Thursday, March 26, 2015

"Adrenal Fatigue", intense exercise and the Paleo diet

Adrenal Fatigue, or the more aptly named HPA axis dysfunction, has seemingly taken the online world by storm.  There are countless support groups, online lifestyle programs, and dietary interventions aimed at preventing adrenal fatigue, but so far we have a fairly limited knowledge of what adrenal fatigue is.  Sure, there is the general notion that as people light the candle at both ends too frequently their autonomic nervous system goes haywire, but what is truly causing it to go haywire?  Are we dealing with a situation where a person's perception of stress has gone wonky, are they exhausting the adrenals to the point they no longer have the raw materials to make cortisol when they experience stress, or is something interfering with the signal?

Honestly, I don't know that everyone experiences the same thing, but looking at biology and the stress response can give us clues to what is considered the most common pathway to adrenal fatigue in the Paleo world: overexercise and nutritional deficiency.  When you look at the symptomology of adrenal fatigue, you get a picture of the systems that are affected:
  • Electrolyte balance
    • Hypotension, dizziness, headaches, frequent urination, cramps
  • Immune system
    • Frequent respiratory infections, prolonged length of infection, parasitic infections
  • Digestive disturbances
    • IBS, loose stools, gas/bloating, parasitic infections
  •  Blood glucose control
    • Low or high blood glucose, irritability, fatigue/low energy
  • Neurological
    • Muscle twitching, heart palpitations/arrythmias, brain fog
  • Hormonal
    • Thyroid issues, sex hormone issues, irritability
While this is merely a small list of the things that people with adrenal fatigue experience, we can use it to look for commonalities between these systems and compare them to some of the things we may expect to see in a person who decides to cut out certain foods from their diet and partake in intense exercise modalities.  This allows us to identify some factors, particularly nutritional, that could be playing a causative role in adrenal fatigue.  Ironically enough, some of these same factors may predispose sedentary over-eaters to the exact same symptoms.

The typical culprit framed for the intense exercise/Paleo diet link to adrenal fatigue is low carbohydrate consumption, but upon further research, I believe other factors related to the type of carbohydrate to be at play.  Many also indicate a link between low carbohydrate intake in general and low thyroid output, but  I don't really feel this link is entirely comprehensive as well.  I do believe carbohydrates, or rather, carbohydrate metabolism, is a central player in this phenomenon.  Where I part ways with this line of thought is when the solution is throwing carbohydrates at the problem.  I believe that merely throwing carbohydrates at the problem can make it much worse if you look at the way cells work.

Understanding cells

Before we move further, it's important to understand how your cells work. All of your cells are constantly interacting with their environment by identifying environmental conditions and performing the biological function that they are programmed to do under those environmental condition via your genes.  For example, when the beta cells in your pancreas identify an increase in blood glucose, they secrete the hormone insulin in to your bloodstream which causes other cells in the body to take in glucose.  Most biological functions occur in this manner, a manner similar to the way the heating system in your house adjusts the temperature.

The thermostat in your house is programmed to the desired temperature and when it senses the temperature drop below that point, it signals your furnace to increase the heat.  An ignitor in your furnace turns on and gas is blown past the ignitor which turns it in to a flame that can distribute heat through the heating duct.  Failure in the system can occur if:
  1. The thermostat doesn't sense the temperature or is improperly programmed
  2. The ignitor fails to turn on, preventing the conversion of fuel to fire
  3. The gas flow doesn't turn on or is obstructed.
This analogy holds for the microscopic physiology of the cell as well as what's happening during adrenal fatigue.  Things like lowering stress, getting better sleep, meditating, and other ways of manipulating lifestyle are, in essence, changing the setting of the thermostat.  Specific enzymes and their cofactors that perform functions within the HPA axis as well as other, related, systems are the ignitor which can be handled with nutritional supplementation.  Finally, the gas flow can be looked at as energy in the system and is most often related to carbohydrate consumption.  While I feel most programs meant to deal with adrenal fatigue take care of resetting the thermostat and increasing gas flow, most fail to address the failed ignitor.

Over-stoking your furnace

While I see no harm and much benefit to changing the setting of the thermostat through meditation, proper exercise, and good stress management, I don't feel the problem is truly being addressed by simply doing these things.  Stress is unavoidable, and it's my opinion that being able to deal with high levels of stress from time to time is important.  I don't feel simply removing all of the stress in one's life is in the best interest of the individual.

