risk of Developing Breast Cancer. Breast Cancer Research and Treatment. May 1; 79(2):265–276

Holick MF, Chen TC 2008 Vitamin D Deficiency: A Worldwide Problem with Health Consequences. The American Journal of Clinical Nutrition. Apr 1; 87(4):1080S–1086S

Jian J, Yang Q, Dai J, Eckard J, Axelrod D, Smith J, Huang X 2011 Effects of Iron Deficiency and Iron Overload on Angiogenesis and Oxidative Stress—A Potential Dual Role for Iron in Breast Cancer. Free Radical Biology and Medicine. Apr 1; 50(7):841–847

Kitagishi Y, Kobayashi M, Matsuda S 2013 Defective DNA Repair Systems and the Development of Breast and Prostate Cancer (Review). International Journal of Oncology. Jan 1; 42(1):29–34

Liehr JG, Jones J 2001 Role of Iron in Estrogen-Induced Cancer. Current Medicinal Chemistry. Jun 1; 8(7):839–49

McDonnell SL, Baggerly C, French CB, Baggerly LL, Garland CF, Gorham ED, Lappe JM, Heaney RP 2016 Serum 25-Hydroxyvitamin D Concentrations ≥ 40 ng/mL Are Associated with > 65% Lower Cancer Risk: Pooled Analysis of Randomized Trial and Prospective Cohort Study. PloS one. Apr 6; 11(4):e0152441

Moore AB, Shannon J, Chen C, Lampe JW, Ray RM, Lewis SK, Lin M, Stalsberg H, Thomas DB 2009 Dietary and Stored Iron as Predictors of Breast Cancer Risk: A Nested Case-Control Study in Shanghai. International Journal of Cancer. Sep 1; 125(5):1110–1117

Pearce EN, Anderson M, Zimmerman MB 2013 Global Iodine Nutrition: Where Do We Stand in 2013? Thyroid. 23(5):523–528

Pierce BL, Ballard-Barbash R, Bernstein L, Baumgartner RN, Neuhouser ML, Wener MH, Baumgartner KB, Gilliland FD, Sorensen BE, McTiernan A, Ulrich CM 2009 Elevated Biomarkers of Inflammation Are Associated with Reduced Survival Among Breast Cancer Patients. Journal of Clinical Oncology. May 26; 27(21):3437–3444

Rappaport J. 2017 Changes in Dietary Iodine Explains Increasing Incidence of Breast Cancer with Distant Involvement in Young Women. Journal of Cancer. 8(2):174–177

Reynolds P, Hurley S, Goldberg DE, Anton-Culver H, Bernstein L, Deapen D, Horn-Ross PL, Peel D, Pinder R, Ross RK, West D 2004 Active Smoking, Household Passive Smoking, and Breast Cancer: Evidence from the California Teachers Study. Journal of the National Cancer Institute. Jan 7; 96(1):29–37

Shao T, Klein P, Grossbard M 2012 Vitamin D and Breast Cancer. The Oncologist. Jan 1; 17(1):36–45

Smyth PP 2003 The Thyroid, Iodine and Breast Cancer. Breast Cancer Research. Jul 29; 5(5):235–238

Teng X, Shan Z, Chen Y, Lai Y, Yu J, Shan L, Bai X, et al 2011 More Than Adequate Iodine Intake May Increase Subclinical Hypothyroidism and Autoimmune Thyroiditis: A Cross-Sectional Study Based on Two Chinese Communities with Different Iodine Intake Levels. European Journal of Endocrinology 164:943–950

 

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

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Coping with the Mental and Emotional Tolls of Cancer

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Jun 012017
 

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By Katybeth Dee

Dealing with a cancer diagnosis and any subsequent treatments and procedures can be overwhelming.  Whether you’re a cancer patient who was just diagnosed or you’re a cancer survivor in remission, you must deal with mental and emotional toll of the diagnosis, treatment, and recovery. Fortunately, there are healthy and meaningful ways to cope.

Activities You Enjoy

Spending some time writing about your cancer journey is another way to cope.  You can write an entire memoir, write poetry, or take a few notes throughout the day. No matter how involved you are, just engaging in the writing process will benefit you.  If words aren’t your cup of tea, you can paint, write music, or make any other artistic expression.  An artistic outlet will allow you to better comprehend and accept your diagnosis, treatment, and recovery.

Writing and artistic expressions shouldn’t be seen as a distraction from cancer.  Instead, they’re a rewarding and meaningful way to analyze everything you are feeling and going through.  Furthermore, it’s inexpensive and doesn’t require physical exertion, so you can use it as a tool even on one of your worst days.

Yoga and Meditation

As the Yoga Journal states, “While it’s not a cure for cancer, yoga enhances physical and emotional wellness and brings a peace many patients had thought they’d lost forever.”  Yoga, meditation, and other relaxation techniques are ways to quiet your mind and body, which allow them to heal.  Relaxation techniques reduce stress as well, which is important because studies have shown that stress can contribute to the development and progress of cancer.

Yoga can increase strength, reduce pain, and improve the overall quality of life.  A yoga session may also include guided relaxation, meditation, and visualization – all things that further promote relaxation and healing.  Furthermore, it’s a great option for cancer patients and survivors because it’s low impact and has a low risk of injury.

Exercise

If you’re feeling up to it, getting some low-impact exercise is good for you. Experts agree that exercise is beneficial for most cancer patients and survivors.  In general, if care is taken and professional advice is followed closely, there’s little risk.  Exercising can boost your energy levels and improve your immune system, helping your body to better deal with cancer and cancer treatments.

Exercise can help improve many of the side effects of cancer and cancer treatments, including anemia, nausea, loss of appetite, fatigue, anxiety, depression, and body weight and composition changes.  You should aim for about 20 minutes of moderate-intensity exercise four or five days a week. As previously mentioned, yoga is one option.  You can also ride a bike, swim, or take your dog for a walk. Dogs also have the added benefits of improving your overall health, boosting your mood, reducing stress, and providing great company.  If you want to take advantage of those great benefits but don’t have a dog, consider finding ways to spend time with someone else’s, either as a dog sitter or the neighborhood dog walker.

Speaking with a Professional

Finding out you have cancer, going through treatment, and even living as a cancer survivor all produce levels of worry and anxiety.  For many people, simply talking about their feelings helps to relieve worry and anxiety.  Choosing the right person to talk with is important. It can be a good friend, a family member, or a religious person, such as a minister.  Many people find speaking with a licensed mental health professional – such as a social workers, psychologists, and psychiatrists – to be comforting and beneficial.

Not only are they expert listeners, they also can teach you valuable coping skills to use outside of your meetings.  “Even one session with a licensed mental health professional can often help you and your family focus on what matters most,” says the American Cancer Society.  If you need help locating a mental health professional, ask your cancer team, family doctor, or insurance company for recommendations.

A cancer diagnosis and the treatments that follow may be the most difficult things you ever do in your life.  Continuing life in remission can be difficult as well. Finding healthy and meaningful ways to cope with the mental and physical challenges of cancer can help you live a better and longer life.

 

 

About

Katybeth Dee created SelfExam.org after her sister received a cancer diagnosis at a young age.  Her aim is to spread awareness about cancer prevention and she strives hard to offer support to those battling cancer.

 

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

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Multiple Sclerosis: The Next Frontier

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Apr 022017
 

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MS Next Frontier Image

By Eugene L. Heyden, RN       

 

It’s just a matter of time.  Things will click.  The future will arrive.  I hope we don’t have to wait long.  Something unexpected has occurred.

“A growing body of evidence in animal models of MS implicates the gut microbiota [bacteria and the like] in the induction of central nervous system (CNS) autoimmunity.”  (Berer and Krishnamoorthy, 2012)

There is growing suspicion that gut bacteria play a pivotal role in initiating and perpetuating the neuroinflammatory disease known as multiple sclerosis (MS).  In a laboratory model of MS, known as experimental autoimmune encephalomyelitis (EAE), the administration of non-absorbing antibiotics “beginning 1 week prior to sensitization, altered the composition of gut flora and, intriguingly, also ameliorated the development of EAE.”  (Yokote et al., 2008)

That bacteria within the gut could influence a disease process occurring in the brain and spinal cord is, indeed, quite surprising.  In the not too distant past, to even consider this would have been crazy.  But not anymore.  We have learned so much!  Suspicions are giving way to conclusions.

