The Best Things in Life are Worth Waiting For…

May 18, 2013 in 2013, The Paleo Approach Excerpts

The Paleo Approach by Sarah BallantyneWell, at least I hope so! I hope that my book is worth waiting for! I also hope that my book is a “best thing”!

By now, if you have pre-ordered my book (and thank you for doing so if you have!!!), you have probably already received an e-mail from amazon letting you know that the expected shipping date has changed. You may have also noticed that I changed the release date in the advertisement on my sidebar.  Yes, the book will be coming out a little later than originally planned–the new release date is October 22nd, 2013.

So, what happened?

No one knew when I started this project just how BIG it was going to be. When we set the release date and my deadlines for turning in the material, the book was only a 24-page outline. This is my first book. So,  I really had no way to gauge just how many words it would take to explain what I wanted to explain and cover all of the topics I wanted to cover. Okay, yes, starting with a 24-page outline should have been a big clue that this book was going to be encyclopedic in scope, but at no time did I anticipate having a conversation with my publisher about the physical limits of book binding.  And my publisher, Victory Belt, who has published most of the best-selling paleo books out there, had no way to anticipate that what I was talking about doing would actually turn into a book of this magnitude. If any of us had known, it probably would have been two books. Or it would have been bound in hardcover and the sticker price would have been double. And, you know what this means? It means that my book is a completely spectacular good deal!

So, what happened is that when we set deadlines and the release date way back when I started this adventure, we were anticipating a book literally a third the size. Victory Belt has never published a book this big with so many different components (or “moving parts” as my publisher likes to call them). We just need more time to edit this beast, pull together all the graphic elements, and make sure that the quality of this book is top notch. For all the time and effort and self sacrifice that I have invested into this book, it’s important to me that we don’t skimp on this process. I want this book to be perfect (yeah, yeah, I know it won’t be perfect and I know typos always get missed, but it’s still a worthy goal). I want this book to help people, to have a real and wide-spread positive impact (and I hope you do too!).

How big is this book? Gargantuan. Think The Paleo Solution, The Paleo Answer and Practical Paleo all in one book, but focused on autoimmune disease. Of course, don’t think this book is just for those with autoimmune diseases because I have gone into details about how foods interact with the gut and the immune system that are broadly applicable to everyone. And I am super proud of my recipes. And my photography, actually (especially given the much lower quality photos I published on the blog when I first started). This book will be useful to anyone who wants to understand how food impacts our health, how lifestyle factors impact our health, and who want a really inventive cookbook too.

Where am I at? I turned in Part 2 of the book and two of the appendices last week (Part 1 was turned in in early April and is already being edited and sent to the graphics design team to start in on the illustrations). AND I turned it in on time!  Woot!  Parts 1 and 2 together are about 187,000 words.  There’s something like 30,000 more words in the appendices and I’m still working on a glossary of terms (there are 1185 references, which comprise about 25,000 words just on their own). I have no way to predict how many words the recipes will add, but I think it’s typically for recipes to add 30-50,000 more words. Just to give you some comparison, Practical Paleo (my favorite paleo resource guide for anyone who is trying to figure out which of the many paleo books out there to buy before mine is available!) was about 90,000 words (including recipes).  I am not exaggerating when I use words like gargantuan. And I am not exaggerating when I say that we are still trying to figure out how to format this book so that we can physically bind it (and still be able to read it!). Maybe we should do a special edition next year in hardcover…

In fact, this book is so big that when I went back to edit Parts 1 and 2 before turning them in, I didn’t remember writing a large proportion of what I was editing (I did write it though! Promise!). It was very surreal, reading my own words but without really remembering writing them… like reading someone else’s book but with a déjà vu type feeling of familiarity (ever accidentally read a novel that you read years and years ago but forgot that you read?… feels kinda like that). The cool thing is that this distances me a little from the writing so I can be a little more objective about it (and while I am still clearly biased, I do have to say that what I am reading is pretty darned good!).

