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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!!

14 replies

Feel better on T4 than you did on Natural Desiccated Thyroid?

Occasionally, hypothyroid patients will exclaim with conviction and truth that they outright feel better on Synthroid or Levothyroxine (T4-only meds) than they did when they tried Natural Desiccated Thyroid (NDT) or even T3-only.  And we believe them.

But…there is an explainable reason which does not mean T4-only is better for you. It really isn’t. Bear with me and read on…

Years ago, as many of us were starting on NDT after being on T4, we were seeing our lives change in a huge way, far more than T4 did! It was like a miracle! Those five hormones really made a difference.

But some others were having problems when raising something so miraculous for others. Huh?? We didn’t get that.

It took awhile longer to finally see why and to answer the “huh?” i.e. we began to see that there were three strong and correctible reasons why someone was not seeing the miracle of NDT as others were, and instead, were blaming the NDT (or T3) and moving back to T4-only…

The three main and correctible reasons why NDT, which gives all five thyroid hormones, seems to fail…

1) NOT BEING “OPTIMAL” WITH YOUR NDT DOSE (it’s NOT about just being in range and not about being held hostage to the TSH)

We all have had a tendency to believe that our doctors know what they are doing with NDT or T3. But, the majority do not. They tend to leave you on too-low doses, and/or pay attention to the lousy TSH. Thus, due to the natural suppression of the feedback loop (hypothalamus to pituitary to thyroid), you will get worse on those lower doses, sooner or later. i.e. you will get more hypo, and/or have rising adrenaline, cortisol, anxiety or other. And because of that, some exclaim “NDT didn’t work for me!” and they rush back to T4-only.  But NDT, with all five thyroid hormones, could have worked well IF you had known to be more optimal. Optimal puts the free T3 towards the top of the range and the free T4 mid-range, and puts the TSH below range…all three…and removes all symptoms. What amount does that is very individual—some start to achieve that in mid-2 grains, others are in the 3-5 grain area, others may be higher.

What if you tried to raise to be optimal, but had worsening problems? Read #2 and #3 below.

2) NOT BEING OPTIMAL WITH YOUR IRON LEVELS (it’s not about just being in range)

When this is brought up to patients who once tried NDT and failed, they will exclaim with all sincerity “But my iron levels were great”. We know that a very small percentage may have had good iron. But what is common with the majority is they did NOT have good levels “Falling in the normal range” does not equal a good level of iron. It’s WHERE one falls that tells the story.

For example, with two types of ranges for serum iron (NOT ferritin):

a) When the range is approx. 40?155: women who have optimal serum iron tend to be close to 110, or 109, or 108, etc. They are NOT in the 90’s and definitely not lower when optimal. Men tend to be in the upper 130’s.
b)  When the range is approx. 7-27: women are optimal around 23ish; men are towards the top.

If they are lower than the latter examples, it messes up the ability to raise NDT and feel great without issue. Why? Inadequate iron levels tend to raise the reverse T3 (RT3) as one is raising their NDT.  As the RT3 goes up due to inadequate iron, you will feel worse. And because of that, some exclaim “NDT didn’t work for me!” and they rush back to T4-only…but if they had had optimal iron, NDT WOULD have worked…as long as they also had optimal cortisol (See #3 below) and were working to find their optimal dose of NDT (see #1)

See more details about iron here: http://stopthethyroidmadness.com/ferritin

3) NOT BEING OPTIMAL WITH YOUR CORTISOL LEVELS (it’s not about just being in range, and it’s NOT about blood cortisol)

We noted years ago that at least 50% of those with hypothyroidism had a cortisol issue as revealed by saliva, not blood. What does a cortisol issue mean? Either their cortisol was too high (due to the stress of being undiagnosed, poorly treated, or being on T4) or was too low (due to the stress of being undiagnosed, poorly treated, or being on T4), or had both high and low (due to the stress of being undiagnosed, poorly treated, or being on T4).

And what happens with a cortisol issue when you are trying to work with NDT? Either RT3 will go too high (the inactive hormone), or one’s T3 will pool in the blood and not make it to the cells, or both…and you won’t feel well or have bad reactions like excess adrenaline, anxiety, shakiness, feel-bads.

And because of having a cortisol issue, some exclaim “NDT didn’t work for me!” and they rush back to T4-only…but if they had…

a) done the 4-point saliva test, not blood
b) compared the saliva results it to the lab-values page (it’s not about that normal range)
c) CORRECTLY treated it (see this page, plus Chapter 6 in the updated revision STTM book if saliva is VERY low, which also applies to Adrenal Cortex),

….they would have soared on NDT…along with good iron and being OPTIMAL on NDT (or T3)

Note: it’s always about the results of a saliva test, NOT blood cortisol.