“Certain populations of commensal [normally found] bacteria are capable of attenuating CNS inflammation.  The gut microbiota has the capacity to affect the development of autoimmune central nervous system (CNS) disorders.”  (Kamada et al., 2013, emphasis added)

“Combined, these data indicate that early dysregulation in MS involves an increase in pro-inflammatory and a decrease in anti-inflammatory gut microbiota milieu.”  (Tremlett at al., 2016, emphasis added)  

To further define the role gut bacteria plays in initiating and in sustaining CNS autoimmunity, some very fascinating studies have been performed.

In one study, investigating the role bacteria play in MS, Lavasani and team were able to reverse experimental MS in mice simply by manipulating their gut flora, using a mix of probiotic bacterial strains to accomplish this end.  “We showed that therapeutic treatment with this new probiotic mixture successfully reversed established EAE.”  (Lavasani et al., 2010)  Success in this study was attributed to an expansion of Treg populations and intensifying their anti-inflammatory actions.   So, what is a Treg?  And why is it important?

A Treg is a migratory immune cell that travels to an area undergoing inflammation.  Given the opportunity, Tregs show up in great numbers.  Their job is to calm things down and promote healing at a time when inflammation is no longer necessary and no longer beneficial.  A Treg cell also prevent unnecessary inflammation from emerging, taking hold, or getting out of hand.  Important to our conversation, Tregs play a key role in preventing and resolving autoimmunity.  Autoimmunity, widely believed to be the cause of MS, is an attack on components of self by an individual’s own immune system.  And in MS, the myelin sheath that covers nerves and aids in impulse transmission is under attack.  Damage ensues.  Loss of function follows.  If I had MS, I would want every Treg I could get my hands on and I would immediately put them to work on my behalf.  This immune cell can apparently reverse autoimmunity.  It can promote healing.  It can stimulate remyelination.  It can be your best friend.

In another study . . .

“Our previous and present studies suggest that differing compositions of gut microbiota could regulate the balance between protection and disease induction in MS and may offer a novel therapeutic approach for disease intervention.”  (Ochoa-Repáraz et al., 2010, emphasis added)

In the study quoted above, the investigators found that no particular gut pathogen is required to induce experimental MS or to protect against its development.  Apparently, all that is needed is a disruption in the balance between various microbial species in the gut, a state called dysbiosis, and the disease appears from out of nowhere in mice genetically predisposed to demyelinating disease.  Along these lines, another study, Chen et al., 2016, reports that patients with relapsing-remitting MS have a distinct (and abnormal) gut microbiota profile, and state: “Thus our study is in agreement with earlier reports that MS patients had dysbiosis of fecal microbiota in the gut.”  (Chen et al., 2016)

These two and many other studies strongly suggest that dysbiosis is behind the pathogenesis of MS.  The authors of one study—identifying dysbiosis present in pediatric MS patients—have reached the following conclusion: “Combined, these data indicate that early dysregulation in MS involves an increase in pro-inflammatory and a decrease of anti-inflammatory gut microbiota milieu.”  (Tremlett et al., 2016)  But that is not to say that a particular pathogen is not involved.   There is now compelling evidence for a bacterial trigger.

Rumah et al., 2013, reports the discovery of a bacterium, never before identified in a human subject, present in a woman with active MS.  This bacterium is a variant of a common soil bacterium called Clostridium perfringens, and emits a toxin that can leave the gut, travel to the brain, cross the blood brain barrier, and bind with myelin.  It’s up to no good.  The toxin is known to create demyelinating disease in grazing animals who never see it coming.  Subsequent to the discovery of this unique bacterium present in a MS patient, this team of investigators tested preserved blood and cerebral spinal fluid samples of patients with MS.  Surprisingly, they found prior exposure to this bacterium was 10 times more prevalent in the samples from MS patients than in the samples of healthy controls.  Very intriguing!

As we learn more about the relationship between MS and the gut, possibilities are emerging.  Could therapy directed at the gut, targeting the microbes within it, be the next frontier in the treatment of MS?  Some seem to think so.

“Although epidemiological studies in man connecting the gut commensal [normally found] bacteria with CNS demyelinating disease have not been reported, perhaps due to the complexity of human microbiome, repopulating the gut microbiota . . . may be a reasonable pathway by which to control disease pathogenesis.”  (Ochoa-Repáraz et al., 2011, emphasis added)   

“It is possible that treatment strategies of MS in the future may include therapeutic intervention designed to affect the microbiome such as probiotics, faecal transplantation and delivery of constituents of organisms isolated from the microbiome, although more work is required.”  (Jangi et al., 2016, emphasis added)

 

And then we have the unexpected

Let me assure you, what I am about to share occurred quite unexpectedly, and at a time when little was known about the role gut bacteria play in MS.  Read the following very carefully (maybe again and again):

“In 2001, Borody et al. reported three wheelchair-bound patients with MS treated with FMT [faecal microbiota transplantation] for constipation.  Bowel symptoms resolved following FMT; however, in all cases, there was also a progressive and dramatic improvement in neurological symptoms, with all three patients regaining the ability to walk unassisted.  Two of the patients with prior indwelling urinary catheters experienced restoration of urinary function.  In one patient of the three, follow-up MRI 15 years after FMT showed a halting of disease progression and ‘no evidence of active disease.'”  (Borody et al., 2014, emphasis added)

There is, perhaps, no better way to both favorably and dramatically alter the gut microbiota than by the strategy known as fecal microbiota transplantation (FMT).  An attempt may be made to delete a problematic bacterial species with antibiotics; however, bacterial diversity takes a hit, as many good bacteria die in the process. Unintended consequences may arise.  One may also put forth the effort to increase bacterial diversity with probiotics, creating unfavorable conditions for pathogenic bacteria to thrive and exert their influence—all in an attempt to modify both local and distant immune responses.  But we don’t have all day.  We need to do something decisive, something capable of creating a dramatic and immediate change.

FMT does not fool around.  It is the gift of a complete, new set of bacteria in an instant.  A donor who is disease-free is chosen, things happen, the procedure is performed, and voilà, a diseased person is transformed.

FMT is nothing new.  Its use dates back some 2,000 years.  Today, it has become somewhat mainstream.  In the hospital where I work, we perform FMT quite regularly.  We do it to reduce morbidity and mortality in the battle against C-diff.

C-diff, is a gut infection that kills between 14,000 and 20,000 Americans each year.  However, expect that number to go down dramatically, as FMT is greater than 90% effective in curing this disease and is becoming more popular and more accessible.  And, it handles this infection both promptly and dramatically.  It is a gift.  For some, the gift of life.  As for MS, there may be nowhere else to turn.

For the three individuals mentioned above, FMT was the gift of a new life.  What seemed to be required for them in their individual battle against MS was an instantaneous, dramatic change in the composition of their gut flora, then the healing could begin.  Are you listening?  Listening carefully?  Perhaps in MS, the therapies we currently use are no match for this “force”—the immense influence exerted by a disruptive, abnormal composition of gut bacteria, an influence that can extend to the brain and the spinal cord.  I believe the next frontier in the battle against MS will be to target this force (and not fool around).  In my humble opinion, there is simply no better way to do this than with FMT.  Next, let’s take a quick look at what this FMT business is all about.

In brief, FMT involves careful donor selection and testing to rule out the presence of transmissible diseases in the donor.  Next comes stool collection and processing.  Also needed, of course, is a recipient who is willing to do just about anything to get well.  Somewhere along the line, and at the appropriate time, a blender is plugged in and asked to do something most unusual.

In preparation for FMT, the recipient typically undergoes a bowel prep the day prior to transplantation, and may have recently completed a course of antibiotics.  Antibiotic therapy is utilized in this situation to kill off the bacteria present within the gut to favor the dominance of good bacteria once the gut is recolonized.   In essence, FMT is a treatment modality that ensures that an improper mixture of gut bacteria is promptly replaced by a bacterial community that is regarded as normal and will not contribute to a disease process.

“The main advantage of FMT over other forms of microbial manipulation, for example antibiotics, prebiotics and probiotics, is that FMT provides the full spectrum of microbial organisms from a healthy individual and therefore can treat as yet uncharacterized dysbiotic conditions, while bypassing the need to decipher the complex composition and functional intricacies of the dysbiosis.”  (Borody et al., 2014)

As reported, the three individuals with long-standing MS experienced a dramatic response to FMT, “with all three patients regaining the ability to walk.”  Most notably, in one patient an MRI at 15 years post-FMT “showed a halting of disease progression and ‘no evidence of active disease.’”  (Borody et al., 2014)  Clearly, what happened in the gut did not stay in the gut.  And clearly something unexpected and profound took place . . . and MS vanished (or substantially improved).