On the other side of the equation, simply increasing carbohydrate consumption can be disastrous if not done properly.  There is a lot of clinical evidence supporting this notion and the refeeding syndrome is simply the clinical manifestation of what happens when you increase gas flow in your furnace without addressing the ignitor.  Going back to the furnace analogy, imagine if the heating system in your house kept calling for gas and the gas kept flowing but the ignitor didn't turn on.  Your house would quickly fill up with gas, a far from ideal situation.  In the refeeding syndrome, introducing carbohydrates before all of the nutrients/cofactors needed to utilize carbohydrates properly have been restored leads to symptoms of vitamin deficiency and electrolyte imbalance(1, 2).  In other words, your heating system is filling your house up with gas, not heat.  Bad idea.

A better approach to dealing with this issue is to adjust the thermostat by bringing stress back to a manageable level through lifestyle change, fix the ignitor by replenishing the enzymes and cofactors that are necessary to kick it on, and then gradually increase carbohydrates to a level that is suitable to your activity level.  The first and third parts are easy, but what are the important steps in fixing the ignitor?  The immediate thought is to simply begin supplementing with vitamins and minerals, but it's not as simple as that.  Unfortunately, this is the direction most people go in and progress drags along slowly for several reasons.

First, many of the things you do in everyday life impact nutrient status, and you are going to have to avoid or cut back on some of these things to restart your ignitor.  If you have adrenal fatigue, you are likely avoiding some of these things but may be doing others.  Second, There are multiple steps in getting nutrients in to cells that become an issue.  This includes absorption, maintaining high levels in the bloodstream, and getting them in to your cells.  While there are many nutrients that are important in restarting your ignitor, there is a large amount of scientific evidence linking one specific nutrient to all of the systems mentioned above, and strong evidence that a deficiency in this nutrient quickly induces stage 1, followed by stage 2, adrenal fatigue.  Deficiency in this nutrient is highly dependent on carbohydrate intake, and deficiency can occur both in people who exercise too intensely and don't ingest enough carbohydrates as well as people who eat tons of carbohydrates while living a sedentary lifestyle.  We will cover that nutrient and all of the ins and outs of it, after the jump.

Monday, February 16, 2015

The Pentose Phosphate Pathway: The missing link between hormonal imbalances and carbohydrate metabolism?

I've taken a bit of time away from blogging because I've been swamped with clients and wanted to spend what free time I have reading.  I've come across some very interesting stuff that I believe plays a significant role in hormonal balance that no one is covering so I'll do my best to break it down in to digestible information.

Anabolic carbohydrate metabolism

When people think of carbohydrate metabolism, they immediately think of glycolysis and maybe even the citric acid cycle.  Both of these reactions are catabolic, they are oxidative processes that make ATP through the breakdown of glucose.  However, there is another pathway of glucose metabolism called the pentose phosphate pathway that is anabolic in nature.  The function of the pentose phosphate pathway is to produce reducing equivalents to power anabolic reactions, to produce ribose 5 phosphate(R5P) for the synthesis of DNA, and to help shuffle carbons between sugars so that they can be utilized again.  But why is this important?  Let's take a look.

Anaerobic glycolysis is the breakdown of glucose in the cytosol of cells.  The first step uses ATP to make glucose 6 phosphate(G6P) which can either continue along the pathway of glycolysis to make ATP or be directed through the pentose phosphate pathway to produce reducing equivalents and/or R5P.  The path that G6P takes is ultimately dictated by cellular needs.  To make this uber-confusing I'll post the steps of both pathways below.

It's not really important that you focus on the steps so much as the parallel pathways that glucose metabolism can take based on cellular needs.  Depending on cell type, there are different levels of pentose phosphate pathway activity.  Cells that are exposed to high levels of oxidative stress, that produce hormones, and that have a high turnover rate tend to have more flux through the pentose phosphate pathway.  But why?

The 2 phases of the pentose phosphate pathway

There are 2 phases of the pentose phosphate pathway, an oxidative phase and a non-oxidative phase, both shown below.