I am now in full cookbook mode, which is Part 3 of The Paleo Approach (okay, the glossary is still science mode, but other than that it’s cookbook time). I am writing shopping lists and meal plans, frantically trying to finish a few recipes I really want to include, rephotograph recipes that I developed early on and that the photography is just not up to par, going through thousands of photos, and typing up the 105 plus recipes that are scribbled in three different notebooks (at this point, I am anticipating about 120 recipes in the book).  And, I’ve got two weeks to finish.

So, I hope you can be patient with me while I continue to focus most of my energy on finishing this book (the rest goes toward being a wife and mom) rather than creating new content for the blog. And I hope that waiting an extra month for my book won’t seem like too much of a hardship.  I am working extremely hard to make sure that it will be worth the wait.

Teaser Excerpt from The Paleo Approach: What about the Goitrogens in Cruciferous Veggies?

April 25, 2013 in The Paleo Approach Excerpts

The Paleo Approach by Sarah BallantyneThere are many topics that I am researching and writing about for the book that I’ve been meaning to write about for the blog for ages (the book just gives me a firm deadline). I have decided take some of these topics (especially the more blog-sized ones) and publish them as teaser excerpts for the book (also because I think this information should be here too).

This excerpt is from Chapter 6, which is the Chapter that details exactly what foods to eat to heal from autoimmune disease (think of it as a 40ish page version of my Autoimmune Protocol post.  One of the challenges I have faced as I write this book is the need to understand what recommendations are broadly applicable and what exceptions there may be for specific autoimmune diseases.  And goitrogenic veggies is a pretty hot topic given the prevalence of autoimmune thyroid diseases (and an important one to get right).

This section comes after a lengthy rationale for eating a large amount and variety of vegetables and fruits, with an emphasis on eating the rainbow and trying to eat something green with every meal.

So, forgive the references to other chapters and page numbers with no number. While you’ll have to wait until the book is out in September to read those sections, in the meantime, please enjoy this part of Chapter 6: The Paleo Approach–Diet

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Those with autoimmune thyroid disorders (Hashimoto’s thyroiditis or Grave’s disease) and those with low thyroid function (which can often accompany other autoimmune diseases) are often advised to avoid consumption of cruciferous vegetables, spinach, radishes, peaches and strawberries due to their goitrogenic properties.  Goitrogens are any compound that  suppress the function of the thyroid gland by interfering with iodine uptake (recall that iodine is a necessary component of thyroid hormones, see page ##).  Thyroid hormones have essential roles in metabolism and even in regulation of the immune system, so supporting optimal thyroid function in everyone is important for healing and for general health.  But avoidance of these foods is actually not well justified.

The cruciferous family of vegetables (a.k.a. brassicas) comprises many of the most antioxidant-, vitamin- and mineral-rich vegetables available, including:

  • horseradish
  • land cress
  • kale, many varieties
  • collard greens
  • Chinese broccoli (gai-lan)
  • Cabbage, many varieties
  • brussels sprout
  • kohlrabi
  • broccoli, many varieties
  • broccoflower
  • broccoli romanesco
  • cauliflower
  • wild broccoli
  • bok choy
  • Mizuna
  • Komatsuna

  • Rapini (broccoli rabe)
  • flowering cabbage
  • napa cabbage (siu choy)
  • turnip, many varieties
  • rutabaga
  • canola/rapeseed
  • mustard, many varieties
  • tatsoi
  • arugula (rocket)
  • field pepperweed
  • maca
  • garden cress
  • watercress
  • radish, many varieties
  • daikon
  • wasabi

This family of vegetables is also particularly rich in a group of sulfur-containing compounds called glucosinolates (see page ##).  When these vegetables are chopped or chewed, an enzyme called myrosinase that is also present in these plants breaks the glucosinolates apart (through hydrolysis) into a variety of biologically active compounds, many of which are potent antioxidants and are known to prevent cancer.  Two of these antioxidant, anti-cancer classes of glucosinolate hydrolysis products are also known goitrogens.  These are isothiocyanates and thiocyanates.