Bottom line, it’s not as simple as “feeling better on T4”. It’s more about that you are NOT experiencing the side effects that you did on NDT from any of the above three problems, which were all correctible. That is different.

“That all sounds like too much trouble–I’m staying on T4-only!”, you may be exclaiming….

There is a big problem with that reasoning that I hope you will be open to….Namely, T4-only outright…

  • CAUSES low iron
  • CAUSES a cortisol problem
  • CAUSES many other issues like lowered B12, lowered Vitamin D, rising blood pressure, rising cholesterol, depression, anxiety, heart issues, bone thinning, chronic pain….and more. The individuality is in who gets which…but T4 users do get problems of their own kind, sooner or later.

Please note that the above is not an empty strong opinion. It’s based on years of reported patient experiences from many who were on T4! i.e. most of the following hypothyroid symptoms were experienced by T4 users!! They were still hypo!

Now you may state “But I know people on T4 who do not have those problems!”.

First, some outright DO have some of those problems, but don’t realize it or they deny it (while others see it in them). Adrenal issues, even those denied, can make certain people awash with defensiveness, argumentativeness, denial, anger, paranoia towards others observations, low patience, moodiness, etc.

Yes, some on T4 do, in fact, do better than others. But you know what we have observed? The longer they stay on T4-only, the more problems WILL, in fact, raise their ugly heads eventually…like either adrenal issues, or low iron, or low B12, or depression, or rising cholesterol, or rising blood pressure, or heart problems, or dry skin and hair, or chronic pain, or bone loss, or rising illnesses…..on and on. Forcing the body to live for conversion alone backfires….sooner or later.

Summary: A working Natural Desiccated Thyroid, or adding T3 to that T4 as a second choice and getting those frees optimal, is a much better way to go than being on nothing but T4, according to years of worldwide patient experiences

A working NDT gives you all five thyroid hormones, and does NOT force you to live for conversion of T4 to T3 alone, i.e. some of NDT is direct T3. Additionally with T4-only, some people have genetic mutations which hinder the conversion of T4 to T3 and may not realize it.

There is a good reason that millions of patients found out that T4-only is not the way to go for many reasons, and NDT is the way to go if you correct the reasons you did NOT to do well...or even adding T3 to your T4 in an OPTIMAL amount. But you will still need optimal iron and cortisol!

P.S. The above three reasons are the most common for not doing well on NDT (or T3) and should be considered first. A 4th less common reason: chronic inflammation of any cause. Read about inflammation. If this is true for you, the sad part is that T4-only will also backfire, as it raises RT3.

Mold exposure can also effect conversion.

Click on the graphic to order an excellent saliva cortisol test.

101 replies

How foods you eat, or don’t eat, can make or break your health!

Headshot StandingWhen you think of doing things that will make you healthy, what do you think of?

But there’s one more way to achieve health: what we eat or don’t eat!  The right food is bigger than we ever imagined for our health and well-being as thyroid patients, especially if you have autoimmune issues. And that is an especially important when the shelves of our grocery stores are filled with rows and rows of over-processed junk!!

The following STTM Guest Blog Post…about FOOD…was written by Jennifer Robins. She was diagnosed with several autoimmune conditions like Hashimoto’s disease, had chronic infections, plus Lyme disease. Jennifer became gravely ill and mostly housebound. When traditional medical treatments failed to help, Jennifer turned to food for healing! Yes, food. She removed grain, dairy and refined sugars and began eating “predominantly Paleo”. And because of that radical change in the way she ate, she started reclaiming her life, one whole food at a time. Read about her interesting story!

I remember growing up eating a standard American diet, missing little to no school, and having more energy than any one person ever could use. While my family did not eat out or frequent drive-through windows routinely, our home had it’s share of boxed “food”. As a family, we were “healthy.” We felt good and rarely visited the doctor.

It’s funny looking back, how people defined “healthy”. Rarely did we think about what goes into our bodies as defining health. Instead, we tended to gauge our health by how we think we feel, how many prescription drugs we are taking, and whether or not we have made any trips to the emergency room.

However, with autoimmune disease and other chronic ailments growing exponentially every year, diet and food sourcing is becoming increasingly more important.

Eight years ago after giving birth to two babies less than a year apart, I felt miserable.