The oxidative phase of the pentose phosphate pathway

The oxidative phase reduces 2 nicotinamide adenine dinucleuotide phosphates (NADP+) to 2 NADPH, the reduced form.  This is important for 2 reasons.  First, NADPH is needed to convert oxidized glutathione to its reduced form.  Everyone and their mother who is trying to optimize health is likely taking some form of supplement or eating foods that promote glutathione production.  Glutathione is known as the master antioxidant as it goes around donating electrons to free radicals before they can react with cellular structures.  The problem is, once glutathione does this it's converted to its oxidized form which can no longer donate electrons.  In this form, glutathione is essentially worthless until NADPH reduces it back to the active form.  This converts NADPH back to NADP+ where the oxidative phase of the pentose phosphate pathway can swing back in and produce more NADPH.  For this reason, any cell that is subject to high levels of oxidative stress such as red blood cells and liver cells has a very active pentose phopshate pathway.  The figure below illustrates the process by which NADPH reduces oxidized glutathione.

Note that selenium is needed in order for glutathione to reduce free radicals and NADPH and riboflavin are needed to reduce oxidized glutathione back to its active form.  Without NADPH, glutathione remains inactive, something you most certainly do not want.  The pentose phosphate pathway is the primary way in which our cells make NADPH for this purpose.

In addition, cells of the immune system used NADPH to kill foreign pathogens through a process called the respiratory burst.  A decrease in the ratio of NADPH:NADP+ ratio will compromise the immune system and provide an environment where pathogens can evade killing by phagocytosis.

The next reason that the oxidative phase is important is because reducing power is needed for all anabolic processes.  This includes the biosynthesis of hormones, so there are high levels of pentose phosphate activity in the adrenal and sex glands.  With insufficient reducing power in the form of NADPH, hormonal balance can be thrown out of whack.  This includes the adrenal and sex hormones as well as the the thyroid, but for a different reason.  Several reversible hormonal conversions are dependent on the ratio of NADPH to NADP+ including:

                                                    DHEA                     <---->  Androstenediol
                                                    Androstenedione   <---->  Testosterone
                                                    Estrone                   <---->  Estradiol
                                                    Cortisone               <---->  Cortisol

NADPH causes the conversions to go from left to right while NADP+ causes them to go from right to left.  So what does this mean?  NADPH will convert androstenedione to testosterone while NADP+ will convert testosterone to androstenedione.  In other words, reduced flux through the oxidative arm of the pentose phosphate pathway will negatively impact testosterone levels in men because there will be more NADP+ than NADPH which favors androstenedione over testosterone. 

I am not expert on women's hormonal issues, but given the fact that estrone is the predominant form of estrogen in postmenopausal women while estradiol is the predominant form in women of reproductive age, I'll go out on a limb and say this conversion is likely detrimental.

On the adrenal side of things, reduced flux through the oxidative arm of the pentose phosphate pathway will negatively impact cortisol levels by favoring cortisone production.  Since cortisol has greater glucocorticoid activity and cortisone has no mineralocorticoid activity, this can have a pretty significant effect on glucose levels, inflammation, and electrolyte balance.

Since these hormonal conversions occur in the endoplasmic reticulum(ER) of cells, the ratio of NADPH:NADP+ within the ER can have a pretty significant effect on hormonal balance.  Reduced flux through the pentose phosphate pathway and high levels of oxidative stress are 2 factors that can decrease this ratio leading to poor hormonal balance.

With the thyroid, the proposed mechanism by which reduced flux through the oxidative arm of the pentose phosphate pathway may negatively impact hormone production is through a reduction in glutathione function.  The thyroid relies on hydrogen peroxide, a free radical, for thyroid hormone synthesis.  Without sufficient levels of reduced glutathione to keep this in check, the thyroid can become damaged, inflamed, and thyroid function can become compromised.

The non-oxidative phase of the pentose phosphate pathway

The non-oxidative arm of the pentose phosphate pathway is also important, especially in tissues with high rates of cell turnover.  The non-oxidative arm of the pentose phosphate pathway essentially interconverts sugars in to different forms.  One of those sugars, R5P, is necessary for DNA production. Cells with high turnover rates such as epithelial cells in the gut are dependent on sufficient flux through the non-oxidative arm to produce enough DNA for replication.  The non-oxidative arm also gives the pentose phosphate pathway flexibility.  By interconverting sugars, the non-oxidative arm can create sugars that can re-enter glycolysis to generate pyruvate or feed back in to the oxidative arm to create more NADPH. 