Isothiocyanates and thiocyanates appear to reduce thyroid function by blocking the activity of the enzyme thyroid peroxidase (a.k.a. thyroperoxidase or TPO).  During thyroid hormone synthesis, TPO is the enzyme that catalyzes the transfer of iodine to a protein called thyroglobulin to produce either T4 thyroid prohormone (a.k.a. thyroxine) or the more active T3 thyroid hormone (a.k.a. triiodotyronine).  When isothiocyanates or thiocyanates are consumed in large enough quantities, this is how they interfere with the function of the thyroid gland (by inhibiting TPO).

Importantly, the evidence linking human consumption of isothiocyanates or thiocyanates with thyroid pathologies in the absence of iodine deficiency is lacking.  This means that these substances have only been shown to interfere with thyroid function in people who are also not consuming adequate amounts of iodine (if you are severely deficient in iodine or selenium, addressing those deficiencies before consuming large amounts of cruciferous vegetables is a good idea; see page ##).  In fact, the consumption of cruciferous vegetables correlates with diverse health benefits, including reducing the risk of cancer (even thyroid cancer!).  In a recent clinical trial evaluating the safety of isothiocyanates isolated from broccoli sprouts, no adverse effects were reported (including no reported reductions in thyroid function).

Perhaps even more compelling, at low concentrations (like what you would get just by including cruciferous vegetables in your diet), thiocyanates actually stimulate T4 synthesis, meaning that consuming these vegetables labeled as goitrogens may actually support thyroid function.  There is also a strong synergy between isothiocyanates and selenium in the formation of the very important enzymes thioredoxin reductase (see page ##) and glutathione peroxidase (see page ##).  This means that the consumption of isothiocyanates in conjunction with selenium is a tremendous support for the body’s antioxidant defense mechanisms and important for cancer prevention.  These are arguments for consuming more cruciferous vegetables, even for those with autoimmune thyroid diseases, not less, especially in the context of adequate dietary iodine and selenium.

Truly, the most important aspect of supporting thyroid function is providing the necessary minerals for thyroid hormone production, the most important of which are iodine, iron, selenium and zinc.  Deficiencies in any one of the minerals may impair thyroid function, but the effect of deficiencies is greatly magnified when more than one of these minerals are not available in adequate quantities.  Iodine is a necessary building block of thyroid hormones and the thyroid cannot function properly if insufficient iodine is available (see page ##).  Iron deficiency impairs thyroid hormone synthesis by reducing activity of TPO (which is heme-dependent, see page ##).  As already discussed in Chapter 3, selenium is required both for the conversion of the T4 thyroid prohormone (a.k.a. thyroxine) to the more active T3 thyroid hormone (a.k.a. triiodotyronine) because the enzymes responsible for this conversion (iodothyronine deiodinases) are selenoproteins.  Selenium is also essential to protect the thyroid gland from the effects of excessive iodide (excessive iodine inhibits the activity of TPO).  Zinc is believed to play an important role in thyroid metabolism, although the details remain unknown.  It appears to play a role in the conversion of T4 to T3 and zinc levels correlate with the levels of thyroid stimulating hormone (TSH), although the precise ramifications of zinc deficiency for thyroid function remain controversial.  All of these minerals are richly found in the foods included in The Paleo Approach.  Supplements are also discussed in Chapter 8.

Barrera, L.N., et al., TrxR1 and GPx2 are potently induced by isothiocyanates and selenium, and mutually cooperate to protect Caco-2 cells against free radical-mediated cell death, Biochim Biophys Acta. 2012 Oct;1823(10):1914-24

 Bonfig, W., et al., Selenium supplementation does not decrease thyroid peroxidase antibody concentration in children and adolescents with autoimmune thyroiditis, ScientificWorldJournal. 2010 Jun 1;10:990-6

 Bosetti, C., et al., A pooled analysis of case-control studies of thyroid cancer. VII. Cruciferous and other vegetables (International), Cancer Causes Control. 2002 Oct;13(8):765-75

 Chandler, J.D. & Day, B.J., Thiocyanate: a potentially useful therapeutic agent with host defense and antioxidant properties, Biochem Pharmacol. 2012 Dec 1;84(11):1381-7