Let me leave you with this:

In summary, we have found alterations of the human gut microbiome in MS that correlate with changes in the immune transcriptome and treatment. It is possible that treatment strategies of MS in the future may include therapeutic interventions designed to affect the microbiome such as probiotics, faecal transplantation and delivery of constituents of organisms isolated from the microbiome, although more work is required. In addition, characterization of the gut microbiome in MS may provide biomarkers for assessing disease activity and could theoretically be an avenue to prevent MS in young at-risk populations.  (Jangi et al., 2016, emphasis added)

 

Related Post

Could Preventing Crohn’s be This Easy?

 

Dedication

In loving memory of Jonna Dybdahl-Buell

 

References     

Berer K, Krishnamoorthy G. 2012 Commensal Gut Flora and Brain Autoimmunity: A Love or Hate Affair? Acta Neuropathologic, May 1; 123(5):639–51

Borody TJ, Brandt LJ, Paramsothy S 2014 Therapeutic Faecal Microbiota Transplantation: Current Status and Future Developments. Curr Opin Gastroenterol, Jan 1; 30(1):97–105

Chen J, Chia N, Kalari KR, Yao JZ, Novotna M, Soldan MM, Luckey DH, et al 2016 Multiple Sclerosis Patients Have a Distinct Gut Microbiota Compared to Healthy Controls. Scientific Reports, 6:28484

Jangi S, Gandhi R, Cox LM, Li N, Von Glehn F, Yan R, Patel B, et al 2016 Alterations of the Human Gut Microbiome in Multiple Sclerosis. Nature Communications, Jun 28; 7

Kamada et al 2013 Role of the Gut Microbiota in Immunity and Inflammatory Disease. Nature Reviews Immunology, May; 13:321–335

Lavasani S, Dzhambazov B, Nouri M, Fåk F, Buske S, Molin G, Thorlacius H, et al 2010 A Novel Probiotic Mix Exerts a Therapeutic Effect on Experimental Autoimmune Encephalomyelitis Mediated by IL-10 Producing Regulatory T Cells. PLoS ONE, Feb; 5(2):e9009

Ochoa-Repáraz J, Mielcarz DW, Ditrio LE, Burroughs AR, Begum-Haque S, Dasgupta S, Kasper DL, Kasper LH 2010 Central Nervous System Demyelination Disease Protection by the Human Commensal Bacteroides fragilis Depends on Polysaccharide A Expression. The Journal of Immunology, 185:4101–4108

Ochoa‐Repáraz J, Mielcarz DW, Begum‐Haque S, Kasper LH 2011 Gut, Bugs, and Brain: Role of Commensal Bacteria in the Control of Central Nervous System Disease. Annals of Neurology, Feb 1; 69(2):240–247

Rumah KR, Linden J, Fischetti VA, Vartanian T 2013 Isolation of Clostridium perfringens Type B in an Individual at First Clinical Presentation of Multiple Sclerosis Provides Clues for Environmental Triggers of the Disease. PloS one, Oct 16; 8(10):e76359

Tremlett H, Fadrosh DW, Faruqi AA, Zhu F, Hart J, Roalstad S, Graves J, Lynch S, Waubant E 2016 Gut Microbiota in Early Pediatric Multiple Sclerosis: A Case-Control Study. European Journal of Neurology, Aug 1; 23(8):1308–21.

Yokote et al 2008 NKT Cell-Dependent Amelioration of a Mouse Model of Multiple Sclerosis. Am J Pathol, 173:1714–1723

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care. It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein. The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy. This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician. The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the resources that are herein recommended.

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

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Six Tips for Keeping Your Family Healthy on a Budget

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Feb 282017
 

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Six tips Image twoBy Katybeth Dee

 

Sometimes at the grocery store, it seems like there’s a choice to make: you can either save money and sacrifice nutrition or shop healthy and go over your weekly food budget.  Alas, there’s good news!  Keeping the whole family healthy on a budget is easier than most people realize.  Here are a few tips for those hoping to maximize their health and budgets at the same time:

 

 

  1. Drink water

Water is free, can be found at any establishment, and has zero calories.  It’s OK for you and your little ones to have juice and other specialty drinks every now and then, but look for easy opportunities to cut back. Instead of a soft drink with lunch, pack a (reusable) water bottle.  Drink a glass of water in the morning instead of a glass of juice. Simple switches can have big results.

 

  1. Turn your scraps into supplies

Make your own chicken stock by saving your vegetable scraps in the freezer and using leftover chicken drumsticks or other bones. Stock is an excellent way to turn just about any other ingredients into a meal, so it’s a great thing to have constantly on-hand and replenished.  Got plenty of stock but too many vegetable scraps?  Freeze them to add to a stew or crock pot recipe. Extra ground beef can be frozen to include in meat pies for dinner next week.

 

  1. Make your food count

Want to see major improvements in your family’s nutrition even more quickly?  Simply focus on buying nutritious food and keeping the junk off your shopping list. Fresh and frozen vegetables are going to be your friend in this endeavor, and that’s a good thing.  Vegetables are nutrient-rich, easy to find, and come in so many varieties that, truthfully, you’re bound to find at least one that you like. Fruit is not only healthful, it’s delicious and can do wonders to kick a serious sugar craving.  Try to stick to whichever produce is seasonal when you go shopping—you’ll usually find better deals.

 

If you think your family may revolt without at least a few of their old favorites, limit it to one or two per person. Make healthy, fiscally smart switches where you can.  Greek yogurt with granola can be a cheap, healthy substitution for a pudding cup, and zucchini bread can give you the essence of indulging in a cake or pastry but with fewer calories.

 

  1. Plan and prepare

Over the weekend, decide with your family what meals you’re going to eat each day of the following week.  Don’t forget snacks! Make your shopping list based on this conversation and don’t deviate from it unless you’re making smart substitutions—substituting the ground beef in your lasagna for the ground turkey that’s on sale.

 

After your trip to the store, set aside a few hours each week to prepare the meals together as a family. You can cook some completely ahead of time and freeze or refrigerate them for the next few days, or you can add fresh ingredients the day you make them.

 

  1. Switch your meat for more legumes

Meat—especially fresh meat— tends to be one of the most expensive items we require of most meals.  It can also be one of the easiest healthy, cost-cutting changes you make! Legumes are actually an excellent source of protein, and best of all they’re inexpensive.  That doesn’t mean you have to cut out meat completely.  Cook smaller portions and supplement them with a hearty serving of legumes and your entire family will leave the table satisfied!

 

  1. Get active together

Exercise just isn’t as fun by yourself, so make it a family activity.  Go to the park and hike a trail together or jump into the pool for a game of water basketball.  When your physical fitness becomes a game, you look forward to doing it. Who needs to join an expensive health club when you’ve got a team to keep you on your toes right at home?

 

Eating on a budget doesn’t have to be unhealthy or unappetizing.  Keep these tips in mind and you’ll be on the road to better living!

 

Copyright © 2017 Katybeth Dee

All Rights Reserved

 

Comment

While www.impactofvitamind.com is dedicated to health and wellness, there is also place on this website for articles on lifestyle, in as much as lifestyle can have an impact on an individual’s health.  Katybeth’s article is all about eating well on a budget.  Nevertheless, the suggestions offered will also help one lead a healthier life.

 

About

Katybeth Dee created SelfExam.org after her sister received a cancer diagnosis at a young age. Her aim is to spread awareness about cancer prevention and she strives hard to offer support to those battling cancer.

 

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

 

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So Cute. But I’m So Worried.

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Feb 202017
 

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IMG_1149By Eugene L. Heyden, RN

 

There’s a real story here. I don’t like it at all.  It’s a sad story—and not just a sad story.  It’s a tragedy.

One by one, too many of our precious African American babies are off to a bad start in life.  And I know why.  I will tell you.  Unfortunately, this story is one of those never-ending stories, unless we do something about it.  I have something in mind.

Likely, the story starts before birth.

“It is well known that vitamin D deficiency is prevalent among pregnant women and pregnant women have significantly lower levels of 25(OH)D than nonpregnant control women.  Approximately two in three pregnant women in the United States have suboptimal vitamin D status, with an even higher prevalence among black and Mexican-American women.”  (Lerchbaum and Obermayer-Pietsch, 2012, emphasis added) 

Vitamin D deficiency during pregnancy is fraught with danger.  This danger threatens women of any color, any ethnicity.  But for mothers with darker skin, vitamin D deficiency is a whole lot easier to come by, making the African American pregnancy—and the unborn baby involved—at heightened risk for some very bad things.  I would say fetal loss is a bad thing.  I would say preeclampsia is a bad thing.  I would say gestational diabetes is a bad thing.  I would say fetal growth restriction is a bad thing.  To all this, let me add an increase in the risk of maternal death.