The non-oxidative arm allows the pentose phosphate pathway and glycolytic pathways to work synergistically to meet cell needs.  There are essentially 4 modes of pentose phosphate pathway activity that can be used to increase energy levels, increase reducing power, provide building blocks for DNA, or a combination of these functions.

Figure 20.24. Four Modes of the Pentose Phosphate Pathway.  
The yield of each mode is:

Mode 1-6 G6P makes 5 R5P
Mode 2-1 G6P makes 1 R5P and 2 NADPH
Mode 3 -1 G6P makes 12 NADPH
Mode 4-3 G6P make 6 NADPH, 8 ATP, & 5 pyruvate and NADH which can be used to create more ATP

As you can see, carbohydrate metabolism is a lot more than simply breaking down glucose to use for energy.  Carbohydrate metabolism also has anabolic effects via the pentose phosphate pathway.  Decreased flux through the pentose phosphate pathway can increase oxidative stress and negatively impact hormonal balance and cellular reproduction.  There is compelling scientific evidence that altered flux through the pentose phosphate pathway may be at the root of adrenal dysfunction, increased inflammation, and some gut pathologies including SIBO.  In addition, many metabolic consequences of Type 2 diabetes can alter flux through the pentose phosphate pathway and there are many blood markers we see in Type 2 diabetes that indicate this.  If there is enough demand I may pull some of that stuff out, so read, like, and share.

Thursday, November 20, 2014

Why your crash diet last New years set you up for this years failure

It's that time of year again.  It's the time of year where people say, "Screw it, I'll get back on the wagon after New Years!"  This statement is followed by unfettered food consumption and little to no physical activity for 6 weeks followed by a crash diet and Tasmanian Devil levels of physical activity to work off what was put on over the holidays, not to mention the other 5 lbs you gained prior to the binge.  What people fail to realize is that their failure was sealed long before they decided to throw caution to the wind and see how many holiday cookies they could eat without getting up on Thanksgiving day.

It's should come as no surprise to anyone that as we get older, our metabolism slows down.  What may come as a surprise to most people, if not all, is that research shows that the crash diet you participated in last year probably jeopardized your chance at success this year.  Hormones controlling everything from appetite to how much energy you burn take a hit from low calorie dieting, and the negative effect 10 weeks of low calorie dieting has on many of these hormones persists for a year or more(1).

This is one of the many reasons I tell people to stay away from anything like the Isagenix or Medifast programs, short-term results for long-term failure.  If you are wondering how I jumped from a low calorie diet to either one of these programs, it's because the low calorie diet in the study above used essentially the same program, Optifast.  They all follow the same template, consume 3-5 of our supplements per day, eat little to no food, and watch the fat melt away.  What's even more disappointing is that these programs often tout that they are perfectly healthy since they provide 100% of the RDI(Reference daily intake) for micronutrients while also creating a caloric deficit.  This may not be the case.

A small study looking at serum and intracellular micronutrient levels in obese people losing weight on the Optifast system paints a starkly different picture.  The study followed obese people after following the Optifast 52 plan for 3 months and through 26 weeks of follow-up.  It's not surprising that the diet of the participants before the study did not meet the RDI for several micronutrients and many were, therefore, found to have insufficient serum and intracellular levels of multiple micronutrients.  What is surprising is that after 3 months of low calorie dieting with shakes that did meet or exceed the RDI of all essential micronutrients, more of the subjects experienced micronutrient deficiencies and some of the micronutrient deficiencies grew worse, particularly Vitamin C, selenium, iron, zinc, and lycopene(2).  That doesn't seem very healthy to me.
Some of this can be explained by increased nutrient demand due to weight loss.  However, if scientists are a little fuzzy on the micronutrient needs of people participating in a weight loss program, how well read up do you think the person who sold you this product is on the topic?  Keep in mind Optifast is only administered by "qualified healthcare providers", which is basically code for someone with an MD who knows nothing about diet.  Do you really think the guy at the gym who is schlepping this stuff to you based solely on his personal experience with it has any idea if it's healthy for you?