I chalked it up to the obvious lack of sleep, the stress of having two babies so close together, and to the fact that my husband was preparing to deploy, leaving me behind with our infant and toddler.

Exhausted, frazzled, irritable, lightheaded, and overheated, I finally headed to my general practitioner to seek advice. She ran thyroid labs and they were “normal”, except for my TSH which read 0. Yes, 0. We agreed to follow up several weeks later and when I did, my labs were all in range, including TSH, FT4, FT3, and reverse T3. My low TSH had resolved yet I felt just as horrible if not worse than the month prior.

Eventually I sought out the help of an endocrinologist who discovered my thyroid antibodies.

My Anti-Thyroglobulin levels were more than double the upper limit. All other thyroid labs were in range, as they fluctuated between hyper and hypothyroid. I was diagnosed with Hashimoto’s and sent on my way. I tossed my prescription for synthetic thyroid replacement, as I just wasn’t ready for that step, whatever that meant.

I ended up reading about the connection between gluten and autoimmune disease as I scoured the internet looking for answers to my affliction. I was desperate to avoid taking thyroid replacement for the rest of my life. I ran the stool test looking for antibodies produced against gluten and came back positive. So I gave up gluten and was very compliant; but within the year resolved to start thyroid medication.

I researched natural desiccated thyroid and knew it was the best fit for me, so I found a doctor willing to prescribe it. Over the next year or so things leveled out, symptoms improved, and I felt like I could at least participate in my life. We moved to another military assignment, I began working out more regularly, started routine acupuncture, and realized I wanted another baby.

After a few months of trying, I got pregnant.

I was elated and I was feeling better than I had in a long time. My pregnancy was fairly uneventful other than managing my thyroid dosage, and my delivery was unmedicated–a goal I had had for awhile. I had 3 healthy children and life was good.

But around 5 months postpartum, I began feeling terrible. 

It was even more terrible than I felt after the first two babies were born. I chalked it up to juggling 3 babies and the hormone shift as well as the need to recalculate my thyroid dosage. I had let my strict gluten free lifestyle go as well and it was time to refocus. So I lowered my meds, cleaned up my diet, and tried to ride it out.

And I got worse. Much worse.

I became so sick in fact that I was housebound 90% of the time and often bedbound. Now I was stricken with neurological symptoms including brain swelling, vertigo, migraines, severe emotional lability (especially when my brain was inflamed), heart palpitations, disorientation, word searching, and more. It was a living nightmare.

I visited a new integrative doctor, in yet another new city and sought help.

She ran labs for viruses, candida, thyroid, adrenals, nutritional deficiencies, and infections and included urine, stool, blood, and hair. The results were overwhelming. I had elevated antibodies for so many types of infections I didn’t know where to start. She noticed I had a few antibody bands come back positive on a western blot for Lyme disease and suggested I test further. I fell down a rabbit hole of more testing, more doctors, and lots of medication recommendations.

Ultimately, I chose to treat the Lyme disease as it was insinuated that this could be the root of all my issues. I began multiple high dose antibiotics that I eventually took for over a year. I was back to strict gluten free eating, took over 40 supplements, probiotics, herbs, and anything else that my doctors recommended. I saw 3 different Lyme literate physicians (LLMDs) over this time.

And I got even worse. Ridiculously worse.

I was assured that this was “herxing” or bacterial die off. So I persisted, I stayed on meds, and life just kept getting more horrendous. I so often begged to die that I wondered daily when my last day on earth would be. I knew I was dying, I just didn’t know when or how long it would take.

But during this time I researched. I read and read and dug until there was nothing left to read. I kept seeing things about the paleo lifestyle for any number of ailments. Be it autoimmune or otherwise, it seemed I was being pointed in this direction for a reason.

Ultimately I made the decision to stop taking antibiotics and start focusing on rebuilding my immune system instead of destroying it.

Giving up the remaining grains and dairy was terribly hard, but it was the first time I began seeing ANY progress in this very long journey. Slowly but surely, I began reclaiming bits of my life back. I began chronicling my recipes, keeping a blog in secret, and eventually sharing it with others. I simultaneously took my already-gluten-free children off of dairy as well, so I needed a place to revisit recipes that kept them nourished and happy too. I noticed changes in all of us. My five year old’s sleep apnea and enlarged tonsils all resolved, my two year old’s enlarged glands in both her groin and neck resolved, and my son’s tummy aches disappeared without gluten and dairy.

I see now how life altering food changes can be.