The bad things mentioned above are unquestionably associated with maternal vitamin D deficiency.  And the crazy thing: this is a problem so easy to detect and so easy to resolve.

“Vitamin D deficiency is often clinically unrecognized, however laboratory measurements are easy to perform, and treatment of vitamin D deficiency is inexpensive.”  (Grundermann and von Versen-Höynck, 2011)

Vitamin D during pregnancy preforms some very valuable roles.  It is not this little nutrient we sort-of need.  It is an essential hormone.  In the context of pregnancy, this vitamin—this hormone—performs a multitude of beneficial actions, many that promote a successful pregnancy.  It should be in adequate supply.  Vitamin D helps protect both baby and placenta against infection.  It allows the blood vessels of the placenta to develop normally, reducing the incidence of placental insufficiency and a serious medical condition called preeclampsia.  Vitamin D has so much to offer.  For many unborn babies, it is the gift of life.  However, for many, vitamin D deficiency is a sentence of death.  And as tragic as this is, it gets worse.  There is a tragedy within a tragedy.  This death sentence is disproportionally carried out.

“In 2005, black mothers were 2.3 times as likely as white mothers to experience an intrauterine fetal death or death of their infant.”  (Bodnar and Simhan, 2010)

In the research paper quoted directly above, Bodnar and Simhan make a strong case that maternal vitamin D deficiency is behind the disparity between black and white pregnancy complications and outcomes, with greater risk of death and complication occurring in those with darker skin.

The reasons why vitamin D deficiency is more prevalent in the African American community are fairly straightforward.  1) Darker skin—developed to withstand exposure to more intense sunlight—needs between 10 to 50 times more sun exposure than light skin to generate an equivalent amount of vitamin D (Bodnar and Simhan, 2010).  Who among us takes the time to generate thousands of IUs (International Units) of vitamin per day by sun exposure, as was common in the distant past?  2) Diet is also a big factor.  Many foods high in vitamin D—such as seafood, reindeer meat, and walrus blubber—are replaced with fast or convenience foods with limited vitamin D content.  A reliance on convenience foods is more prevalent in the African-American community.  3)  Dairy avoidance also contributes to vitamin D deficiency.  Our society fortifies milk and dairy products with vitamin D.  Thus, milk and dairy have become significant sources of vitamin D.  However, a large percentage of black individuals are lactose intolerant and are unable to benefit from this important resource.  4) Supplementation with vitamin D, at least in adequate amounts, occurs less frequently in blacks as opposed to whites.  5) Obesity rate is higher in African Americans than in whites.  Obesity is a risk factor for vitamin D deficiency because fat cells act as storage depots for vitamin D, such that the more you have, the more likely vitamin D will wind up being stored rather than becoming available for immediate use by the mother as well as her developing baby.   The following should be of no surprise:

“Not surprisingly, there is a striking black–white disparity in the prevalence of vitamin D deficiency.”  (Bodnar and Simhan, 2010)

And given all that vitamin D has to offer during pregnancy, is it any wonder that so many little ones who just happen to be black, are off to a bad start in life?

“Compared to white women, black women are at 1.5- to 2.5-fold greater risk of delivering a preterm birth, or very preterm birth, as well as a term low birth weight infant.

“Black infants are four times as likely as whites to have been exposed to in-utero vitamin D deficiency.  They also die at a rate more than twice that of their white counterparts, and experience more frequent morbidity.”   (Bodnar and Simhan, 2010)

Are you getting the picture?  Black babies on average are disproportionately off to bad start in life.  Vitamin D deficiency is a big part of the picture.  So what is being done about the problem?  Basically nothing.  The professional excuse for doing basically nothing goes something like this: “We need further studies to elucidate the issues more clearly before we can arrive at a consensus on what steps to take in the future.”  Clearly, there is no sense of urgency and no real action plan to eliminate vitamin D deficiency during pregnancy—any pregnancy, black, brown, or white.  And we wonder why avoidable death and complication rates remain basically unchanged, decade after decade.

Now I don’t know for sure if the little guy up there was born premature or not, but I do know he made it out alive!  Many do not.  And let’s give the little guy a break and assume that Mom was vitamin D sufficient during pregnancy, offering him a great start in life.  If true, that would be nice.  But even if he was born vitamin D sufficient, this likely has not lasted.

Separated at birth from both mother and her circulating level of vitamin D, a newborn baby only has about an 8-week supply of vitamin D on board, even under the best of circumstances (Dawodu and Wagner, 2007).  So if baby is nursing, Mom better be taking a lot of vitamin D (or making a lot by sun exposure) or her breast milk will be deficient.  Studies have shown that it takes at least 2,000 IU—better yet 4,000 IU to 6,000 IU of vitamin D intake per day—or precious little vitamin D will show up in breast milk (Hollis and Waggoner, 2004; Hollis et al., 2015).  Knowing that this level of supplementation is unlikely, experts highly recommend that the nursing baby be supplemented with vitamin D.  If not, rickets, a condition characterized by bone weakness and deformity, may develop.

In the USA and in this day and age, rickets is more likely to occur in the exclusively breast-fed African American baby.  If the African American baby is taking formula, there is at least enough vitamin D included to prevent rickets, at least for a while.  Surprisingly, rickets can develop outside of infancy, even in the adolescent (Wagner et al., 2008).  A child complaining of muscle pain, often occurring in rickets or a related condition called osteomalacia, should be investigated for vitamin D deficiency.  Actually, every child—black, white, or somewhere in between—should be investigated for vitamin D deficiency, but our African American children are clearly at a greater risk for rickets and osteomalacia than children with lighter skin.

According to FamiliesUSA.org, compared to ethnic groups with lighter skin, African American babies have twice the rate of infant mortality and are twice as likely to die from SIDS (Sudden Infant Death Syndrome).  With respect to SIDS, “Bone pathology in sudden infant death syndrome (SIDS) was investigated by British researchers, who found 87% of the SIDS babies less than one year of age showed histopathological [tissue pathology] of rickets.”  (Post and Ernst, 2013)  FYI: Rickets is almost exclusively caused by vitamin D deficiency.  Go ahead, connect the dots.

As the African American baby advances beyond infancy, FamiliesUSA report a doubling of the risk of asthma and a three-fold increase of death from asthma as compared with a white child.  Vitamin D deficiency has clearly been associated with an increased risk of asthma.  There is more bad news.  And this is big!

Obesity is 73% higher in black children as compared to white children, as reported by FamiliesUSA.  Obesity leads to many health problems including diabetes.  And speaking of diabetes, type 1 diabetes (formerly known as juvenile-onset diabetes) rates in black children have apparently surpassed the type 1 diabetes rates in white children (source: Endocrinology Today, 2006)  Vitamin D deficiency is clearly a risk factor for type 1 diabetes.  “Astonishingly, they found that children who received vitamin D supplementation at the recommended 2,000 IU/d [day] had reduced the risk of developing diabetes type 1 by 80%.”  (Holick, 2002)     So, may I ask, why do policy makers recommend a mere 600 IU of vitamin D in infancy and childhood?  And if the infant/child is obese, just where do you think most of the vitamin D will go?  Off to be stored in the fat cells, that’s where it will go!  It won’t go into the battle against type 1 diabetes, that I can tell you.

There are other diseases that occur more frequently in our African American kids than in our white kids, many associated with vitamin D deficiency.  Multiple sclerosis readily comes to mind.  This neurological disease causes devastation on so many fronts, including various degrees of visual impairment and an impaired ability to initiate and control body movement.  WebMD reports: “Black Americans may be at higher risk for multiple sclerosis than whites, according to study findings that contradict a widely held belief that blacks are less likely to develop the neurological disease.”  (Preidt, 2013-2015)  And yes, little black kids get multiple sclerosis, too.  I have a case report on my desk outlining 6 cases of multiple sclerosis in African American kids, ages ranging 8 years old to 17 years old.  (see Zelink et al., 1991)  How sad.  No!  How tragic!  Multiple sclerosis is clearly associated with vitamin D deficiency.  Listen up!