Interestingly, the participants in the second study who were able to maintain the fat loss through follow up were able to improve these deficiencies as they began eating real food.  If they were able to maintain the weight loss eating real food, why not just start there and not risk long term hormonal dsyregulation due to the low calorie diet?  The first study we looked at showed this altered hormonal state lasts a year and, unfortunately, follow up in this study only lasted 26 weeks.  Who knows if that weight loss was maintained or not?  Maybe this holiday season would be better spent with sane levels of holiday food consumption and high levels of physical activity followed by a nutritious whole food diet at a slight caloric deficit and intelligently programmed exercise?

Thursday, November 13, 2014

Fibrolmyaglia and Non-celiac Gluten Sensitivity: Two peas in a pod?

Some newer research looking at remission in fibromyalgia recently caught my eye for a few reasons.  First, I worked on a clinical trial in fibromyalgia at the University of Pennsylvania a few years back and formed several opinions on what I thought may be predisposing factors to the syndrome.  Second, over the course of the last few years I have expanded my knowledge on gut health and gut bacteria to the point where I keep coming back to my thoughts on fibromyalgia and many of the things I thought were potential contributing factors.  This new study renewed my interest because it may be shedding light on potential lifestyle modifications that can send fibromyalgia in to remission.

Before I go in depth in to the research, I have to point out that you really cannot make very many hard scientific conclusions based on this information.  For one, this data is merely a short communication pinpointing clinical findings of the use of a gluten free diet in people with fibromyalgia.  Secondly, this wasn't a random sample of people with fibromyalgia.  These people were selected based on certain criteria, specifically that they did not have Celiac disease, they had intraepithelial lymphocytosis, and their symptoms improved on a gluten free diet.  While this very specific set of symptoms makes it hard to generalize these results to everyone with fibromyalgia, they honestly make this data far more interesting.

In Fibromyalgia and non-celiac gluten sensitivity: a description with remission of fibromyalgia, physicians in Madrid, Spain chronicle their success at putting patients with fibromyalgia in to remission with a gluten free diet.  The study followed 20 patients who met the above criteria of the study and who were willing to try a gluten free diet.  The results found all patients had improvement in their pain with 15 of the 20 patients having complete remission of their pain.  Fatigue, depression, migraines and GI symptoms all improved with pain and 2 people with psoriatic arthritis and spondylarthritis, 2 autoimmune conditions, saw remission of those conditions as well.

This data is interesting or a few reasons.  First, all but one of the patients had some sort of digestive tract abnormality/issue, and the patient who didn't was the patient who had been diagnosed with fibromyalgia for the shortest period of time(3 years).  Indigestion, IBS, constipation, and GERD were the most commonly reported digestive issues.  Oral aphthae was also an interesting finding in 2 of the patients.  Oral aphthae is essentially recurrent canker sores in the mouth.  I've always thought this condition was a barometer of total GI health, and the presence of immune cells in the intestine provide support for this notion.

Next, none of the patients had villous atrophy, a flattening of the villi associated with Celiac disease, but all had intraepithelial lymphocytosis.  This isn't a finding because this was part of the inclusion criteria, but it provides significant evidence for the existence of non-celiac gluten sensitivity.  Intraepithelial lymphocytosis essentially means something is triggering intestinal inflammation, but it cannot be assumed that gluten is the specific cause just because there is inflammation.  Resolution of the problem via a gluten free diet and re-occurence of symptoms in 7 people who reintroduced gluten indicate gluten may be one of, if not the causative factor.  The picture below illustrates the stages of progression from normal small intestinal tissue to the damaged villi seen in Celiac disease.

Notice how the normal tissue on the left has projections, called villi, that erode over time in to flat tissue.  This is villous atrophy and is caused by intraepithelial lymphocytosis, which is illustrated by the little black dots that slowly infiltrate the intestinal tissue gradually from left to right.  As the villi become flattened, a person's ability to absorb nutrients is decreased and they may eventually become deficient in one or several nutrients.  In addition, inflammation can dump in to the circulation and cause problems elsewhere in the body.  This is where it gets interesting.