 Ertek, S., et al., Relationship between serum zinc levels, thyroid hormones and thyroid volume following successful iodine supplementation, Hormones 2010, 9(3):263-268

 Hodkinson, C.F., et al., Preliminary evidence of immune function modulation by thyroid hormones in healthy men and women aged 55-70 years, J Endocrinol. 2009 Jul;202(1):55-63

Jakubíková, J., et al., Effect of isothiocyanates on nuclear accumulation of NF-kappaB, Nrf2, and thioredoxin in caco-2 cells, J Agric Food Chem. 2006 Mar 8;54(5):1656-62

 Magnusson, R.P., et al., Mechanism of iodide-dependent catalatic activity of thyroid peroxidase and lactoperoxidase, J Biol Chem. 1984 Jan 10;259(1):197-205

 McDanell, R., et al., Chemical and biological properties of indole glucosinolates (glucobrassicins): A review, Food and Chemical Toxicology. 1988; 26(1):59-70

 Shapiro, T.A., et al., Safety, tolerance, and metabolism of broccoli sprout glucosinolates and isothiocyanates: a clinical phase I study, Nutr Cancer. 2006;55(1):53-62

 van Bakel, M.M., et al., Antioxidant and thyroid hormone status in selenium-deficient phenylketonuric and hyperphenylalaninemic patients, Am J Clin Nutr. 2000 Oct;72(4):976-81

 Virion, A., et al., Opposite effects of thiocyanate on tyrosine iodination and thyroid hormone synthesis, Eur J Biochem. 1980 Nov;112(1):1-7

 Zimmermann, M.B. & Köhrle, J., The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health, Thyroid. 2002 Oct;12(10):867-78

Teaser Excerpt from The Paleo Approach–The Importance of Sleep

April 4, 2013 in Practical Tips, Stress and Sleep, The Paleo Approach Excerpts

The Paleo Approach by Sarah BallantyneThere are many topics that I am researching and writing about for the book that I’ve been meaning to write about for the blog for ages (the book just gives me a firm deadline). I have decided take some of these topics (especially the more blog-sized ones) and publish them as teaser excerpts for the book (also because I think this information should be here too).

The book also contains a detailed (yet easy-to-follow) description of the components of the immune system, including a great quick reference guide to help you as you read through the book.  So, when you read this section in the book, you’ll already know why modulating Th1, Th2 and Th17 cells is important and you’ll already understand the essential role that regulatory T-cells play in the immune system.  

For a quick primer: Th1, Th2 and Th17 cells are subtypes of lymphocytes (white blood cells) that can be over-activated in autoimmune disease and cause damage. Regulatory T-cells are another subtype of lymphocyte that are supposed to keep all the other immune cells in check and suppress both over-activation of the  immune system and autoimmunity (they tend to be deficient in autoimmune disease). Cytokines are chemical messengers of inflammation. Monocytes and neutrophils are types of white blood cell responsible for generalized inflammation (part of the innate immune system whereas B-cells and T-cells are part of the adaptive immune system).  B-cells are the type of lymphocyte that produce antibodies.

So, forgive the references to Chapter 7 and page numbers with no number. While you’ll have to wait until the book is out in September to read those sections, in the meantime, please enjoy this part of Chapter 4:  Lifestyle Factors That Contribute to Autoimmune Disease.

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Want to help spread the word about my book?  Please share this post and other teaser excerpts.  Thank you!

“A good laugh and a long sleep are the best cures in the doctor’s book.”

–Irish Proverb

In the last 50 years, the average amount of time that Americans sleep each night has decreased by 1.5–2 hours.  That’s a staggering amount of sleep—equivalent to a full month of continuous sleep every year—that we need but are not getting.  Epidemiological studies show a strong correlation between short or disturbed sleep and obesity, diabetes and cardiovascular disease.  In fact, lack of adequate sleep has been associated of increased morbidity and mortality from all causes.  This means that if you consistently don’t get enough sleep, you have a much higher risk of getting sick and/or dying.  Period.  Studies have also evaluated the role that sleep plays in healing from specific diseases, like breast cancer, and show that the less you sleep, the less likely you are to survive.