“Early sun avoidance seems to precede the diagnosis of multiple sclerosis (MS).  This protective effect is independent of genetic susceptibility to MS.  (Islam et al., 2007, emphasis added)

Early life sunlight exposure and dietary vitamin D supplementation diminish the risk of MS(Chaudhuri, 2005)

Living above the 35 latitude [above Los Angeles or Atlanta, for example] for the first 10 years of life imprints on a child for the rest of his or her life a 100% increased risk [double the risk] of developing multiple sclerosis no matter where they live thereafter.  (Holick 2006, emphasis added)

Another study checked the vitamin D intake in more than 187,000 women from two separate cohorts (study groups) . . . and found a 40% reduction in the risk of multiple sclerosis among women who used supplemental vitamin D.  (Arnson et al., 2007)

Mice that were pretreated with 1,25(OHO)2D3 [the active form of vitamin D] before they were injected with myelin to induce a multiple-sclerosis like disease were immune from it.  (Holick, 2005)

Given all the damage and heartache caused by vitamin D deficiency, can you see why I’m so worried about the little guy up there?  But it really doesn’t matter if a child is black or white (or somewhere in between), any little guy or gal can become vitamin D deficient unless decisive actions are taken to prevent it.

 

Related Posts

I Didn’t Plan on Any for This, Did You?

What Will Happen to Me, If I Don’t Get Enough Vitamin D?

 

References

Arnson Y, Amital H, Shoenfeld Y 2007 Vitamin D and Autoimmunity: New Aetiological and Therapeutic Considerations.  Ann Rheum Dis; June 8; 0:1–6

Bodnar LM, Simhan HN 2010 Vitamin D May Be a Link to Black–White Disparities in Adverse Birth Outcomes. Obstetrical & Gynecological Survey. Apr; 65(4):273–284

Chaudhuri A 2005 Why We Should Offer Routine Vitamin D Supplementation in Pregnancy and Childhood to Prevent Multiple Sclerosis. Medical Hypothesis 64:608–618

Dawodu A, Wagner CL 2007 Mother–Child Vitamin D Deficiency: An International Perspective. Arch Dis Child 92:737–740

Endocrinology Today 2006 Type 1 Diabetes Rates in Black Children Higher Than in White Children. healio.com  http://www.healio.com/endocrinology/diabetes/news/print/endocrine-today/%7Bfd504871-4c42-4d1d-8e8f-e72ea6e23898%7D/type-1-diabetes-rates-in-black-children-higher-than-in-white-children

Families USA 2014 African American Health Disparities Compared to Non-Hispanic Whites http://familiesusa.org/product/african-american-health-disparities-compared-to-non-hispanic-whites

Grundmann M, von Versen-Höynk F 2011 Vitamin D—Roles in Women’s Reproductive Health? Reproductive Biology and Endocrinology 9:146

Holick MF 2002 Vitamin D: The Unappreciated D-Lightful Hormone that is Important for Skeletal and Cellular Health. Current Opinion in Endocrinology & Diabetes 9:87–98

Holick MF 2005 The Vitamin D Epidemic and Its Health Consequences.  J. Nutr. 135:2739S–2748S

Holick MF 2006 Resurrection of Vitamin D Deficiency and Rickets. The Journal of Clinical Investigation 116(16):2062–2072  

Hollis BW, Wagner CL 2004 Assessment of Dietary Vitamin D Requirements during Pregnancy and Lactation. Am J Clin Nutr 79:717–726

Hollis BW, Wagner CL, Howard CR, Ebeling M, Shary JR, Smith PG, Taylor SN, Morella K, Lawrence RA, Hulsey TC 2015 Maternal Versus Infant Vitamin D Supplementation During Lactation: A Randomized Controlled Trial. Pediatrics; Oct 1; 136(4):625–34.

Islam T, Gauderman WJ, Cozen W, Mack TM 2007 Childhood Sun Exposure Influences Risk of Multiple Sclerosis in Monozygotic Twins. Neurology 69:381–388

Lerchbaum E, Obermayer-Pietsch B 2012 Vitamin D and Fertility: A Systematic Review. European Journal of Endocrinology 166:765–778

Post JL, Ernst JZI 2013 Controversies in Vitamin D Recommendations and Its Posible Roles in Nonskeletal Health Issues. J Nutr Food Sci 3(4): doi:10.4172/2155-9600.1000213

Preidt R 201–2015 Black People May Face Higher MS Risk Than Whites. WebMD News from HealthDay http://www.webmd.com/multiple-sclerosis/news/20130506/blacks-may-face-higher-risk-of-ms-than-whites

Zelnik N, Gale AD, Shelburne Jr SA 1991 Multiple Sclerosis in Black Children. Journal of Child Neurology. Jan; 6(1):53–7

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and is not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care.  It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein.  The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy.  This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician.  The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the references used in this article.

 

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

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What Will Happen to Me if I Don’t Get Enough Vitamin D?

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Feb 192017
 

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IMG_1140By Eugene L. Heyden, RN

 

I actually hate to tell the little guy.  It seems like I’m always dwelling on the negative.  But since he wants to know, I think I will tell him.  I owe it to him to be honest.  And he looks a little worried at the moment, don’t you think?  Did I mention his name is Jimmy?

Well, little Jimmy, sadly, you are at risk for some very bad things.  Type 1 diabetes is a bad thing.  Crohn’s disease is a bad thing.  Multiple sclerosis is a bad thing.  (Soon, you will learn that a spanking is a bad thing.  I can’t help you there.)

I know, I can’t shield you from every evil, but I may be able to shield you from some.  However, it won’t really be me.  More likely, it will be your mom or your dad, or both, who will be setting in motion something so powerful that it can shield you from the evils of which I speak.  What I hope for you, little Jimmy, is that all the major players in your life—Mom, Dad, and the fine physician who is watching over you—will recognize the dangers of vitamin D deficiency and do what it takes to make and keep you vitamin D sufficient.  But apparently not everybody is recognizing the dangers and acting to eliminate the problem.

“In the United States, it is estimated that 50% of Children 1–5 years and 70% of children age 6–11 years are vitamin D deficient or insufficient. This has potentially serious consequences.”  (Holick, 2012)

Jimmy, I think it is safe to say that you are probably vitamin D deficient at this very moment—I see no attractive suntan, and I doubt if you will be crawling out from under that blanket anytime soon.  And because you are nursing, likely your vitamin D needs are not being met.  Breast-fed babies are notoriously vitamin D deficient (Misra et al., 2008).  So, unless Mom has a lot of vitamin D already on board or you are receiving vitamin D supplementation in relevant amounts, I’m afraid you are headed down the wrong path.  The wrong path often starts before birth—vitamin D deficiency is extremely common during gestation and often continues through infancy and beyond.  But I’m getting a little ahead of my story.  Let’s talk lunch.

No, little Jimmy, there is nothing wrong with Mom.  She has what it takes to provide you with generous amounts vitamin D in her breast milk, but most likely she herself is vitamin D deficient with little to pass on to you.  It takes somewhere between 4,000 to 6,000 IUs of vitamin D each day (or frequent, relevant skin exposure to the sun between 10 AM and 3 PM) for mothers to be able to pass enough vitamin D along to make their babies vitamin D sufficient (Mulligan et al., 2010; Wagner et al., 2008).  I’m sure she would like to get outdoors and have some fun in the sun—and in this manner generate generous amounts of vitamin D for her own needs and to share with you—but, you are filling your diapers so fast and furiously, dealing with this issue alone leaves her little time for anything else.  Besides, it’s winter now, a time when little to no vitamin D is created from sunlight exposure no matter how hard one tries (Weydert, 2014).  So, as you can see, vitamin D deficiency is so easy to come by.  Mom is in danger, too—vitamin D deficiency can harm her as easily as it can harm you.  But now my focus is on you.  And to be quite honest, I’m a little worried about the parenting advice Mom may have received.

If you listen to those in the dermatology community, they want you to stay under that blanket for at least six months, recommending no sunlight exposure for infants during the first six months of life because they feel that babies’ skin is too sensitive and too vulnerable to damage by the sun’s UV rays (American Academy of Dermatology, 2015).  Others in the medical community may recommend that unless vitamin D deficiency is clearly established, “vitamin D supplements should not be provided in early infancy.”  (Pérez-López, 2007)  And since there is no real push to supplement nursing mothers with thousands of International Units of vitamin D per day (instead of the recommend hundreds of units per day day), is it any wonder the vitamin D deficiency is very common during infancy?  In view of all this, what are the consequences?

 Infections occur more frequently in babies who are vitamin D deficient.  It is well known that vitamin D is intimately involved in our defense against bacteria and other pathogens, and a deficiency of vitamin D weakens our immune defenses.

