inflammation Archives - Stop The Thyroid Madness

A way to bring up serum iron without taking iron supplements?

Yes, it appears so…with lactoferrin. But first…

It is common for hypothyroid or Hashimoto’s patients to get low iron

Why? The most common reason is being on T4-only like Synthroid or Levothyroxine. The latter leaves most with lingering hypothyroidism, sooner or later. Thus, continued hypothyroidism lowers one’s stomach acid, and lowered stomach acid means you aren’t going to absorb nutrients well. So iron can fall, as can B12, Vitamin D and more.

The second most common reason is being underdosed on Natural Desiccated Thyroid (NDT) or T3 for a long period of time…usually due to a doctor who goes by the TSH or doesn’t understand how to get you optimal.

The third most common reason? Being undiagnosed for awhile, once again due to doctor’s clueless reliance on the lousy TSH lab test. The TSH can be “normal” for years before it rises high enough to reveal your thyroid problem.

But before I get into the topic of this post, please know that the vast majority of thyroid patients with inadequate levels of iron have successfully raised it with the right amount of iron supplements and for years! It’s all explained on the iron page.

How do I know if I have low iron?

It’s about four iron labs, NOT just ferritin–the latter which too many doctor rely upon solely, and is a mistake. You can have low ferritin and good or high iron due to a methylation problem! Those four iron labs are serum iron, % saturation, TIBC and ferritin. Yes, all four. Then you compare your results to this page: https://stopthethyroidmadness.com/lab-values

Your results have NOTHING to do with just falling anywhere in those ridiculous ranges. Compare to above link!! It’s serum iron you treat.

And if ferritin is high with lower serum iron, that means inflammation you’ll need to treat and get DOWN, otherwise taking iron will raise your high ferritin even more.

How I found out about a new way other than iron supplements

I do coaching calls. And one call in particular was impressive! This young man raised his serum iron from 77 to 130 without taking a single supplement of iron. How did he do it? With nothing more than lactoferrin. He was also taking astaxanthin, but I’ll explain later.

BUT PLEASE NOTE: We have NOT seen just lactoferrin work for anyone else since I wrote this blog post. ~Janie

What is lactoferrin?

Lactoferrin is a protein, also called a “glycoprotein” because it has both a carb and a protein. Lactoferrin is primarily found in a mother’s breast milk at the beginning of nursing and it’s at quite high levels–seven times higher than it will be later, or in regular milk¹. And what does lactoferrin do for infants who breast feed, as well as adults who use it as a supplement? It plays a fabulous role in enhancing your immune response, making it antibacterial, for one, plus anti-viral, anti-parasitic and even anti-fungal. Lactoferrin is also stated to be anti-cancer, and also known to promote bone health.

And for all of us, lactoferrin envelopes (binds) iron, constraining the iron from feeding a bacterial or viral infection, from feeding candida, from being too toxic in our bodies, or causing too high levels of free radicals! But there is evidence that it also helps raise low iron.

Some ask about the lactose in lactoferrin since it comes from a mother’s milk–it’s very very low.

So has research also shown that lactoferrin supplementation can raise iron levels?

Yes!

Here’s a 2006 study of 300 women, part taking lactoferrin and part taking just iron supplements, and the women taking lactoferrin saw a definite rise in their serum iron as did those taking supplements, but the former had even better results! It was 100 mg lactoferrin twice a day vs 520 mg once a day of ferrous sulfate. https://www.ncbi.nlm.nih.gov/pubmed/16936810

And here’s a 2009 study showing that with one group using iron supplements and another group using lactoferrin…the outcome was the same–each had raised their iron status comparably! results! https://www.ncbi.nlm.nih.gov/pubmed/19639462

In 2014, a study with pregnant women showed the same as above–that transferrin did the job in raising iron as much as iron supplementation and with fewer potential side effects. Transferrin also lowered inflammation. https://www.ncbi.nlm.nih.gov/pubmed/24590680

And there are more studies which scientifically validate that power of lactoferrin to bring up iron from the iron content in foods you eat. Most studies show participants taking 100 mg twice a day, to equal a total of 200 mg.

How have we used lactoferrin before?

Stop the Thyroid Madness–the mothership of patient experiences and wisdom rather than empty strong opinion, has always mentioned using lactoferrin with your iron supplementation to envelope the iron and carry it around, besides protect you from the toxicity of iron. That is especially true if your liver isn’t making much transferrin as revealed by a lower TIBC–an indirect measure of your liver’s ability to make transferrin. Transferrin is in the same family of proteins as lactoferrin, thus lactoferrin supplements are ideal.

But now we have evidence that lactoferrin ALONE may do the trick. And guess what…there are even lactoferrin receptors in your body.

Will lactoferrin supplementation do the trick for everyone in raising low iron?

We don’t know yet. We need more patient feedback on their experience with it. But as mentioned above, there is evidence both in experience and research that is a bit exciting and interesting. And you probably need to take it while eating foods rich in iron, too.

Which lactoferrin should I get if I want to try raising my confirmed low iron?

Most brands seem to be fine; most lactoferrin supplementation is shown to be safe; they come from bovine sources. But I would choose a brand you have read about and/or trust.

There is a brand of lactoferrin by Life Extension that says it’s the apolactoferrin form, meaning iron depleted. Regular lactoferrin in most other brands do contain a little iron which is not depleted. I would personally go with other brands, not Life Extension, but that’s me.

What about the astaxanthin mentioned above?

If you have inflammation, iron will tend to go high into storage (aka ferritin), instead of supplying your serum iron levels. For women, you can suspect inflammation if your ferritin is nearing 100 or much higher, and for men, if you ferritin is going above the 130’s. With either men or women, your serum iron will be lower than it should be if ferritin is revealing inflammation!!