For the most part, it has always been assumed that forming antibodies to something called tissue transglutaminase has been the cause of problems outside of the gut due to ingestion of gluten.  In Celiac disease, it is believed that tissue transglutaminase binds with gluten and the immune system recognizes this complex as foreign.  From there it has been assumed that the immune system mistakes other body tissues as foreign because tissue transglutaminase is found in every cell in the body, but the patients in this study were not forming antibodies to tissue transglutaminase.  Therefore, this data does not support the notion that antibodies to tissue transglutaminase is the issue in fibromyalgia, at least not in those who fit the inclusion criteria in this study.  So what could be causing the pain?

Interestingly enough, inflammation is known to induce the release of something called nerve growth factor.  Nerve growth factor(NGF) has many functions in the body, in response to inflammation that role is to attempt to reduce it under certain circumstances.  NGF is produced locally in tissues but can also be produced by cells of the GI tract and may circulate throughout the body to help maintain homeostasis(1).  However, continually assaulting the body with a food that increases inflammation, in this case gluten, will cause more (NGF) to be produced.

Another one of NGFs functions is that it increases pain sensitivity both acutely and chronically in an inflammatory state(2, 3, 4) and administration of anti-NGF drugs reverses this increased sensitivity rapidly(5, 6).  Notably, the biggest finding in this short communication is that removal of gluten from the diet of these patients reduced or eliminated their widespread pain.  Below is an illustration of the tender points known to be extremely sensitive to touch in people with fibromyalgia.

People with fibromyalgia have an extreme sensitivity to touch in these areas, the slightest brush to the area can cause tremendous pain.  In the study I was part of, we directly measured the amount of pressure with a dolorimeter and the difference in pain tolerance between someone with fibromyalgia and someone without it is pretty striking.  However, these areas tend to be tender for most people indicating that they may have a greater supply of nerve endings than the surrounding tissue.  Fascia, a body-wide matrix of connective tissue that runs throughout muscle tissue, is richly innervated with pain receptors.  Therefore, it is tempting to hypothesize that the fascia may be involved in the widespread pain associated with fibromyalgia.  A recent study found pain receptors in the fascia to be highly prone to the pain sensitizing effects of NGF, and that effect lasted up to 2 weeks(7).

When I worked on the AT101 clinical study on fibromyalgia at UPENN, researchers elsewhere were looking at levels of something called Substance P in the cerebrospinal fluid of people with fibromyalgia as a way to diagnose the syndrome as it is elevated in patients with fibromyalgia.  In an interesting twist of fate, Substance P levels in cerebrospinal fluid appear to be tied to cerebrospinal NGF levels and cerebrospinal NGF levels have been shown to be 4x higher in people with primary fibromyalgia than in healthy controls and 2x higher than people with other pain conditions(8).

I have yet to find anything on how blood levels of NGF relate to levels of NGF in cerebrospinal fluid, and NGF appears to play a dual role in inflammation, acting as pro-inflammatory or anti-inflammatory depending on the situation.  However, in LPS induced sepsis, NGF appears to have a pro-inflammatory role(9) and this state is similar to what one would experience in non-celiac gluten sensitivity with bacteria from inside the intestine leaking in to the bloodstream due to a leaky gut.  Whether NGF functions as pro- or anti-inflammatory is irrelevant, however, since an increase in NGF that accompanies inflammation likely induces increased sensitivity to pain, the hallmark of fibromyalgia.

I would love to go more in depth with the science aspect in this blog, but it gets rather dry.  The take-home message is that a gluten free diet is a potential therapeutic approach that most people with fibromyalgia likely don't use to their advantage.  Even in those who have tried it, the results are variable and can take some time.  I've worked with people to eliminate gluten and it's hard enough to get them to go without it for a week, let alone for several months.

In the short communication discussed in this blog, some patients saw quick relief over the course of a few months while others took much longer and the results came along much more slowly.  I have a feeling this may have had to do with how damaged their GI tract was as well as how strictly they followed the diet or whether they ate foods that may have cross-reactivity with gluten or that the person is reacting to separately.  Even a small dose of gluten can be problematic for someone who is reacting to it, and a diet containing something the body senses as foreign with a structure similar to gluten, such as oats or eggs, can have the same effect as eating gluten itself.  For more on gluten cross-reactivity go here.  A study looking at a gluten free diet found persistent intraepithelial lymphocytosis in people with Celiac disease despite a long term gluten free diet.  The offending nutrient was oats(10), which do not contain the problematic proteins associated with wheat and barley. Cross-contamination may be a potential contributing factor in this study.