Frankly, scientists still don’t really understand why we need sleep, why we need as much as we do, and what our bodies are actually doing while we sleep.  But, it is obvious that sleep is important for human health.  Studies that evaluate the physiological changes caused by not sleeping or not getting enough sleep can be very instructive in understanding just how critically important sleep is.  For those with autoimmune disease, it is especially important to understand the role that sleep has in inflammation, stimulating the immune system, and regulating hormones (which themselves modulate the immune system).

Just plain old not getting enough sleep causes inflammation even in young, healthy people.  A variety of studies evaluating the effects of acute sleep deprivation (typically by restricting sleep to 4 hours per night) for several consecutive days (typically 3 to 5) have shown increases in markers of inflammation and the numbers of white blood cells in the blood.  Specifically, even just three consecutive nights of not enough sleep can cause increased monocytes, neutrophils and B-cells in the blood, increased proinflammatory cytokines (including cytokines known to stimulate maturation of naïve T-cells into Th1, Th2, and Th17 cells), increased C-reactive protein (a marker of inflammation), increased total cholesterol and increased low density lipoprotein cholesterol (LDL).

Even just one night of lost sleep (40 hours without sleep) causes inflammation in young, healthy people.  Just pulling a single all-nighter dramatically increases markers of inflammation in the blood, including C-reactive protein and proinflammatory cytokines.  Studies that evaluated not just sleep deprivation but also recovery after sleep restriction (with the idea of simulating a typical workweek where someone might get less sleep for 4 or 5 nights straight and then try to make up for it on the weekend) have also shown that the proinflammatory cytokine known to stimulate Th17 cell development persists for at least two days after increasing sleep to 8 hours per night, even though other markers of inflammation have recovered.  This means that even if you try and “catch up” on your sleep during the weekend, the stimulation to the immune system keeps going.  If you follow this stereotypical pattern of not getting enough sleep during the week and sleeping in on the weekend, you still run the risk of cumulatively causing detrimental changes in the immune system.  Certainly, you can recover from lack of sleep, but it takes persistence, consistency and commitment—even during the week.

Sleep deprivation is also associated with increased susceptibility to infection.  In fact, the less sleep you get, the more likely you are to catch the common cold.  Getting adequate sleep can also protect you from infection.  One study even showed that the longer the sleep duration, the lower the incidence of parasitic infections in mammals.

Inadequate sleep also has profound effects on hunger hormones and metabolism (recall that hunger hormones such as insulin, leptin, ghrelin, and cortisol are important modulators of the immune system, see page ##, ## and ##).  For example, when food intake is measured following sleep deprivation (5 consecutive days of 4 hours sleep), people tend to eat substantially (20%!) more than normal.  However, it doesn’t take five full days of inadequate sleep to see dramatic effects on insulin, cortisol, and leptin.  One study showed that even a single night of partial sleep (4 hours) causes insulin resistance in healthy people.  Another study showed that a single night of partial sleep (3 hours, in this case) caused reduced morning cortisol levels (when cortisol should be its highest) and elevated afternoon/evening cortisol (when cortisol should be gradually decreasing) and elevated morning leptin levels.  This means that one night of three or four hours sleep causes insulin resistance, dysregulated cortisol and increased leptin.  One late bedtime because you went to a late night movie or a party at the boss’ house.  One.

Inadequate sleep has also been investigated as a possible cause of autoimmune disease. In an animal model of psoriasis, sleep deprivation caused significant increases in proinflammatory cytokines, cortisol levels, and increases in specific proteins in the skin associated with symptoms of psoriasis (like the flaking, dry, scaly skin).  In an animal model of multiple sclerosis, mice subjected to sleep deprivation developed the disease earlier than mice that slept normally.  Once the mice developed multiple sclerosis, sleep deprivation caused increased disease activity and pain sensitivity.  Furthermore, sleep disturbances are commonly reported by people with chronic inflammatory conditions (such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease and asthma).  Whether the sleep disturbances cause the disease or the disease causes the sleep disturbances is not well understood.  However, such sleep disturbances are known to worsen the course of the disease, aggravate disease symptoms such as pain and fatigue, increase disease activity and lower quality of life.  Yes, sleep is important.