And it’s your serum iron levels you are supposed to be treating, NOT ferritin… unless you have inflammation! Thus, taking inflammation lowering supplements are important, as lowering inflammation is the only way to raise low serum iron! Astaxanthin² is one (such as a minimum of 12 mg and possibly twice a day?), but so is curcumin twice a day (in higher doses than bottles say) or other anti-inflammatory supps of your choice. Take the time to check out this page–we all have to be educated to get well: —-> https://stopthethyroidmadness.com/inflammation

Bottom line?

1. We now have science showing the efficacy in using lactoferrin to raise low serum iron levels, plus solid patient experience in doing so, as well.

2. Lactoferrin supplementation may prevent you from getting low iron in the first place.

3. If you are someone who has serious gastrointestinal issues with taking iron to correct low serum iron (not low ferritin–it’s about correcting low serum iron), this is a new possibility to explore. Even if you have no issues taking iron, the possibility that taking lactoferrin can raise iron is interesting, besides the fact that it also improves your immune function, is anti-viral, anti-bacterial, anti-fungus, anti-parasites and anti-cancer! Wow!

4. If you have low serum iron with high ferritin, the latter points to inflammation. Important to get that inflammation down to help raise your serum iron, even if you use lactoferrin.

5. Studies above used 100 mg twice a day to equal 200 mg daily. If you have gained any experience with using JUST lactoferrin to raise iron, please let us know how long it took you, how much lactoferrin you used, and what your results were.

P.S lF YOU ARE RECEIVING THIS BLOG POST via email because you signed up to do so (bottom right of any page on STTM), do NOT reply to the email. No one will see your reply. Click on the title of the post, which will take you to the actual blog post on STTM. Comment there!

Footnotes:

1. https://en.wikipedia.org/wiki/Lactoferrin

2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4454080/

This information about lactoferrin can be a supplement to your STTM books! Print and insert. Here they are: https://laughinggrapepublishing.com

August 9th 2018 67 replies

Gut Health — One more part of your health and well-being as thyroid patients

When I was first creating the Stop the Thyroid Madness website, plus the books, it was all to empower you in both the doctor’s office and without.

And it never even dawned on me or others to look at gut health. It’s probably because I never had any obvious signs of a gastrointestinal problem. But many others do!

Over the years, though, it’s become a hot topic, and rightly so!

What is gut health?

Gut Health is a catchy phrase referring to all the right things that should go on within your gastrointestinal tract. The latter refers to all those organs which are involved in digestion–the breakdown of what you consume! They include your…

1) Esophagus

2) Stomach

3) Small intestine

4) Large intestine

5) Liver

6) Gallbladder

7) Pancreas and more

Why is digestion so important?

Healthy digestion is the process your body goes through to break down the food, liquids and supplements you put in your mouth so your body can use what is contained within for its health and energy–i.e. nutrients.

Your digestion also helps you move out waste products in a timely manner. Healthy digestion helps proteins you consume break down into amino acids, helps any carbs you eat break down into simply sugars, helps fats break down to important fatty acids.

What can be obvious symptoms that I have a gut health problem?

Bloating (especially due to excess bacteria in the gastrointestinal tract)
Excess Gas (some gas is very normal throughout the day–this is about far too much)
Constipation (very common with undiagnosed or poorly treated hypothyroid)
Diarrhea (no gall bladder, intolerance to raw products, lactose intolerance, irritable bowel syndrome, etc)
Chronic Inflammation (symptoms can include that spare tire, or any of the above; gluten intolerance)
Heartburn (can be related to low stomach acid or a damaged gut lining)
Sugar cravings (candida/excessive yeast, possible nutrition deficiencies, etc)
Bad breath (acid reflux, ulcers due to a stomach bacteria, poor dental hygiene, etc)
Food allergies/sensitivities (overreactive immune response; possibly GMO products; genetics)
Depression or being moody (which could also be hypothyroid symptoms)
Skin problems like eczema (due to poorly performing gastrointestinal tract)
Diabetes, mostly including Type 2, but also those with Type 1 (inability of insulin to control sugar levels)
Autoimmune diseases (leaky gut, genetics)
Immune suppression (having frequent illnesses)

What I even discovered about me and good bacteria

I have never tended to have gastrointestinal problems. But some are silent, as I found out about me! I did the 23andme.com genetic testing and found out that because of mutations, I never have enough of the bifada good bacteria in my system.

We all need good bacteria in our gut. That bacteria helps fight disease. It helps neutralize some of the toxins released by digestion, and can reduce harmful substances. The right amount also discourages the build up of bad bacteria and yeast.

OOPS. I’ve also recently discovered that I need to stop licking the bowl after making cake mix, because the raw ingredients do not sit well with my gastrointestinal tract. Darn. lol.

Where can I read more to find answers?

Here is a great article that though it can focus on Hashimoto’s disease patients especially, you don’t have to have Hashi’s to greatly benefit: https://stopthethyroidmadness.com/10-gut-health-questions/

Here is a compilation of issues to read about from Dr. Axe: https://draxe.com/category/health-concerns/gut-health/

Here’s an article with great pictures and easy to understand from the National Institute of Diabetes and Digestive and Kidney Diseases: https://www.niddk.nih.gov/health-information/digestive-diseases/digestive-system-how-it-works

This video is kinda cool, taking a camera through your gastrointestinal tract!! https://www.youtube.com/watch?v=-1aZj6v6dxc

We would love to hear from you about your own gastrointestinal issues as a thyroid patient and how you have treated them. I am not an expert on them, so you may not see me comment. Hopefully others who have gained knowledge can reply.