Another confounding dietary issue could be the presence of small intestinal bacterial overgrowth, or SIBO.  A recent study found that 100% of the people enrolled in the study(42 out of 42) who had fibromyalgia also had SIBO(11).  We do not know if this is cause or effect, but eating a reduced FODMAP diet is likely a good idea to help normalize the gastrointestinal flora as SIBO can induce intestinal inflammation.  Finally, consumption of foods that contain or cause the release of histamine may be problematic due to the inflammatory effects of histamine..  For more information on histamine, check out this blog.

Now, to the bottom line.  If you have fibromyalgia, the autoimmune paleo protocol low in FODMAPs and histamine containing and releasing foods is likely the best dietary protocol to help calm down the immune activation in the gut.  Below are a couple of links to foods that fit the FODMAP and histamine criteria.  After a couple of weeks the hope is that the pain sensitizing effects of NGF will wear off, but it wouldn't surprise me if results took longer.  There are other strategies that have to do with exercise, stretching and physical activity that would speed up the process, but we'll save that blog for another day.

A final interesting note on this study.  The predominant theory is that once an autoimmune process starts, it will continue throughout life if the environmental trigger is reintroduced.  In other words, it would mean lifelong elimination of gluten from the diet.  However, this study does not support fibromyalgia as a classic autoimmune disease in that antibodies are not being produced, at least not to tissue transglutaminase.  In theory, this means that once the gut is healed, a person may be able to eat gluten in sane quantities provided their gut is healthy and the majority of their diet is centered on maintaining a healthy gut.  This would mean that once their gut is healed, it would be beneficial to gradually increase FODMAPs and other types of fiber to promote a more acidic GI tract and to limit inflammation, once the SIBO is cleared.  However, there is the potential that people with fibromyalgia are forming different antibodies when they ingest gluten, but I don't imagine the science will pick up on that for quite some time.

Histamine in foods

Foods low in FODMAPS

Thursday, November 6, 2014

What the Kale happened to my Iodine?!?!?! Please pass teh almund milkzz!!!!!!

There always seems to be a ginormous pendulum swing every time a food is classified as a "superfood".  A relatively obscure food goes from unknown and untouched to eaten 5 times a day with the hope that it will somehow prolong your life or help you lose 15lbs.  This pendulum swing is no different when we look at kale.  Five years ago no one knew what kale was, now everyone and their mother is eating kale chips, drinking kale smoothies, and eating kale salads at Whole Foods.  In some instances, this is not a good thing.

While kale is certainly something that can be part of a healthy diet, we must look at a food from root to tip to determine how big of a part of our diet it should be.  There is a lot going for kale from a nutrient standpoint, but there is also a significant drawback, notably that it contains goitrogenic compounds.  Goitrogens are substances that can interfere with thyroid function by binding to receptors where iodine should attach.  The thyroid turns iodine in to thyroid hormones and a deficiency can lead to thyroid dysfunction.  When goitrogens attach to iodine receptors in the thyroid, the thyroid is unable to make thyroid hormones.  In theory, if you consume enough goitrogens, you could be getting enough iodine and still be in an iodine deficient state.

I don't believe that this is the typical route that a person consuming kale would be getting themselves in to trouble.  In moderation, I don't think kale would have any significant effect on thyroid function.  It could interfere with thyroid function when consumed in excess and under the proper conditions, though.  First, other cruciferous vegetables such as broccoli, cauliflower, and cabbage also contain goitrogens so you would have to take a look at these other goitrogens in the diet.  Second, cooking inactivates some of the goitrogens so people who cook their kale are less likely to have a problem than someone who eats kale smoothies or eats cups of it a day in their salad.  Finally, even if you did consume a good amount of kale, it's only likely to become a problem if you aren't taking in sufficient iodine.  This is where I think a  problem can set in.

Goiter, a swelling of the thyroid due to iodine deficiency was once a significant problem in the United States.  It was so big that the landlocked and mountainous areas where goiter was common was referred to as the goiter belt.