So, how much sleep do you need?  There is no clear answer to this.  Consensus is that healthy adults need 7-10 hours of sleep per night.  If you are trying to heal from an autoimmune disease, don’t be surprised if what your body needs is on the longer end of that range (say 9 to 10 hours) or even exceeding that range (some people with autoimmune disease report needing 12 hours of sleep every night to heal).

Getting enough sleep isn’t just about preventing inflammation; it’s also about repairing the body and modulating the immune system.  Certainly, the process of tissue repair in the body is predominantly performed during sleep.  However, an important study showed that regulatory T-cell activities follow a circadian rhythm, meaning that, just like many functions within the human body, they increase and decrease throughout the day.  In healthy people, regulatory T-cells are highest in the blood at night with lowest numbers in the morning (similar to melatonin production and the opposite of cortisol). The activity of the regulatory T-cells also follows a circadian rhythm, having the highest suppressive activity during sleep and lowest in the morning.  When volunteers were subjected to sleep deprivation, the suppressive activity of their regulatory T-cells was decreased (even though the actual numbers of T-cells remained the same).  This implies that sleep is required for the suppressive activity of regulatory T-cells, meaning that if you want to modulate your immune system and reverse your autoimmune disease, sleep is critical.

If you have an autoimmune disease (I generally assume you do if you are reading this book) and aren’t getting 8 hours of good sleep every night, I cannot emphasize enough the importance of putting sleep on the top of your priority list.  You need sleep.  Now.  Tonight.  Every night.  Seriously, stop reading and go to bed.  Strategies for prioritizing sleep and what to do if you are trying to get more sleep but just can’t are discussed in Chapter 7.

Bollinger, T., et al., Sleep-dependent activity of T cells and regulatory T cells, Clin Exp Immunol. 2009 Feb;155(2):231-8

Bosy-Westphal, A., et al., Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women, Obes Facts. 2008;1(5):266-73

Boudjeltia KZ, et al., Sleep restriction increases white blood cells, mainly neutrophil count, in young healthy men: a pilot study, Vasc Health Risk Manag. 2008;4(6):1467-70.

Donga, E., et al., A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects, J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8.

Frey, D.J., et al., The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults, Brain Behav Immun. 2007 Nov;21(8):1050-7

Heslop, P., et al., Sleep duration and mortality: The effect of short or long sleep duration on cardiovascular and all-cause mortality in working men and women, Sleep Med. 2002 Jul;3(4):305-14.

Hirotsu, C., et al., Sleep loss and cytokines levels in an experimental model of psoriasis, PLoS One. 2012;7(11)

Lehrer S, et al., Insufficient sleep associated with increased breast cancer mortality, Sleep Med. 2013 Mar 4 pii: S1389-9457(12)00384-X. doi: 10.1016/j.sleep.2012.10.012. [Epub ahead of print]

Lucassen EA, et al., Interacting epidemics? Sleep curtailment, insulin resistance, and obesity, Ann N Y Acad Sci. 2012 Aug;1264(1):110-34

Meier-Ewert HK, et al., Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk, J Am Coll Cardiol. 2004 Feb 18;43(4):678-83.

Palma, B.D., et al., Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus, Am J Physiol Regul Integr Comp Physiol. 2006 Nov;291(5):R1527-32.

Palma, B.D. & Tufik, S., Increased disease activity is associated with altered sleep architecture in an experimental model of systemic lupus erythematosus, Sleep. 2010 Sep;33(9):1244-8.

Ranjbaran, Z., et al., The relevance of sleep abnormalities to chronic inflammatory conditions, Inflamm Res. 2007 Feb;56(2):51-7.