Need a gut group? This is one I know about. Note that mentioning it means I’m making no guarantees about any group mentioned on here and you take full responsibility for outcomes in using any group: https://www.facebook.com/groups/FTPOGluten/ It’s now a privately run Gut Group.

TIP:

DO YOU HAVE NIGHTTIME SLEEP WAKE UPS? I have always been a total NDT user. For the last few months, I had to switch to mostly T3 with a smaller amount of NDT to counter high RT3 due to chronic inflammation (which is now fixed). But during that time, I would wakeup too easily in the middle of the night, and I knew I didn’t have adrenal problems, which also causes this problem. Well guess what? I tried to take a small amount of T3 right at bedtime (in addition to what I was already taking during the day). It was perhaps a third of a 25 mcg tablet. And guess what? I SLEPT BETTER!!

March 1st 2018 14 replies

In Loving Memory of Dr. William Trumbower, a Contributor to the STTM II book

With great sorrow, I want to announce that Dr. William D. Trumbower of Missouri, who contributed the chapter Nutrition and Hypothyroidism in the Stop the Thyroid Madness II book, has recently passed away.

I adored Dr. Trumbower. He had great humility. When I asked him to be in the book, he stated that he “agonized over it as I am not in the same category as the other authors”. Posh!! I knew that was totally wrong. He was smart, open-minded, insightful and fabulous.

What I loved about his chapter is his take on the effects of either inflammation, malnutrition or toxicity on one’s hypothyroid state. He talked about the gut and the problem one can have from gluten, besides all the problems we can encounter from refined sugars and industrial-processes oils–all which he explained can cause more inflammation.

In one section of his chapter, he discussed the problems on our thyroid and health in general due to toxicity from halogens, heavy metals and xenoestrogens. I kept thinking about that when I discovered myself with high copper and lead last year, as well as high barium!! He was also keenly aware of the importance of knowing if one has the MTHFR mutation, which in itself can cause high heavy metals.

Dr. Trumbower believed that “almost all hypothyroidism begins as a nutritional disorder”. Patients haven’t always found that to be true for them if genetics are involved, but we agree that a high body of us could fall in that nutritional problem category!! So what a perfect chapter subject for him to focus on.

But here’s what I have NEVER forgotten about Trumbower: He followed his own advice about nutrition and stated that his “thyroid dose dropped from 150 mg of desiccated thyroid to 30 mg daily”. That has always blown me away. His experience underscored how important it is for all of us to know our nutritional status and treat it! I definitely do. I had found myself to be low in B-vitamins, l-carnitine and CoQ10 and definitely treat those. I also tend to fall too low in magnesium, so that’s an important nutrient for me to supplement. Dr. Trum certainly underscored it.

After the STTM II book came out, he explained to me in his own humorous way how it had changed his professional life. He stated: “I now have credibility instead of being an old outlying radical doc.” Don’t you love it?? Now you know why I found him to be so endearing. And one way he blessed me in return is in stating that even he used the revised STTM book to guide his own thyroid journey! You make this girl proud.

In 2015, Dr. Trumbower and his daughter Elisabeth created a fully integrated clinic that combined aesthetics, wellness and bioidentical hormone therapies, called Pela Cura Anti-Aging & Wellness. What a blessing that must have been to worked with his own beloved daughter!

I have included his bio from the book below, just for you to know more about him and what a wonderful person and doctor he was!

Rest in Peace, Dr. Trumbower. Your chapter in the STTM II book will forever inspire thyroid patients, just as your presence and open-mindedness in the lives of so many of your patients have done the same.

********************

I, William D. Trumbower MD, am a 69-year-old OB/GYN (no longer doing obstetrics or surgery), practicing in the, medium size, college town of Columbia, Missouri. I am blessed in my practice, as my eleven partners do not require me to take call any more. I am able to spend my time, in my office, performing annual exams on many people I have known for well over 30 years, as well as being able to concentrate on bioidentical hormones, thyroid, chronic fatigue and other areas that no one seems to be very interested in, probably because they are not extremely profitable.

I did not mean to be an alternative thyroid hormone physician. Nothing in my training would have given me any hint that this was to be my destiny. During my residency, I was obsessed with surgery, high-risk obstetrics and obstetrical anesthesia. I was fortunate enough to to stay on the teaching faculty, at the University of Missouri — Columbia, for three years, as an assistant professor. I left the University of Missouri and entered private practice, in 1979.

I suppose I can trace much of my interest in alternative thinking to my parents, who were both extremely bright and well-read individuals. My father, who had been a captain, in World War I, was the product of a classic East coast education and seemed to know everything about everything. My mother was a registered nurse and she was the one who directed me into medicine, by forcing me to get a job, in the summer of my high school graduation, in 1963, as an orderly, at the University of Missouri Teaching Hospital, in Columbia, Missouri. When I think back to my youth, one of the turning points, at the age of 15, was reading Immanuel Velikovsky’s book’s Worlds in Collision and Earth in Upheaval. I realized, after reading these books the important issue for me was not whether Dr. Velikovsky was right or wrong about his theories (I believe he was right, about most things), but how the scientific establishment dealt with someone who dared to question consensus views. This attitude of not accepting what everyone assumes is the truth has stuck with me for the rest of my life.

Another turning point, for me, and my career, occurred early in my private practice, in the 1980s, when I was confronted with patients with cyclic mood problems, which my training had not prepared me to deal with, at all. The only thing that I could think of, for people like this, was hysterectomy and putting them on Premarin. One of my patients directed me to the works of Dr. Katharina Dalton, in London, England. When I tried some of her techniques of supplemental natural progesterone, I was astonished to find that it worked remarkably well. As a result, my family and I took a trip to London, where I spent a week with Dr. Dalton learning her techniques. When I returned home, full of enthusiasm to share my new knowledge, I was shocked to find that most of my colleagues were very negative and wanted nothing to do with this information. It literally drew a line in the sand, with me on one side and most of my colleagues on the other. However, when I looked around, most of the patients were on my side of the line.