“As early as birth a child is often deficient in vitamin D, which may not only affect their bone metabolism but also modulate their immune function, contributing to the increased susceptibility to many infections seen early in life.”  (Battersby et al., 2012)

And consider this:

“Vitamin D deficiency seems to be a risk factor for severe respiratory infection in children <5 years of age.”  (Laaksi et al., 2010)

Of course, many infections—pneumonia included—require prompt medical attention.  Uh oh!  Here come the antibiotics!  And here come the unintended consequences.  One study found, “Those receiving one of more dispensations of antibiotics were at a 2.9 times the odds . . . of being an IBD [Crohn’s disease or ulcerative colitis] case.” (Shaw et al., 2010)  Surprisingly, this study also found that “individuals diagnosed with pneumonia before 5 years of age were at almost three-fold the odds of developing pediatric CD [Crohn’s disease].”  Another study found that Crohn’s disease can occur in as little as three months following several courses of antibiotics (Hviid et al., 2011).  So, let’s talk about Crohn’s disease for a few moments.

“Vitamin D deficiency has been linked to several different diseases, including the immune-system diseases ulcerative colitis and Crohn’s disease.”   (Cantorna et al., 2004)

“Hildebrand et al. found that individuals diagnosed with pneumonia before 5 years of age were at almost three-fold the odds of developing pediatric CD [Crohn’s disease], compared to those with no recorded pneumonia diagnosis.”  (Shaw et at., 2010)

Crohn’s disease affects thousands upon thousands of kids in North America alone.  It is a horrible disease.  Those suffering with Crohn’s disease experience intense inflammation of the intestinal tract, abdominal pain, and a variety of other symptoms to deal with.  It can be very difficult to treat, and sometimes the treatments, in and of themselves, can be exceptionally harmful, even deadly.  Without question, Crohn’s disease occurs more frequently in those who are vitamin D deficient.  And since antibiotics disrupt the normal protective bacteria in the gut, antibiotic use can lead to Crohn’s.  So, here we see two ways to become more at risk for developing Crohn’s disease—vitamin D deficiency and antibiotic use.  Add them both together, and I see trouble ahead.  You didn’t know any of this, did you little Jimmy? (Don’t be embarrassed, neither does Mom.)  Let’s move on.

“Early life sunlight exposure and dietary vitamin D supplementation diminish the risk of MS [multiple sclerosis].”  (Chaudhuri, 2005)

“Higher sun exposure during childhood and early adolescence is associated with a reduced risk of multiple sclerosis.”  (van der Mei, et al., 2003)

“Early sun avoidance seems to precede the diagnosis of multiple sclerosis (MS). This protective effect is independent of genetic susceptibility to MS.”  (Islam et al., 2007)

Multiple sclerosis (MS) is a disease prompted by vitamin D deficiency.  Approximately 200 Americans receive this diagnosis each and every week.   In MS, a degeneration of the nerves that control movement and other bodily functions occurs, leading to a whole host of problems to deal with day-in and day-out.  It is like being destroyed from within . . . slowly . . . over time.  Nobody is particularly excited about the overall success we are having with treating MS.  They still call it incurable.  The evidence is strong; vitamin D deficiency in childhood and youth—even during gestation—makes it a lot easier to contract this disease.  What should be kept in mind is this: a situation or an event occurring during pregnancy, infancy, childhood, or later in life, may set the stage for a disease process to develop years later.  This seems to be what is occurring with MS. It also seems to be what is occurring with type 1 diabetes.

“In a Finnish study, children who received 2000 IU of vitamin D per day during the first year of life had an 80% reduction in the risk of the development of type 1 DM during a follow-up period of 30 years. In contrast, children who were vitamin D-deficient or who were suspected to have rickets at 1 year had a 2.4-fold increased risk of the development of type 1 DM.”  (Mulligan et al., 2010, emphasis added)

Type 1 diabetes claims approximately 15,000 new child victims each year.   And that’s just in the United States!  In the United States, type 1 diabetes chews up about $14.4 billion health care dollars each year with an average annual cost of over $9,000 per child.  In this disease, the cells of the immune system attack and progressively destroy the insulin-producing cells of the pancreas.  Since insulin is required to allow glucose to enter the cells, with less insulin production the cells of the body are starved of fuel.  Without treatment, death occurs.  Luckily, we can use injectable insulin to smooth things over.  But still, these kids have a lot of health issues to deal with for life.

Did you take notice that the kids in the Finnish study, who became remarkably resistant to contracting type 1 diabetes, received 2,000 IUs of vitamin D . . . in their first year of life?!  Say, let’s not learn a thing here and continue to supply little if any vitamin D supplementation to the little Jimmies (and the little Susies) of the world.  On second thought, let’s not do that.  That wouldn’t be right.

So, as you can see, little Jimmy, bad things can happen to you if you don’t get enough vitamin D.  I didn’t mean to scare you.  But now I mean to scare you—you, along with Mom, Dad, and the fine physician who is watching over you.  There is something perhaps worse than the evils we have discussed thus far.  Can little Jimmy say “Schizophrenia?”

“In utero or early life vitamin D deficiency has been linked to an increased risk of type 1 diabetes, asthma, and schizophrenia. ” (Bodnar et al., 2007)

“The absence of vitamin D supplementation during infancy was associated with an increased risk of schizophrenia.”  (McGrath et al., 2004)

Schizophrenia is a disease of the mind.  Thoughts become distorted.  Reality can be in short supply.  Sometimes it is a nightmare you never wake from.  Surprisingly, vitamin D deficiency in early life—a time when the brain is rapidly developing—can lead to a distortion of the structure and an alteration of the function of the brain, giving rise to this unfortunate state of existence.  Now this is interesting: The Finnish children who were found to have an 80% less chance of contracting type 1 diabetes if supplemented with 2,000 units of vitamin D per day during their first year of life also had a greatly reduced (77% less) risk of developing schizophrenia, at least in the male subjects of the study.  (McGrath et al., 2004).  It is still something of a mystery why no females in the study group came down with schizophrenia.  It may be that their higher estrogen levels offered them a degree of protection against developing this condition (Cannell, 2008).

Jimmy, I could tell you more, but I need to bring things to a close.  I smell something a little funny.  It may be your diaper.  Once again, I see Mom putting on her nose plugs.  So, for obvious reasons, I will bring our little discussion to a close.  I won’t take the time to mention your increased risk of autism, asthma, allergies, dental cavities, depression, and many other evils that occur more frequently in babies who live the vitamin D deficient life.  Word of advice:  Jimmy, don’t live the vitamin D deficient life.

“The world is currently facing an unrecognized and untreated pandemic of vitamin D deficiency. Sensitizing pediatricians to recognize and treat this pandemic would have great impact on child health in the 21st century.”  (Rathi and Rathi, 2011)

 

Related Post

What I Want My Mommy to Know About Vitamin D

 

References

American Academy of Dermatology 2015 The First Steps of Sun Protection: How to Keep Your Baby Safe. https://www.aad.org/media/news-releases/the-first-steps-of-sun-protection-how-to-keep-your-baby-safe

Battersby AJ, Kampmann B, Burl S 2012 Vitamin D in Early Childhood and the

Effects on Immunity to Mycobacterium Tuberculosis. Clinical and Developmental Immunology doi: 10.1155/2012/430972

Bodnar LM, Simhan HN, Powers RW, Frank MP, Cooperstein E, Roberts JM 2007 High Prevalence of Vitamin D Insufficiency in Black and White Pregnant Women Residing in the Northern United States and Their Neonates. J. Nutr. 137:447–452

Cannell  JJ 2008 Autism and Vitamin D. Medical Hypotheses 70:750–759

Cantorna MT, Zhu Y, Froicu M, Wittke A 2004 Vitamin D Status, 1,25Diydroxyvitamin D3, and the Immune System. Am J Clin Nutr 80(Suppl):1717S–1720S

Chaudhuri A 2005 Why We Should Offer Routine Vitamin D Supplementation in

Pregnancy and Childhood to Prevent Multiple Sclerosis. Medical Hypothesis 64:608–618

Hviid A, Svanström H, Frisch M 2011 Antibiotic Use and Inflammatory Bowel Disease. Gut 60:49–50

Holick MF 2012 The D-Lightful Vitamin D for Child Health. Journal of Parenteral and Enteral Nutrition; January; 36(Suppl 1):9S–19S

Islam T, Gauderman WJ, Cozen W, Mack TM 2007 Childhood Sun Exposure Influences Risk of Multiple Sclerosis in Monozygotic Twins. Neurology 69:381–388

