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


Ingredients

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

Directions

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

Ingredients

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

Directions

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

Thursday, October 16, 2014

Spanish Fries

Ingredients

2 TBSP of bacon grease
1/2 large onion, diced
1 large jalapeno pepper, cut in half length-wise and sliced into half discs
2 peeled potatoes, cut with a fry cutter
Garlic powder to taste

Directions

Preheat oven to 425F.  Place large cast iron skillet on low heat and add bacon grease.  Place cut potatoes in a container with a lid, pour half of grease over fries, add garlic powder, cover, and shake.  Place fries on a baking sheet and put in preheated oven.  Add onions and peppers to the skillet once its hot and stir.  At 10 minutes, shake the fries and put back in for 10 more minutes.  When the fires are finished, dump on plate and put onions and peppers on top.  Salt to taste.

Nutrition information

Makes 2 servings
270 cals
13g fat
35g carbs
3g fiber
4g protein
669mg potassium
10mg sodium

Monday, October 13, 2014

Candida albicans and its effect on hormonal balance

In my previous blog, found here, I went over some of the research on Candida albicans.  This opportunistic fungus is the leading cause of fungal infection in humans and can cause issues ranging from mild skin and connective tissue irritation to vaginal yeast infections and hormonal disturbances in those with a candida overgrowth.  In this blog I will show the connection behind all 3 of these issues.

To better understand how Candida albicans can cause a hormonal imbalance, it's important to understand the basic physiology of the stress response.  The stress response is carried out by the HPA axis.  HPA is an acronym for Hypothalamus-Pituitary-Adrenal.

Stress 101

The stress response begins when stress is perceived, which causes the hypothalamus, a part of your brain that is essentially the master control center, to release something called corticotropin releasing hormone(CRH).  CRH, in turn, triggers a projection off of your hypothalamus called the the pituitary gland to release adrenocorticotropic hormone (ACTH).  ACTH travels in the bloodstream until it reaches an area on top of the kidneys called the adrenal glands and signals them to produce corticosteroids such as cortisol and aldosterone.  In turn, as cortisol is pumped out by the adrenals, it eventually makes its way back to the hypothalamus via the bloodstream and shuts off CRH production, which causes the pituitary to reduce production of ACTH which reduces cortisol production by the adrenal glands.  This is called a negative feedback loop as higher levels of cortisol help tell the hypothalamus to chill out with requesting more cortisol.  While the stress response is far more complicated than this, this is all you need to know to understand Candida albicans' role in causing hormonal disturbances.

Recall from my last blog that Candida albicans possesses a corticosteroid receptor capable of binding corticosterone and cortisol.  When Candida albicans binds cortisol, it prevents cortisol from binding to cells that need it, while at the same time blocking the negative feedback loop cortisol has on CRH production by the hypothalamus.  This can cause the hypothalamus to pump out more and more CRH as it never receives the "Cool it" signal which, in hormonal terms, means the perception of chronic stress.  It doesn't end here for the impact on hormonal balance, however.  By causing something called pregnenonlone steal, HPA axis mis-signaling due to Candida albicans can cause problems with sex hormones and, therefore, reproductive success.

Pregnenolone-hormonal stem cell

As far as hormones go, pregnenolone is the last common ancestor of all hormones.  All steroids begin as pregnenolone and are created based on the body's needs.

Pregnenolone is synthesized from cholesterol and becomes whichever steroid the body needs based on hormonal signaling. When cortisol is bound by Candida albicans and the negative feedback loop it has on the HPA axis is broken, CRH sends the signal to the adrenal glands via ACTH that pregnenolone should be converted in to the corticosteroids, particularly cortisol.  As pregnenolone is directed towards the corticosteroids, less can be used for formation of sex/reproductive hormones causing a hormonal imbalance.  In men, this can cause low testosterone and in women it can cause low testosterone and low levels of estrogens.  Estrone, estriol, and estrogen are estrogens and Candida albicans can directly bind estrogen.  Ironically, you really don't have to learn anything else to understand how Candida albicans can affect the skin and GI tract because it is by the same mechanism.

The HPA axis in the skin

In addition to the central HPA axis that regulates the stress response, humans have a peripheral HPA axis within the skin and hair follicles that actively produce the same hormones and contains the same negative feedback system of the central HPA axis(1, 2, 3, 4) with the only difference being that the end product of the skin HPA axis is corticosterone instead of cortisol.  The skin and hair follicles are also rich sources of collagen which is high in the amino acid L-Proline, the amino acid of choice for the conversion of yeast to hypha in Candida albicans.  When you look at the effect of unmitigated CRH secretion in the skin and GI tract, you can see how Candida albicans can wreak havoc in these tissues.

By binding corticosterone in the skin, Candida albicans can break the negative feedback loop in the skin's HPA axis which may cause CRH levels in the skin to increase.  CRH causes mast cells in the skin to release histamine, an immune compound that increases inflammation and the primary target of antihistamines, pharmaceuticals used to decrease allergic responses(3, 5).  Unfettered stimulation of mast cells by CRH could cause skin inflammation to grow out of control and cause major skin hypersensitivity reactions.  Increased levels of CRH in the skin are thought to play a role in skin conditions such as eczema, psoriasis, hypersensitivity to chemicals, poison ivy reactions, urticaria, acne, and certain types of hair loss.

Effects of CRH outside of the skin

High levels of CRH activate mast cells and cause them to release histamine in the intestinal tract, increasing intestinal(6, 7) permeability.  CRH is thought to have a major role in IBS(8, 9) which would jibe with the relationship between a exaggerated stress response and IBS.  Finally,  CRH activates mast cells in the brain and increase permeability of the blood brain barrier(10).  An additional effect of chronically high CRH levels in the brain is impaired function of the hippocampus(11), an area of the brain crucial for consolidating information from short-term to long-term memory as well as spatial memory. It is interesting that brain fog is often listed as a potential symptom of candida overgrowth as impaired hippocampal function would certainly be a mechanism for brain fog.

Conclusion

Above I have laid out possible mechanisms for the symptoms associated with overgrowth of Candida albicans.  It is important to point out that this doesn't mean that if you have one of these symptoms that you have an overgrowth of Candida albicans.  If Candida were disrupting signaling within the HPA axis, you wouldn't have a single symptom, you would have a suite of them.

It is interesting to note that many of the symptoms of a Candida overgrowth overlap with symptoms of what was once referred to as adrenal fatigue and is now more appropriately labeled HPA axis dysregulation.  Another interesting thing that pops up is that many of the symptoms of HPA dsyregulation are caused by an electrolyte imbalance.  It is important to note that the adrenal hormone aldosterone is one of the chief regulators of electrolyte balance, and corticosterone is the precursor to aldosterone.  Candida could only play a role here if it invaded the adrenal gland directly.

If these mechanisms turn out to be correct, overgrowth of Candida albicans causes HPA axis dysregulation.  That is not to say it is the only cause or even the most common cause, other commensal organisms could potentially bind hormones that are part of the HPA axis and could, therefore, cause it to function improperly if they grow out of whack.  The important thing to realize if this is the case is that nutrient deficiencies aren't causing the problem, blocking steps in a tightly regulated system is.  Therefore, taking high doses of nutrients that are used to manufacture cortisol won't fix the problem until you fix the signaling issue.

***I will likely follow this up with a blog on therapeutic approaches to fixing the problem.  However, I need a break from writing these super long, heavily referenced blogs as they take a ton of time and I am currently working on something work related.  Please stay patient and hopefully I will get to it soon if that was what you were waiting for.  I know, it sucks, but there are only so many hours in the day.