I see that what you put in your body has everything to do with not only how you feel from day to day but also has the capability of healing a leaky gut and truly managing autoimmune conditions. This does not mean that food always takes the place of medication or of medical care. But we cannot overlook nutrition as being instrumental in our healing.

In my own story, my body could not even begin to heal until I removed inflammation-causing foods, despite the multiple medications, supplements, and other lifestyle changes. My healing has been gradual, with those expected setbacks that have made me feel as if I was failing. But over the past 2+ years of eating this way, I have finally seen glimpses of the old me. Before my body began attacking itself, before I became a shell of the person I was, and before my immune system became my own worst enemy.

I consider myself a work in progress as I truly believe that once you have a chronic ailment, you must always take extra care in respecting your body and its limitations. But I am living again. I am an active parent, a contributing citizen and am no longer just a spectator of my own life. And for that my heart will never be able to exScreen Shot 2015-08-16 at 2.56.40 PMpress the joy and gratitude to have been born once again.

ABOUT JENNIFER ROBINS: Jennifer is the voice and whole foodist behind the popular food blog Predominantly Paleo and is best selling author of the fabulous book of recipes and information called Down South Paleo: Delectable Southern Recipes Adapted for Gluten-free, Paleo Eaters
–filled with gorgeous photos of the recipes she includes. You can also visit her Facebook page Predominantly Paleo which has some really delicious recipes on it, too.

P.S. I, Janie, have her book Down South Paleo: Delectable Southern Recipes Adapted for Gluten-free, Paleo Eaters and it is fabulous.

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11 replies

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

Screen Shot 2015-08-11 at 8.43.39 PMThyroid 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-α)

A pro-inflammatory cytokine referred to as TNF-α 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-α 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….

 ©2013-2014

 

References:

  1. TUOMISTO, K., ET AL. “C-REACTIVE PROTEIN, INTERLEUKIN-6 AND TUMOR NECROSIS FACTOR ALPHA AS PREDICTORS OF INCIDENT CORONARY AND CARDIOVASCULAR EVENTS AND TOTAL MORTALITY. A POPULATION-BASED, PROSPECTIVE STUDY.”THROMBOSIS HAEMOSTATIS, 95, NO. 3 (MAR 2006): 511-18.
  2. 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.
  3. RÃœCKERL, 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.
  4. AGGARWAL, B.B., ET AL. “INFLAMMATION AND CANCER: HOW HOT IS THE LINK?”BIOCHEMICAL PHARMACOLOGY, 72, NO. 11 (NOV 2006): 1605-21.
  5. 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.
  6. 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.
  7. 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.
  8. ARKAN, M.C., ET AL. “IKK-BETA LINKS INFLAMMATION TO OBESITY-INDUCED INSULIN RESISTANCE.”NATURE MEDICINE, 11, NO. 2 (JAN 2005): 191-98.
  9. WÃœLLNER, U. AND KLOCKGETHER, T. “INFLAMMATION IN PARKINSON’S DISEASE.”JOURNAL OF NEUROLOGY, 205, NO. 1 (FEB 2003): 35-38.
  10. 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.
  11. LEE, Y.J., ET AL. “INFLAMMATION AND ALZHEIMER’S DISEASE.”ARCHIVES OF PHARMCAL RESEARCH, 33, NO. 10 (OCT 2010): 1539-56.
  12. 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.
  13. 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.
  14. 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.
  15. O’CONNELL, R.M., RAO, D.S. AND BALTIMORE, D. “MICRORNA REGULATION OF INFLAMMATORY RESPONSES.”ANNUAL REVIEW OF IMMUNOLOGY, 30 (2012): 295-312.
  16. 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.
  17. EDELMAN, D., ET AL. “A MULTIDIMENSIONAL INTEGRATIVE MEDICINE INTERVENTION TO IMPROVE CARDIOVASCULAR RISK.”JOURNAL OF GENERAL INTERNAL MEDICINE, 21, NO. 7 (2006): 728-34.
  18. 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.
  19. 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.
  20. 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.
  21. 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.
  22. 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.
  23. 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.
  24. 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.
  25. 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.
  26. 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.
  27. WONG, N.D., ET AL. “MYELOPEROXIDASE, SUBCLINICAL ATHEROSCLEROSIS, AND CARDIOVASCULAR DISEASE EVENTS.”JACC: CARDIOVASCULAR IMAGING, 2, NO. 9 (SEP 2009): 1093-99.
  28. 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.
  29. 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.
  30. 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.
  31. BROOK, R.D., ET AL. “PARTICULATE MATTER AIR POLLUTION AND CARDIOVASCULAR DISEASE.”CIRCULATION, 121 (MAY 2010): 2331-78.