Laaksi I, Ruohola J-P, Mattila V, Auvinen A, Ylikomi T, Pihlajamäki H 2010 Vitamin D Supplementation for the Prevention of Acute Respiratory Tract Infection: A Randomized, Double-Blinded Trial among Young Finnish Men. The Journal of Infectious Diseases 202(5):809–814

McGrath J, Saari K, Hakko H, Jokelainen J, Jones P, Järvelin M-R, Chant D, Isohanni M 2004 Vitamin D Supplementation During the First Year of Life and Risk of Schizophrenia: A Finnish Birth Cohort Study. Schizophrenia Research 67:3237–3245

Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M 2008 Vitamin D Deficiency in Children and Its Management: Review of Current Knowledge and Recommendations. Pediatrics 122:398–417

Mulligan ML, Shaili SK, Riek AE, Bernal-Mizrachi C 2010 Implications of Vitamin D Deficiency in Pregnancy and Lactation. Am J Obstet Gynecol; May; 202(5):429.e1–429.e9

Pérez-López FR 2007 Vitamin D The Secosteroid Hormone and Human Reproduction. Gynecological Endocrinology; January; 23(1):13–24

Rathi N, Rathi A 2011 Vitamin D and Child Health in the 21st Century. Indian Pediatrics 48:619–625

Shaw SY, Blanchard JF, Bernstein CN 2010 Association Between the Use of Antibiotics in the First Year of Life and Pediatric Inflammatory Bowel Disease. The American Journal of Gastroenterology 105(12):2687–2692

van der Mei IA, Ponsonby AL, Dwyer T, Blizzard L, Simmons R, Taylor BV, Butzkueven H, Kilpatrick T 2003 Past exposure to sun, skin phenotype, and risk of multiple sclerosis: case-control study. BMJ; Aug 7; 327(7410):316

 

Wagner CL, Taylor SN, Hollis BW 2008 Does Vitamin D Make the World Go

“Round”? Breastfeeding Medicine 3(4):239–250

Weydert JA 2014 Vitamin D in Children’s Health. Children. Sep 12; 1(2):208–226.

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and is not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care.  It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein.  The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy.  This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician.  The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the references used in this article.

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

Download a PDF of this page

 

As Always, There Are at Least Two in There

 Comments Off on As Always, There Are at Least Two in There
Feb 192017
 

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By Eugene L. Heyden, RN

 

It’s quite obvious.  You’re having a baby.  We’re glad.  And we all want what you want—a healthy, happy baby.  However, with all the focus on baby—meeting his or her needs for proper development—we often overlook the needs of someone else.  You’re also having a placenta.  Yes, placentas are people, too.  And just like babies, placentas are part mom as well as part dad.

Or course, the goal of this pregnancy is not to welcome a healthy, happy placenta into your loving arms.  The goal is to welcome a healthy, happy baby into your loving arms and take it from there.  However, a placenta that is abnormal may stand directly in the way.  Worst case, an abnormal placenta may take the life of the baby.  It may even take the life of the mother.  I’m fairly confident, this kind of placenta—one that has gone over to the dark side—is not what you have in mind.  You probably want a good one.  Luckily, what is good for baby is also good for placenta, so creating a healthy placenta may be easier than you think.

The scientists who intently study these issues want you to have a good placenta, too.  Their work is paying off.  They are making remarkable discoveries that you should pay close attention to.  Your doctor should also play close attention to what is being discovered.  But unfortunately, because you and your girlfriends as having babies so fast, our doctors seem to be having trouble keeping up with all that is new.  They finally got around to paying attention to folic acid to prevent birth defects—but it took about 25 years of delay and neglect before folic acid supplementation before and at the beginning of pregnancy went from being a great idea to a universal practice.  So, Mom, it’s up to you to become cutting edge.  Pay close attention to what follows:

“Adequate vitamin D intake is essential for maternal and fetal health during pregnancy, and epidemiological data indicate that many pregnant women have sub-optimal vitamin D levels. Notably, vitamin D deficiency correlates with preeclampsia, gestational diabetes mellitus, and bacterial vaginosis, and an increased risk for C-section delivery. Recent work emphasizes the importance of nonclassical roles of vitamin D in pregnancy and the placenta. The placenta produces and responds to vitamin D where vitamin D functions as a modulator of implantation, cytokine production and the immune response to infection.”  (Shin et al., 2010, emphasis added)

Relevant to the issues at hand, what the scientists have discovered is that vitamin D deficiency has a negative impact on the health of the placenta.  Vitamin D is not this little nutrient you sort of need.  It is actually a steroid hormone, one we cannot do without, one that the placenta heavily relies upon so you can have the baby of your dreams.  Normal placental development depends on vitamin D being in adequate supply.  This hormone is what the body uses to allow normal growth to occur (for both baby and placenta), and it is critical for the life-and-death struggle against those who are evil.  Surprisingly, a life-and-death struggle occurs even in the placenta!  There are bacteria living there—even in a healthy placenta—so keeping bacteria in check is most important.  There is a baby at stake.

“The placenta is one of the most poorly understood human organs, particularly with regard the presence of microbes within it.”  (Nuriel-Ohayon et al., 2016)

No longer should we consider the placenta to be a sterile environment.  Quite the contrary, the placenta is home to many bacteria.  Bacteria can also be found living in the amniotic fluid and in the vascular network that connects baby to placenta, the umbilical cord.  (see Nuriel-Ohayon et al., 2016)  So—and this is important—bacteria need to be controlled or there will be no baby.  Enter the power of vitamin D.

Vitamin D triggers or supports many of the physiological actions required to mount a lethal immune response directed toward bacteria, yet it does so in a controlled manner that does not harm the little one the placenta is trying to nourish and protect.  Even in a healthy pregnancy there are enemies lurking in the shadows.  They want to destroy Baby.  Vitamin D sufficiency defends against this.  So why are so many mothers-to-be allowed to remain vitamin D deficient?  Are we looking for another 25-year period to pass before the following happens?

“The routine monitoring of vitamin D levels in antenatal period [period before or during pregnancy] is mandatory.  Early preventative measures should be taken at the slightest suspicion of vitamin D deficiency in pregnant women, to reduce morbidity during pregnancy and lactation, as well as its subsequent impact on the fetus, the newborn and the child.”  (Urrutia-Pereira and Solé, 2015)

I am fairly certain of this: The placenta you want is one that is properly constructed, one that functions normally and adequately supports fetal growth.  And to achieve this, you will need vitamin D on your side.  You really have no choice in the matter.

“Vitamin D is considered as having a major role in the synthesis and regulation of genes that are effective in the early development phase of the placenta.”  (Bakacak et al., 2015)

“The placenta plays a crucial role in fetal health, and it is well known that placental pathologies, specifically vascular lesions, affect fetal growth.

“Inadequate growth in utero is not only linked to immediate morbidity and mortality risk of offspring but also lifelong risk of chronic disease.”  (Gernand et al., 2013, emphasis added)

The science is clear; vitamin D aids in the proper development of the placenta, particularly with respect to its vasculature (blood vessels).  The science is equally clear about the fact that vitamin D deficiency impairs placental vascular development (Gernand et al., 2013).  Little scrawny infants, with their pathetic, immature little organs—ill prepared for life on the outside—are produced by placentas that are developmentally impaired.  In the face of vitamin D deficiency, the blood vessels of the placenta can become insufficient in the task of supplying all the nutrition the baby needs.  And after birth, often a premature birth, these infants are off to a poor start in life.  Some are damaged for life.  Some have their lives taken away.  We have a name for this: fetal growth restriction.  Fetal growth restriction should be avoided at all costs.  You don’t want any part of this!  Vitamin D deficiency can lead to this, which is why you will be reading the following:

“Maternal vitamin D deficiency has been associated with many poor birth outcomes, including fetal growth restriction.  A recent Cochrane Review showed that vitamin D supplementation reduces the incidence of low birth weight . . . by 52%.”  (Gernand et al., 2013, emphasis added)

And let me remind you: Vitamin D deficiency is very common in ladies who make babies.  And it may be that there are more vitamin D deficient pregnant moms and women in their child-bearing years than there are those who have a healthy vitamin D level—you should read the statistics I read!   Vitamin D deficiency is so common during pregnancy, and a lot of problems follow in its wake.  Fortunately, some of this may be corrected when this vitamin, this hormone, is provided in adequate supply.  “Vitamin D deficiency is implicated in reduced fetal growth, which may be rescued by supplementation of vitamin D.”  (Murthi et al., 2016)  However, some of the damage may never be corrected, making prevention and early intervention extremely important actions to take.