Because of my age, I did some of my training in the days before Synthroid dominated the market and natural products, such as Armour, were still in wide use. My mother was hypothyroid and I watched as her new doctors switched her to modern medicines, leaving her with a continued weight problem and fatigue. Because of this, I was open-minded enough to prescribe Armour, if patients requested it, but I really did not know much about it until I met another physician from Columbia, Missouri, Dr. Mark Starr. Mark was from Columbia and moved back here to start a practice. He is the author of the book Hypothyroidism Type 2. I realized that he had a lot to offer my patients and so I began to communicate with him. He is the one who directed me toward the work of Dr. Broda Barnes and opened my mind about thyroid. Since then, I have continued to read and study, extensively, about thyroid. My education was enhanced when I was diagnosed with Hashimoto’s thyroiditis, in the last decade.

Interestingly enough, one of my patients had brought me one of the first editions of Stop the Thyroid Madness, prior to my diagnosis. I actually used many of the techniques and suggestions, in the book, to guide me through my own hypothyroid treatments, including a trial of Synthroid, finding elevated reverse T3, having to use T3 only and, finally, settling on desiccated thyroid, which I have been on since that time.

When Janie Bowthorpe called me to ask me to write a chapter, for her new book, I was dumbfounded to find that anyone knew who I was. I was likewise astonished at the other authors in the new book, many of whom are people whose works I regularly read. My hope is that this chapter will provide a small overview of my view on thyroid disease and the general approaches that I take with it. I will end by saying that the most powerful tool that anyone has to control their health destiny is what they eat every day

** Dr. Trumbower’s obituary http://www.columbiatribune.com/obituaries/bill-trumbower/article_60ba8e47-c38f-5f03-ad9a-a87978dfa9ef.html

March 10th 2016 26 replies

Inflammation Kills!! A pertinent article for thyroid patients by Yusuf Saleeby, MD

Thyroid patients are wiser!! They now know what thyroid treatment works, and what doesn’t.

And they’ve also noted common issues that they share with a large percentage of each other…one being INFLAMMATION.

Sometimes, thyroid patients don’t even know where the inflammation exists in their body, except that their high ferritin reveals it, or their C-Reactive Protein or ESR (erythrocyte sedimentation rate or sed rate) lab tests reveal it. Other times, it’s obvious by the pain they notice in their bodies.

Some ways to deal with inflammation, especially for Hashimotos patients, is removing gluten from the diet. Others have to ascertain if they have Lyme disease that needs treatment. Some have neither problem, but inflammation exists anyway!

Many thyroid patients take supplements to help lower that inflammation, which range from Astaxanthin to Ginger to NAC to Curcumin/Turmeric…and/or a combination of them all.

Here’s a great article written by Yusuf Saleeby, MD. He happens to also be a contributor to the new STOP THE THYROID MADNESS II book, which you should read, and/or give to someone you love as a Christmas present!!

The following published in May/June 2014 edition American Fitness magazine.

It has been well known and understood for years that inflammation is harmful. Inflammation essentially kills. Well, not right away or in a big flashy way, but it does hurt our chances for a healthy disease-free existence and does shorten our lifespan. Inflammation has been proven to increase your risk for heart disease, heart attacks and strokes.^1-3 Inflammation is also known to increase a person’s risk for cancer.^4,5 It is also linked to obesity and metabolic syndrome; even implicated in Parkinson’s and Alzheimer’s Disease.^6-8,9-12

In 2011, researchers at Ohio State University found a link between inflammation and a molecule called microRNA-155 (miR-155). What they discovered was in chronic inflammatory conditions, levels of miR-155 rise and this molecule stimulates and allows for spontaneous mutations of cells contributing to tumorigenesis, the mechanism whereby normal cells become cancerous cells.^13-16 While cancers are devastating diseases, all deaths due to cancer do not even come close to numbers of Americans who succumb to heart disease and stroke. So for the purpose of this article we will focus on how inflammation is a big silent killer regarding our hearts and brains; our attention will be on cardiovascular and cerebrovascular disease.

To put it simply, inflammation causes undesirable reactions on the inner lining of blood vessels. The combination of inflammation and circulating lipids is a dangerous recipe that produces something called “foam cells”. Foam cells attach to the endothelial lining of our blood vessels, such as the arteries that feed our heart and brain, and once they mature over months to years form arterial plaques. These plaques narrow the blood vessels making it an eventual challenge for oxygen carrying blood cells to pass. Distal tissues to these narrowing arteries are the ones that suffer. When cells do not get the oxygen they need the result is tissue necrosis in the form of a heart attack or a stroke. Another pathogenesis of inflammation is its impact on maturing plaques. It just happens that inflammation can cause, in a rather short time frame, the rupture of these vessel plaques. In doing so, that plaque can quickly obstruct all blood flow quite abruptly and results in significant damage downstream. One of the biomarkers we shall discuss is FDA-cleared for assessment of plaque rupture and risk of stroke.¹⁶ Specific clinically available inflammatory markers are now available for the diagnosis and management of chronic inflammatory states which can impact life and health.