To combat this problem, iodine was added to table salt.  The result, steep declines of goiter as Americans in the goiter belt were now getting sufficient levels of iodine.  I would like to say this is where the story ends, but I don't believe that to be the case.  While adding potassium or sodium iodide to table salt helped correct the iodine deficiency, Americans have been turning from table salt to sea salt, which doesn't contain iodine.  While I cannot know for sure, I'd imagine this switch is highly prevalent in the kale crowd.

There are other sources of iodine in the American diet.  Bread used to have significant amounts of iodine in it until they started using bromine, which happens to also be a goitrogen.  Cow dairy also contains significant amounts of iodine.  I say this as large swaths of people switch from cow's milk to almond milk while I am still frantically trying to find the teats of an almond.  Again, this is a switch I feel is safe to say is quite prevalent in the kale crowd.

So where does this put us with regard to kale?  Kale can be a healthy part of your diet provided that the diet is diverse, doesn't focus on kale as an excessive green of choice, and that you get sufficient iodine.  Good sources of iodine tend to come from the sea.  Kelp and other seaweeds are very good sources as are eggs.

The underlying issue, however, is that people take good foods and call them superfoods to elevate them to the level that they can be consumed endlessly without issue.  Kale is a great food, but for someone who is already eating cruciferous vegetables regularly there really isn't any added benefit to eating a lot of kale.  It's high in fiber, vitamins A, C and K, and that's about it; these are nutrients that are typically high in vegetables.  Kale is also a good source of the omega 3 fatty acid ALA, which would be great except for the fact that humans convert ALA to usable omega-3 fatty acids at less than a 5% rate.

Many boast about the high ORAC score of kale, which is basically a way of measuring how well a food helps the body quash free radicals.  Kale is high on the ORAC list...If you don't count berries, about 2 dozen other fruit, pretty much every spice in the world, and at least half a dozen other greens that are freely available at any supermarket such as arugula and beet greens.  My point here isn't to prevent you from eating kale, it's to show you that it really isn't appreciably better than most vegetables.  So why is it a superfood again?

Monday, October 27, 2014

Zucchini pasta with red sauce


2 TBSP olive oil
1/4 pound ground beef
2 zucchinis, whole
6 large tomatoes, quartered or chopped
1 yellow bell pepper
1 orange bell pepper

1 1/4 cup yellow onion, diced
1 cup of mushrooms, chopped
6 cloves of garlic, chopped
2/3 oz fresh basil leaves(8 leaves), chopped
2/3 oz fresh oregano, chopped
2 teaspooons of ground black pepper
Salt to taste


Place cast iron skillet on medium heat and add olive oil.  Once heated, add spices and stir.  Add onion, peppers, and mushrooms and continue to stir until coated with oil.  As the veggies soften, add in the meat and cook until browned.  Place tomatoes in a crockpot on low heat and add contents of skillet.  Leave on low heat for 6 hours, stir occasionally to break up quartered tomatoes or you can puree in a blender once finished.  Once finished, use a vegetti or julienne slicer to make "noodles" out of the zucchini.  Serve sauce over zucchini noodles.

Nutrition information

Makes 2 servings, each with 6 cups of vegetables
513 cals
21g fat
70g carbs
19g fiber
24g protein
3000mg potassium
1236mg sodium (Assuming 1 tsp of salt)

Monday, October 20, 2014

Asian Hash


1lb of ground turkey sausage
2 TBSP of coconut oil
1/2 large onion, diced
12oz bag of Asian slaw or Rainbow salad  OR
     1/2 cup of broccoli, shredded
     1/2 cup of cauliflower, shredded
     1/2 cup of carrots
     1/2 cup of red cabbage
4 cloves of garlic
1 teaspoon of roasted red pepper
1 teaspoon of black pepper
2 teaspoons of coconut aminos


Place large cast iron skillet on medium heat and add 1 TBSP of coconut oil and add garlic, roasted red pepper and black pepper, coating with oil.  Add sausage and brown.  Once sausage is brown, add in other TBSP of coconut oil, Asian slaw, and onions and stir, slowly adding in coconut aminos.  Cover for 5-10 mins or until veggies are soft.  Salt to taste.

Nutrition information

Makes 2 servings
519 cals
29g fat
19g carbs
7g fiber
47g protein
1188mg potassium
1451mg sodium