Reynolds AC, et al., Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men, PLoS One. 2012;7(7)

van Leeuwen WM, et al., Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP, PLoS One. 2009;4(2)

Teaser Excerpt from The Paleo Approach: The Trouble with Stevia

March 11, 2013 in Baking Ingredients, Is It Paleo?, Sugar/Carbs, The Paleo Approach Excerpts

The Paleo Approach by Sarah BallantyneI get often get asked why I do not endorse the consumption of stevia (see my post Is Sugar Paleo? for more information on what sugars/sweeteners I do endorse).  So, as I found myself including a section on the trouble with stevia for The Paleo Approach, I felt like this was a good topic to include as a book teaser on the blog.  I have a section of Chapter 3 that describes the role that sugars, blood sugar regulation, insulin sensitivity, fructose, sugar alcohols and nonnutritive sweeteners play in propagating inflammation in autoimmune disease.   This excerpt is included as a standalone text box following the subsection on nonnutritive sweeteners.

This excerpt is from Chapter 3 (The Diet Link to Autoimmune Disease chapter).

Stevia is often recommended as a natural sugar substitute because it comes from the leaf of a plant (Stevia rebaudiana Bertoni).  It tastes sweet on the tongue, requires very small quantities to sweeten baking, and contains no sugar.  While some experts advise caution against purified and manufactured forms of stevia, green leaf stevia is typically endorsed.  On the surface, it sounds like a perfect solution.  However, I do not recommend the consumption of stevia, even in its most natural form.  The chemicals responsible for the sweet taste of stevia are called steviol glycosides (there are at least ten different steviol glycosides present in the stevia plant).  Purified/manufactured forms of stevia often isolate one or two of these steviol glycosides whereas green leaf stevia (which is simply the dried and powdered leaves of the stevia plant) contain all ten.

Steviol glycosides are synthesized in the same pathway and end up being structurally very similar to the plant hormones gibberellin and kaurene.  This means that steviol glycosides have a hormone structure.  The majority of toxicological studies establish that stevia is safe, however there are some studies showing that it can act as a mutagen and may increase the risk of cancer (these studies are in the minority and tend to use quite high concentrations, so they are readily discarded in discussions of the overall safety of consuming stevia).  Whether or not stevia causes genetic mutations is not the only cause for concern, however (even if safety studies focus on this particular property).  For those with autoimmune disease, in which hormones have such a dramatic impact on disease development and progression, the impact of consuming stevia on hormone regulation is relevant.

There is evidence that steviol glycosides have contraceptive effects in both males and females.  In particular, one specific steviol glycoside, called stevioside, has been shown to have potent contraceptive properties in female rats, implying that stevia may have an impact on estrogen, progesterone or both.  In another study, male rats fed stevia extracts showed a decrease in fertility, reduced testosterone levels and testicular atrophy, potentially attributable binding of steviol glycosides with an androgen receptor.  Although no studies have been conducted evaluating the impact of stevia on fertility in humans, the stevia plant was traditionally used to control the fertility of women by the Guarani Indians in southern Brazil.  While small and occasional consumption of stevia likely has little to no impact on general health, it should not be consumed on a regular basis especially by those with altered hormone balance and dysfunctional immune systems.

Brusick DJ. A critical review of the genetic toxicity of steviol and steviol glycosides. Food Chem Toxicol. 2008 Jul;46 Suppl 7:S83-91.

Mazzei Planas G and Kuć J. Contraceptive properties of Stevia rebaudiana. Science. 1968 Nov 29;162(3857):1007.

Melis MS Effects of chronic administration of Stevia rebaudiana on fertility in rats Journal of Ethnopharmacology 1999 Nov 67(2):157–161

Melis MS. Chronic administration of aqueous extract of Stevia rebaudiana in rats: renal effects.  Journal of Ethnopharmacology 1995. July 47(3):129–134

Oliveira-Filho RM et al.  Chronic administration of aqueous extract of Stevia rebaudiana (Bert.) Bertoni in rats: Endocrine effects.  General Pharmacology: The Vascular System. 1989. 20(2):187–191