With the recent availability of advanced laboratory testing with a number of inflammatory biomarkers, the clinician has the obligation of identifying inflammation and stomp it out before it puts patients at risk for some ugly disease processes. Identifying overt acute inflammation is as easy as feeling a hot knee joint for example, or identifying fever, stiffness, swelling or pain. Measuring it or quantifying it has typically been with the use of the time tested but non-specific erythrocyte sedimentation rate (ESR) and more recently the C-reactive protein (CRP) tests. However, newer, more specific and diagnostically advanced biomarkers of inflammation have arrived on the playing field to help doctors assess and gauge inflammation. They are sensitive enough to pick up harmful levels of inflammation that may go unnoticed to the casual observer (both patient and doctor). Once identified, the measured inflammation can be watched and carefully reduced by prescriptive medications (statin drugs or anti-inflammatory agents as an example), orthomolecular therapies such as glutathione (NAC), resveratrol or turmeric, and lifestyle modifications (smoke cessation, exercise and weight loss).^17,18 Reassessing these inflammatory biomarkers allows clinicians to better guide their patients and assure the reduction of this disease causing entity. This article will discuss a few of these cutting edge inflammatory biomarkers that are currently being used in some clinical practices to identify people at risk for heart disease, stroke, neurodegenerative disorders and diabetes. There are other biomarkers available, many used in research and not clinically applicable or practical. At some point in the future they may find clinical application. Scientists are likely to discover even better biomarkers with more specificity and selectivity for certain conditions as research continues in this field. However, for the time being we will examine the PLAC test, the high sensitivity C-Reactive Protein, Fibrinogen, F₂-Isoprostanes, Myeloperoxidase, Interleukins 6 & 17a, and Tumor Necrosis Factor-alpha. Preventive medicine physicians are measuring and monitoring these inflammatory markers to reduce the risk of end-organ damage and degenerative disease in their patients.

Lipoprotein-Associated Phospholipase A₂ (Lp-PLA₂, or PLAC)

The Lp-PLA₂ biomarker is an enzyme associated with plaques in the arteries. Carried mostly by LDL-Cholesterol this enzyme in high levels of circulation is found when inflammation is high and plaque rupture in eminent. When levels of this inflammatory marker remain high for long periods of time there is a very high chance for cardiovascular events and risk of ischemic stroke. Prolonged activity of this enzyme is associated with coronary calcification or ‘’hardening of the arteries”. The PLAC test was recently cleared by the FDA to assess the risk of both coronary heart disease and ischemic stroke associated with atherosclerosis.¹⁶ Nicotinic acid as well as fenofibrate therapy has effectively treated elevations in Lp-PLA₂.^19,20

High sensitivity C-Reactive Protein (hs-CRP)

Much like the ESR this biomarker of inflammation is non-specific; it is formed in the liver as a reaction to inflammation occurring in other parts of the body. The high sensitivity CRP is a measure of minuscule amounts of this protein that are typically associated with vascular inflammation. The chronic elevation of this acute phase reactant is used to predict risk of heart attack and undesirable events in those with angina and in those who are having a heart attack. Elevated CRP may be a better predictor of heart disease than elevations in LDL-cholesterol.²¹ While Lp-PLA₂ elevations can double the risk for heart attack and stroke, having both the Lp-PLA₂ and hs-CRP elevated increases heart disease four-fold and stroke risk by a factor of ten. This inflammatory protein responds remarkably well to exercise.²¹

Fibrinogen

Fibrinogen will convert to fibrin as blood clots form. So fibrinogen, a protein, is a good measure of acute inflammation and is associated with risks of heart disease. Elevated fibrinogen can cause platelets to clump together or aggregate, increase the viscosity of blood and embellish other clotting factors. There is a strong correlation between elevated levels of fibrinogen and acute ischemic stroke.²² Fibrinogen is therefore a good tool for evaluation of stroke risk and prediction of a future heart or brain event. To reduce this pro-thrombotic state, a reduction of fibrinogen can be accomplished by routine aerobic exercise, smoke cessation, aspirin therapy and omega-3 fish oil supplementation and increasing endogenous glutathione with N-AcetylCystine (NAC) or bioavailable oral/IV glutathione (S-AcetylGlutathione).²³

F₂-Isoprostanes (F₂-Isops)

While the initial implementation of exercise can often raise the F₂-Isops levels, eventually sustained regular exercise lowers it to safer levels. F₂-Isoprostanes are prostaglandin like compounds which are formed by the oxidation of free fatty acids by free-radicals in circulation. Poor diets, too rich in red meat, a sedentary lifestyle and cigarette smoking all contribute to the elevation of this inflammatory marker. F₂-Isops is a strong predictor of coronary heart disease (CHD) as elevated levels cause oxidative stress on arterial walls and the production of atherosclerotic plaques. These isoprostanes also act as potent vasoconstrictors, which can further limit passage of blood cells through already narrowed arteries. Control of triglycerides (TG), diet and exercise combat this marker. Eicosapentaenoic acid (EPA) and docosapentaenoic acid (DHA) are two omega-3 fatty acids that are generally shown in multiple research studies to lower F₂-Isoprostanes.^23-26

Myeloperoxidase (MPO)

Particular white blood cells (WBC) called polymorphonuclear leukocytes and monocytes produce an enzyme called myeloperoxidase, this enzyme help your immune system fight infections only when your body uses it correctly. With chronic inflammation there is too much MPO released into circulation from WBCs and this hampers the function and bioavailability of nitric oxide. Nitric oxide (NO) is crucial to proper endothelial function in our arterial walls. MPO also causes the oxidation of HDL-C (good cholesterol) and impairs its ability to pull bad cholesterol (LDL-C) away from arteries for recycling. Additionally, the oxidizing effect of MPO on LDL-C contributes to the formation of foam cells and increases the likelihood of plaque rupture. Elevated levels of MPO in the presence of coronary artery calcium (CAC) raise the risk for a coronary event. Aspirin therapy, statin drug therapy (such as atrovastatin (Lipitor®) for example) and proper diet rich in omega-3 fatty acids (fish oil) all help lower MPO.²⁷ Of all the biomarkers discussed here, probably the most detrimental when found elevated is the MPO. Aggressive measures should be taken to reduce this marker, especially over the long term.