Besides fetal growth restriction, an abnormal placenta can lead to preeclampsia, “a disorder involving dysregulated placental vascularization that affects up to 10% of pregnancies.”  (Liu et al., 2011)  Vitamin D deficiency is implicated here, too, as one might expect.  One study found, “patients with 25(OH)D levels 15 ng/mL [quite low, but common] had a 5-fold increase in the risk of preeclampsia, despite receiving prenatal vitamins.”  (Mulligan et al., 2010, emphasis added)  Other studies have found pretty much the same thing.  For example:

“In a recent study, the odds of severe preeclampsia decreased by 38% for every 10 nmol/L increase in 25(OH)D [vitamin D].”  (Christensen et al., 2012)

“Almost all cross-sectional studies have reported a significant association between vitamin D deficiency and risk of pre-eclampsia.”  (Tabesh et al., 2013)

“Women with vitamin D deficiency (<20 ng/ml) were more likely to have low levels of placental growth factor, which is associated with an increased risk of preeclapsia.”  (Fanos et al., 2013) 

I won’t go into the details of preeclampsia at this time.  I need to bring this presentation to a close.  However, I will take the time to tell you that you don’t want anything to do with preeclampsia.  There is danger there.  Yet sadly, even though it is known that vitamin D deficiency threatens the pregnancy and harms and kills babies (and placentas), we pay such little attention to vitamin D during this important period in life.

“Vitamin D deficiency is often clinically unrecognized, however laboratory measurements are easy to perform, and treatment of vitamin D deficiency is inexpensive.”  (Grundermann and von Versen-Höynck, 2011)

“Vitamin D is important to maternal health, fetal development, and postnatal life.  Current prenatal care does not include the monitoring of vitamin D levels, which is an unfortunate oversight because deficiency is easily treated.”   (Mulligan et al., 2010) 

Before I let you go, I should probably tie up a few lose ends.  Earlier, in this article I wrote “what is good for the baby is also good for the placenta.”  Obviously, smoking is totally out of the question—very harmful to the vascular health of the placenta (Zdravkovic et al., 2005).  A healthy diet, one that includes adequate amounts of “calcium, magnesium, selenium and vitamin A and C,” along with vitamin D in generous supply, will help you construct a healthy placenta (Bakacak et al., 2015).  Your prenatal supplement will help deliver some of the things you need, but clearly it will not provide you with enough vitamin D to make you or keep you vitamin D sufficient (McCullough, 2007).  And if you are taking a prenatal supplement without iodine, I will have to track you down and make you read my birth defect book.  (During gestation, a baby can be damaged, sometimes severely damaged, when his or her mother is low in iodine.)

Also earlier, I wrote this:Mom, it’s up to you to become cutting edge.”  By this, I mean that I invite you become aware of the issues surrounding vitamin D and pregnancy, and not remain part of the problem.  Year after year I read paper after paper detailing the discoveries and conclusions of the experts, yet little change can be detected in how we address a clearly-defined problem that harms and destroys, namely vitamin D deficiency.  Year after year, the belief that only a little vitamin D is required during pregnancy is tightly held.  No sense of urgency is detectable.  No change is in sight.  This needs to end.  It can start with you.  You can request a vitamin D level to see where you stand.  You can insist on effective treatment, as indicated.

I will conclude with this:

“Finally, let us discuss a scenario that occurs thousands of times daily in the United States.  A pregnant woman visits her obstetrician, who prescribes prenatal vitamins containing 400 IU (10µg) vitamin D.  The patient and physician both assume that this supplement will fulfill all the nutritional requirements for the duration of the pregnancy.  However, in the case of vitamin D, it will not even come close unless the pregnant woman has adequate sun exposure.  The woman, especially if African American, and her developing fetus are at high risk of remaining vitamin D deficient during the entire pregnancy.  Even if the physician were to prescribe a vitamin D supplement of 1,000 IU/d (25 µg), the mother would likely remain vitamin D deficient.  As scientists and health care providers, we simply cannot accept this any longer.”  (Hollis and Wagner, 2004)

 

Related Post

 

I Didn’t Plan on Any for This, Did You?

 

References

Bakacak M, Serin S, Ercan O, Köstü B, Avci F, Kılınç M, Kıran H, Kiran G 2015 Comparison of Vitamin D Levels in Cases with Preeclampsia, Eclampsia and Healthy Pregnant Women. International Journal of Clinical and Experimental Medicine. 8(9):16280

Christensen HT, Falkenberg T, Lamont RF, Jørgensen JS 2012 The Impact of Vitamin D on Pregnancy: A Systematic Review. ACTA Obstetrica et Gynecologica 91(2012):1357–1367

Fanos M, Vierucci F, Saggese G 2013 Vitamin D in the Prenatal Period: An Update. Journal of Pediatric and Neonatal Individualized Medicine 2(2):e020202

Gernand AD, Bodnar LM, Klebanoff MA, Parks WT, Simhan HN  2013 Maternal Serum 25-hydroxyvitamin D and Placental Vascular Pathology in a Multicenter US Cohort. The American Journal of Clinical Nutrition. Aug 1; 98(2):383–8

Grundmann M, von Versen-Höynk F 2011 Vitamin D—Roles in Women’s Reproductive Health? Reproductive Biology and Endocrinology 9:146

Hollis BW, Wagner CL 2004 Assessment of Dietary Vitamin D Requirements during Pregnancy and Lactation. Am J Clin Nutr 79:717–726

Liu NQ, Kaplan AT, Lagishetty V, Ouyang YB, Ouyang Y, Simmons CF, Equils O, Hewison M 2011 Vitamin D and the Regulation of Placental Inflammation. The Journal of Immunology. May 15; 186(10):5968–74

McCullough ML 2007 Vitamin D Deficiency in Pregnancy: Bringing the Issues to Light. The Journal of Nutrition. Feb 1; 137(2):305–6

Mulligan ML, Shaili SK, Riek AE, Bernal-Mizrachi C 2010 Implications of Vitamin D Deficiency in Pregnancy and Lactation. Am J Obstet Gynecol; May; 202(5):429.e1–429.e9

Murthi P, Yong HE, Ngyuen TP, Ellery S, Singh H, Rahman R, Dickinson H, Walker DW, Davies-Tuck M, Wallace EM, Ebeling PR 2017 Role of the Placental Vitamin D Receptor in Modulating Feto-Placental Growth in Fetal Growth Restriction and Preeclampsia-Affected Pregnancies. Frontiers in Physiology. 7

Nuriel-Ohayon M, Neuman H, Koren O 2016 Microbial Changes during Pregnancy, Birth, and Infancy. Frontiers in Microbiology. July; 7 (Article 1031)

Shin JS, Choi MY, Longtine MS, Nelson DM 2010 Vitamin D Effects on Pregnancy and the Placenta. Placenta. Dec 31; 31(12):1027–34

Tabesh M, Salehi-Abargouei A, Tabesh M, Esmaillzadeh A 2013 Maternal Vitamin D Status and Risk of Pre-eclampsia: A Systematic Review and Meta-analysis. The Journal of Clinical Endocrinology & Metabolism. Jun 19; 98(8):3165–3173

Urrutia-Pereira M, Solé D 2015 Vitamin D Deficiency in Pregnancy and Its Impact on the Fetus, the Newborn and in Childhood. Revista Paulista de Pediatria. Mar; 33(1):104–13

Zdravkovic T, Genbacev O, McMaster MT, Fisher SJ 2005 The Adverse Effects of Maternal Smoking on the Human Placenta: A Review. Placenta. Apr 30; 26:S81–6

 

Disclaimer: This article is presented solely for informational purposes. The information contained herein should be evaluated for accuracy and validity in the context of opposing data, new information, and the views and recommendations of a qualified health care professional, and is not to be substituted for professional judgment and guidance or to provide reason to neglect or delay appropriate medical care.  It is the reader and reader only who bears the responsibility for any actions that could be construed as being a response to the information contained herein.  The statements and opinions expressed by the author have not been reviewed or approved by the FDA or by any other authoritative body, nor is the author endorsing any product or specific therapy.  This article is offered to the reader to broaden his or her understanding of the issues discussed and to help identify options that may be suitable for the individual to pursue, on behalf of self or others, under approval and direction of a qualified physician.  The author and publisher offer no guarantees of the accuracy or validity of the quotations incorporated into this article or the accuracy or validity of the information presented by the references used in this article.

Copyright © 2017 Eugene L. Heyden, RN

All Rights Reserved.

Download a PDF of this page