******

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What thyroid patients should know about Oxidative Stress

20130817_151332With a recent Italian study hypothesizing a significant correlation between T4-only levothyroxine use and lung cancer because of “oxidative stress” (possibly due to the serum peak of T4), or the same oxidative stress simply from the hypothyroidism itself, it spurs curiosity as to what oxidative stress is about and what we, as thyroid patients, can learn from this biological phenomena!

Oxidation–what the heck is that?

I have a shampoo holder that hangs from the shower nozzle, and to my dismay, it started to rust underneath the coating. (Note to self: don’t buy a hanging shampoo holder from a garage sale, even if it does look brand new).  And this rust is an example of “oxidation”, i.e. when the iron comes into contact with oxygen (also via moisture), an oxidized corrosion will form called “rust”. Other examples of oxidation are the greenish patina you see on copper, the fading of paint on your house, or the brown coating you’ll see on an exposed cut apple…all due to the substance coming in contact with oxygen.

In your body, oxidation is a constant and normal chemical reaction going on every hour, every day and occurring when your cells come into contact with oxygen. It’s a required process to supply your body and all its cells with energy. Oxidation helps your body to get rid of old cells in favor of new cells. Your immune system also uses oxidation to attack and kill off pathogens.

Biologically, oxygenation describes the process of any particular molecule (which is made up of connected atoms) coming into contact with oxygen (making it an “oxygenated molecule”), resulting in the loss of an electron–a subatomic particle with a negative electric charge that surrounds any of those atoms. This oxygenated-molecule-minus-an-electron will frantically try to connect with another molecule which does NOT have this electron loss, and this constant attempt of connection produces an unstable “free radical”. And free radicals can cause all sorts of havoc.

Fortunately, a healthy and balanced body has a built-in ability to keep these unstable free radicals in check with anti-oxidant defense mechanisms…or at the very least, slow the havoc of a free radical down. Those heroes include several anti-oxidant enzymes, also called free radical scavengers, which can neutralize all those frenzied free radicals. Our body will also use nutrients in what we eat to squelch those free radicals, such as Vitamin C and E. Our bodies have the ability to repair DNA and tissue damage from free radicals, as well as zap damaged cells to death!

When Oxidation become “Oxidative Stress”

On the negative side, sometimes your body can lose the ability to take care of all the free radicals caused by the constant oxidation. (Collectively, all these free radicals are called “reactive oxygen species” (ROS).) The body then becomes overwhelmed by the excess of oxygenated free radicals, causing all sorts of damage. And this is all termed “oxidative stress”. 

Alarmingly, oxidative stress can cause the loss of one of your key and internally-natural antioxidants: glutathione. Glutathione is a powerful antioxidant produced by your own cells, and it neutralizes those free radicals/reactive oxygen species. It also works expertly with antioxidants vitamin C and E. And as your glutathione levels fall, a cascade of toxic deterioration and damage can also begin, from cells to tissues to organs. Scientists theorize, and studies propose, that this is what leads to conditions like:

Oxidative stress may also be negatively affecting your methylation process, such as the MTHFR enzyme.

Dr Andrew Weil explains :

Although we need oxygen to live, high concentrations of it are actually corrosive and toxic. We obtain energy by burning fuel with oxygen – that is, by combining digested food with oxygen from the air we breathe. This is a controlled metabolic process that, unfortunately, also generates dangerous byproducts. These include free radicals – electronically unstable atoms or molecules capable of stripping electrons from any other molecules they meet in an effort to achieve stability. In their wake they create even more unstable molecules that then attack their neighbors in domino-like chain reactions.

Some Causes of oxidative stress

There are quite a few situations mentioned in articles and studies which can cause your body to be overly stressed from the results of oxidation and all the reactive oxygen species. They include, but are not limited to:

  • excess endurance exercising
  • excess weight lifting
  • lack of key antioxidant nutrients like Vitamin C, Vitamin E, Selenium, Magnesium and other minerals
  • excess radiation or sunlight
  • smoking (huge cause of oxidative stress)
  • excessive drinking or drug use
  • over-exposure to toxins in our air, water and foods like pesticides, chemicals, heavy metals and more
  • prescription medications
  • processed foods with all their artificial dyes, additives or flavorings
  • excess physical trauma
  • Graves disease aka hyperthyroidism
  • excess copper levels from the MTHFR defect