Interleukin-6 (IL-6)

Interleukin-6 (IL-6) is a pro-inflammatory cytokine. Cytokines are proteins that act as cell-signaling molecules in the immune system. IL-6 can increase the aggregation of platelets causing clumping and infarction when blood vessels are narrow and blood flow is impeded. IL-6 augments the synthesis of CRP and is thus associated with increased risk of cardiovascular disease (CVD). Elevated levels of IL-6 are associated with a 2 fold increase in diabetes risk and an even higher (3-fold) risk of CVD. We know the blockade of IL-6-receptors by drugs like tocilizumab (Actemra®) in patients with rheumatoid arthritis is helpful, but whether this drug will have a similar effect on reduction of the ill effects of this circulating inflammatory cytokine on the heart or brain remains to be seen.²⁸

Interleukin-17a (IL-17a)

Another inflammatory cytokine that has a role in vascular remodeling and function is Interleukin-17a. Elevated levels of IL-17a are responsible for vascular dysfunction and are found at increased levels in the presence of unstable angina and heart attacks. However, one study pointed out that low levels of circulating IL-17a in the presence of an acute myocardial infarction (AMI) or heart attack had poor outcomes for survival. While some studies show it as a risk factor in the asymptomatic individual, this may be untrue in the acute setting. More research is needed. Hence, blocking this interleukin too aggressively may have unwanted outcomes.²⁹

Tumor Necrosis Factor-alpha (TNF-Î±)

A pro-inflammatory cytokine referred to as TNF-Î± is excreted from macrophages (immune system cells that fight infecting microbes). People with the autoimmune and inflammatory disease systemic lupus erythematosus (SLE) are known to be at higher risk for CVD. There is a correlation between the inflammatory TNF marker which is elevated in SLE patients and their CVD risk. Some researchers are inclined to believe that this is what causes the increased risk of heart attacks in this subset of patients. Elevated levels of this cytokine can have a negative effect on sugar metabolism by interfering with insulin receptors. Elevated TNF-Î± levels result in a two fold increase in CVD risk. Weight loss and statin drug therapy can lower these levels. Controlling this marker’s levels may also reduce the risk of acquiring diabetes.³⁰

So the take home message here is that chronic inflammation is bad for your health and wellbeing. Even acute bursts of inflammation can significantly raise the risk of an acute event such as a heart attack or stroke. A very good illustration of this is found in a study in Mexico City, where air pollution levels are monitored in one of the most polluted cities in the western hemisphere. There were correlations made with rises in AMIs in a population of nursing home patients on particularly dirty air quality days in that city. The elevated air particle count attributed to an acute increase in inflammatory biomarkers and thus triggered heart attacks.³¹

Besides the impact on cardiovascular health, inflammation is to be avoided for many other reasons, from neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease to development of cancers to destructive and degenerative diseases of our skeletal system. We are now at the cusp of clinically available, specific biomarkers of inflammation that allow doctors to identify those at risk and diligently (with periodic monitoring of serum and urine levels) evaluate therapy that reduce harmful inflammation.

ABOUT THE AUTHOR: Yusuf (JP) Saleeby, MD is a contributing editor for American Fitness magazine. He practices preventive integrative medicine and age management in Murrells Inlet & Greenville, SC. Dr. Saleeby is regional director of a direct access testing site that offers analysis of inflammatory bio-markers. He can be reached at www.saleeby.net or by e-mail at jpsaleeby@aol.com. You can also see his other website here: http://www.getmythyroidfixed.com/

SEE MORE BELOW THE REFERENCES….

References:

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DANESH, J., ET AL. “C-REACTIVE PROTEIN AND OTHER CIRCULATING MARKERS OF INFLAMMATION IN THE PREDICTION OF CORONARY HEART DISEASE.”THE NEW ENGLAND JOURNAL OF MEDICINE, 350, NO. 14 (APR 2004): 1387-97.
RÜCKERL, R., ET AL. “AIR POLLUTION AND MARKERS OF INFLAMMATION AND COAGULATION IN PATIENTS WITH CORONARY HEART DISEASE.”AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 173, NO. 4 (2006): 432-41.
AGGARWAL, B.B., ET AL. “INFLAMMATION AND CANCER: HOW HOT IS THE LINK?”BIOCHEMICAL PHARMACOLOGY, 72, NO. 11 (NOV 2006): 1605-21.
HUSSAIN, S.P. AND HARRIS, C.C. “INFLAMMATION AND CANCER: AN ANCIENT LINK WITH NOVEL POTENTIALS.”INTERNATIONAL JOURNAL OF CANCER, 121, NO. 11 (DEC 2007): 2373-80.
LEE, Y.H. AND PRATLEY, R.E. “THE EVOLVING ROLE OF INFLAMMATION IN OBESITY AND THE METABOLIC SYNDROME.”CURRENT DIABETES REPORTS, 5, NO. 1 (2005): 70-75.
GENCO, R.J., ET AL. “A PROPOSED MODEL LINKING INFLAMMATION TO OBESITY, DIABETES, AND PERIODONTAL INFECTIONS.”JOURNAL OF PERIODONTOLOGY, 76, NO. 11 (SUPPL.) (NOV 2005): 2075-84.
ARKAN, M.C., ET AL. “IKK-BETA LINKS INFLAMMATION TO OBESITY-INDUCED INSULIN RESISTANCE.”NATURE MEDICINE, 11, NO. 2 (JAN 2005): 191-98.
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DOURSOUT, H.F., ET AL. “INFLAMMATORY CELLS AND CYTOKINES IN THE OLFACTORY BULB OF A RAT MODEL OF NEUROINFLAMMATION; INSIGHTS INTO NEURODEGENERATION?”JOURNAL OF INTERFERON & CYTOKINE RESEARCH, 33, NO. 7 (JUL 2013): 376-83.
LEE, Y.J., ET AL. “INFLAMMATION AND ALZHEIMER’S DISEASE.”ARCHIVES OF PHARMCAL RESEARCH, 33, NO. 10 (OCT 2010): 1539-56.
TUPPO, E.E. AND ARIAS, H.R. “THE ROLE OF INFLAMMATION IN ALZHEIMER’S DISEASE.”INTERNATIONAL JOURNAL OF BIOCHEMISTRY AND CELL BIOLOGY, 37, NO. 2 (FEB 2005): 289-305.
O’CONNELL, R.M., ET AL. “MICRORNA-155 IS INDUCED DURING THE MACROPHAGE INFLAMMATORY RESPONSE.”PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 104, NO. 5 (JAN 2007): 1604-09.
TILI, E., ET AL. “MUTATOR ACTIVITY INDUCED BY MICRORNA-155 (MIR-155) LINKS INFLAMMATION AND CANCER.”PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 108, NO. 12 (MAR 2011): 4908-13.
O’CONNELL, R.M., RAO, D.S. AND BALTIMORE, D. “MICRORNA REGULATION OF INFLAMMATORY RESPONSES.”ANNUAL REVIEW OF IMMUNOLOGY, 30 (2012): 295-312.
BALLANTYNE, C.M., ET AL. “LIPOPROTEIN-ASSOCIATED PHOSPHOLIPASE A2, HIGH-SENSITIVITY C-REACTIVE PROTEIN, AND RISK FOR INCIDENT ISCHEMIC STROKE IN MIDDLE-AGED MEN AND WOMEN IN THE ATHEROSCLEROSIS RISK IN COMMUNITIES (ARIC) STUDY.”ARCHIVES OF INTERNAL MEDICINE, 165, NO. 21 (2005): 2479-84.
EDELMAN, D., ET AL. “A MULTIDIMENSIONAL INTEGRATIVE MEDICINE INTERVENTION TO IMPROVE CARDIOVASCULAR RISK.”JOURNAL OF GENERAL INTERNAL MEDICINE, 21, NO. 7 (2006): 728-34.
TILI, E., ET AL. “RESVERATROL DECREASES THE LEVELS OF MIR-155 BY UPREGULATING MIR-663, A MICRORNA TARGETING JUNB AND JUND.”CARCINOGENESIS, 31, NO. 9 (SEP 2010): 1561-66.
GARZA, C.A., ET AL. “ASSOCIATION BETWEEN LIPOPROTEIN-ASSOCIATED PHOSPHOLIPASE A2 AND CARDIOVASCULAR DISEASE: A SYSTEMATIC REVIEW.”MAYO CLINIC PROCEEDINGS, 82, NO. 2 (2007): 159-65.
KEI, A., ET AL. “LIPID-MODULATING TREATMENTS FOR MIXED DYSLIPIDEMIA INCREASE HDL-ASSOCIATED PHOSPHOLIPASE A2 ACTIVITY WITH DIFFERENTIAL EFFECTS ON HDL SUBFRACTIONS.”LIPIDS, 48, NO. 10 (OCT 2013): 957-65.
RIDKER, P.M. “C-REACTIVE PROTEIN: A SIMPLE TEST TO HELP PREDICT RISK OF HEART ATTACK AND STROKE.”CIRCULATION, 108, NO. 12 (2003): E81-85.
NAPOLI, M.D. AND SINGH, P. “IS PLASMA FIBRINOGEN USEFUL IN EVALUATING ISCHEMIC STROKE PATIENTS: WHY, HOW, AND WHEN?”STROKE, 40, NO. 5 (2009): 1549-52.
MAS, E., ET AL. “THE OMEGA-3 FATTY ACIDS EPA AND DHA DECREASE PLASMA F(2)-ISOPROSTANES: RESULTS FROM TWO PLACEBO-CONTROLLED INTERVENTIONS.”FREE RADICAL RESEARCH, 44, NO. 9 (SEP 2010): 983-90.
NIKOLAIDIS, M.G., KYPAROS, A. AND VRABAS, I.S. “F2-ISOPROSTANE FORMATION, MEASUREMENT AND INTERPRETATION: THE ROLE OF EXERCISE.”PROGRESS LIPID RESEARCH, 50, NO. 1 (JAN 2011): 89-103.
MILNE, G.L., MUSIEK, E.S. AND MORROW, J.D. “F2-ISOPROSTANES AS MARKERS OF OXIDATIVE STRESS IN VIVO: AN OVERVIEW.”BIOMARKERS, 10, SUPPL. 1 (2005): 10-23.
LYNCH, S.M., ET AL. “FORMATION OF NON-CYCLOOXYGENASE-DERIVED PROSTANOIDS (F2-ISOPROSTANES) IN PLASMA AND LOW DENSITY LIPOPROTEIN EXPOSED TO OXIDATIVE STRESS IN VITRO.”JOURNAL OF CLINICAL INVESTIGATION, 93, NO. 3 (1994): 988-1004.
WONG, N.D., ET AL. “MYELOPEROXIDASE, SUBCLINICAL ATHEROSCLEROSIS, AND CARDIOVASCULAR DISEASE EVENTS.”JACC: CARDIOVASCULAR IMAGING, 2, NO. 9 (SEP 2009): 1093-99.
HINGORANI, A.D. AND CASAS, J.P. “THE INTERLEUKIN-6 RECEPTOR AS A TARGET FOR PREVENTION OF CORONARY HEART DISEASE: A MENDELIAN RANDOMISATION ANALYSIS.”LANCET, 379, NO. 9822 (MAR 2012): 1214-24.
SIMON, T., ET AL. “CIRCULATING LEVELS OF INTERLEUKIN-17 AND CARDIOVASCULAR OUTCOMES IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION.”EUROPEAN HEART JOURNAL, 34, NO. 8 (FEB 2013): 570-77.
SVENUNGSSON, E., ET AL. “TNF-ALPHA: A LINK BETWEEN HYPERTRIGLYCERIDAEMIA AND INFLAMMATION IN SLE PATIENTS WITH CARDIOVASCULAR DISEASE.”LUPUS, 12, NO. 6 (2003): 454-61.
BROOK, R.D., ET AL. “PARTICULATE MATTER AIR POLLUTION AND CARDIOVASCULAR DISEASE.”CIRCULATION, 121 (MAY 2010): 2331-78.