Your thyroid condition and Oxidative Stress

In addition to all the above, there are a vast amount of documentation about the strong relationship between hypothyroidism and Oxidative Stress. In just four examples of many:

  1. Oxidative stress and enzymatic antioxidant status in patients with hypothyroidism before and after treatment :  concludes that “increased ROS levels in hypothyroidism may result in a pro-oxidation environment, which in turn could result in decreased antioxidant PON1 activity, increased MDA (malondialdehyde) and NO (nitric acid) levels”. ROS stands for Reactive oxygen species, which are chemically reactive molecules containing oxygen
  2. Serum Lipids and Oxidative Stress in Hypothyroidism : found relationship between high Total Cholesterol, Triglycerides, LDL and MDA levels in hypothyroid patients with oxidative stress
  3. Oxidative Stress and Antioxidant Status in Hypo- and Hyperthyroidism  “Despite some contradictory reports, the aforementioned results provide strong evidence that thyroid hormones induce oxidative stress in target tissues.”
  4. Oxidative stress status in hypothyroid patients.  “Hypothyroidism undeniably can be risk factor for in- creased oxidative stress; can eventually lead to many other complications. Antioxidant therapy and antioxidant diet should be advised along with thyroid hormone replacement therapy to diminish further complications.”

What we might conclude as informed thyroid patients

Plenty of research studies and articles underscore that lack of optimal thyroid hormones are strongly associated with your anti-oxidative status in a negative way, meaning the lack of adequate thyroid hormones means oxidative stress. And worldwide thyroid patient reports underscore the reality of a potential, hypothyroid-induced “oxidative stress profile” with their chronic inflammation and finding themselves more frequent illnesses, besides lowered levels of important nutrients (due to hypothyroid-induced low stomach acid) which can end up contributing to oxidative stress. In other words, all too many patients have reported continued hypothyroidism while being on T4-only, or they reporting seeing symptoms of hypothyroidism creep up the longer they stay on T4-only. Continued hypothyroidism can occur if you are undertreated even on Natural Desiccated Thyroid or T3-only thanks to being held hostage to the TSH lab test (or issues with untreated low cortisol).

Conversely, informed thyroid patients could surmise that proper treatment of their hypothyroid state, in addition to their acquire low iron, low nutrient, low cortisol state, could strongly improve their anti-oxidative status in a positive way. And reported patient experience in the use of Natural Desiccated Thyroid may be underscoring this, as well. Namely, patients who switch from T4 to NDT report far better health outcomes i.e. less sicknesses, better well-being, lowered inflammation.

In the meantime, the same four Italian researchers who did the study on T4-only, lung cancer and oxidative stress may eventually provide us with more tips to counter this issue.

Ten suggested strategies for informed thyroid patients to consider to counter oxidative stress

  1. Be on a thyroid treatment which gives the best results, and thus, may play a role in lowering your oxidative stress, which reported patient experience reveals to be natural desiccated thyroid (or adding T3 to your T4 treatment, or even being on T3-only).
  2. Get a wide variety of antioxidants in foods.
  3. Optimize and balance your blood sugar levels
  4. Identify and address your food intolerances
  5. Optimize your gut health
  6. Treat your low cortisol
  7. Dr. Kharrazian recommends the following nutrients: N-acetyl-cysteine (NAC), Alpha Lipoic Acid (ALA), L-Glutamine, Selenium, Cordyceps, Gotu kola and Milk thistle. (Learn about each before using)
  8. Consider meditation and/or Yoga or any other stress-busting activities
  9. Find ways to laugh…and laugh….and laugh!
  10. Get plenty of sleep.

Discuss all the above with your doctor so he or she can be included in your team approach to your health and well-being. Let’s STOP THE THYROID AND OXIDATIVE STRESS MADNESS! 🙂

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

** Want to chat with other patients concerning this oxidative stress issue? See a list of good thyroid patients groups.

** Need a good doctor to be in partnership with you? Here are strategies to help you.

** Like to learn in book form about better thyroid treatment? Order the Bible of better thyroid treatment as learned by patients (and the publishing company, with each order of the STTM book, is giving away a FREE 4-page handout on Herbs which help thyroid patients, for a limited time!)

** Check out this neat video by Tyler DeWitt explaining the difference between an atom and a molecule.

** For a very technical description of free radicals, check out the “Radical” Wikipedia article.

** See a list of diseases and conditions caused by oxidative stress on the Oxidative Stress Resource website. . http://www.oxidativestressresource.org/

 

16 replies