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** WANT TO ORDER THE STTM BOOKS?? They are:

1) The Bible of Thyroid Treatment–all based on years of patients experiences and wisdom, called Stop the Thyroid Madness: A Patient Revolutions Against Decades of Inferior Thyroid Treatment.

2) A physician-written STTM BOOK, called Stop the Thyroid Madness II: How Thyroid Experts are Challenging Ineffective Treatments and Improving the Lives of Patients. Dr. Saleeby contributed Chapter 3 in this book and it’s a knockout of more information from the minds of medical professionals!

Or if you want BOTH, go here.

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December 3rd 2014 18 replies

Exercise reduces T3, Vitamin C lowers high cortisol, Interesting theory about iodine…and more.

DESICCATED THYROID QUOTE OF THE DAY: “I had potbelly pigs as pets for 18 years (my kids were allergic to cats and dogs). I took darn good care of them! Now pigs are taking care of me! :c)” ~Thyroid Patient Tula

THE STOP THE THYROID MADNESS BOOK IN SPANISH IS COMING OUT LATER THIS MONTH!

Look for a future announcement! It will only be available via the publishing company at first, which is here: //www.laughinggrapepublishing.com

CAN ENDURANCE EXERCISE AFFECT YOUR THYROID?

There has been some hoopla around the net about the possibility of endurance training affecting thyroid function in a negative way, especially in women (but could happen to men). And when women stop their endurance or cardio training, they see their T3 levels come back up where they should be. One article cites 80 difference references about problems caused from excess training or exercise. But what I fail to see mentioned in many articles is the potential physiological reason why. First, more intensive exercise raises cortisol levels (in those with healthy adrenal function–not in those with sluggish adrenal function). Both higher levels of cortisol, as well as increased inflammation, inhibit the conversion of T4 to T3. This inhibition raises the levels of Reverse T3, which lowers the cellular receipt of T3. And here’s something quite interesting also found in this article:

“….low intensity exercise (40%) does not result in significant increases in cortisol levels, but, once corrections for plasma volume reduction occurred and circadian factors were examined, low intensity exercise actually resulted in a reduction in circulating cortisol levels.”

The above biological fact about exercise and cortisol is another reason why intense exercise becomes a no-no if saliva testing proves you already have an adrenal (sluggishness) or HPA feedback issue.

VITAMIN C AFTER A WORKOUT CAN HELP LOWER HIGH CORTISOL–IS THERE SIGNIFICANCE FOR THYROID PATIENTS??

I thought I knew a lot about Vitamin C until thyroid Patient Kristian told me about Vitamin C helping to lower high cortisol. Well Blimey and Blow me down!! This article reveals, via certain studies, that taking 1,000 mg of vitamin C before a workout lowered high cortisol even 2 and 24 hours after the workout, or taking 1500 mg Vitamin C for eight days put cortisol 57% lower….and more. So perhaps we have another treatment for thyroid patients who find themselves with high cortisol (as revealed by a saliva test, NOT a blood test) or a mix of highs and lows. This Psychology Today article says Vitamin C might be an essential part of stress reduction, which a mix of highs and lows in which saliva testing reveals.

IODINE DEFICIENCY MAY NOT BE FROM LACK OF IODINE IN OUR SOIL?

From 2004, the article titled “Nutrition, evolution and thyroid hormone levels — a link to iodine deficiency disorders?” proposes that iodine deficiency may be more about historical changes in what humans now eat rather than a decrease of iodine from the environment. He explains that T3 is actually dependent on the amount of carbs we eat. He states:

While our Paleolithic ancestors subsisted on a very low carbohydrate/high protein diet, the agricultural revolution about 10,000 years ago brought about a significant increase in dietary carbohydrate. These nutritional changes have increased T3 levels significantly. Higher T3 levels are associated with an enhanced T3 production and an increased iodine requirement. The higher iodine requirement exceeds the availability of iodine from environmental sources in many regions of the world, resulting in the development of IDD.

DON’T DISMISS THE INFLAMMATION PROBLEM WITH THYROID DISEASE…

Normally, inflammation is a naturally healthy and positive response of your immune system to counter the infectious problem of a virus, bacteria or fungal excess. It can also be activated by an irritant (picture a splinter in your finger) or damage to your cells from an injury.

But in thyroid patients, especially those who have remained undiagnosed or poorly treated on T4-only meds, the inflammation response can become chronic and problematic! You might even get the diagnosis of Fibromyalgia because of it! And while many thyroid patients may be clear they have inflammation, others may have it with no clue! See the newest page on Stop the Thyroid Madness concerning the problem of inflammation, how to detect it, and what you need to do about it.

May 29th 2013 27 replies

Category: inflammation