Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
July 24th, 2016 

Lynn’s Clinical Pearl on Stress

Over the last few days, I’ve been speaking with people, either in a coaching capacity or on a call, and as they explain the messages their body is giving them, they usually tell me it involves hormone-deficiency symptoms such as hot flashes, vaginal dryness, decreased libido, difficulty sleeping, increased anxiety, etc. In asking the questions that we learn through our Nutritional Endocrinology Practitioner Training, a basic theme comes through – stress.

As in many responses, stress begins in the brain. As we come upon a situation, it enters our brain response through either sight, sound, smell, or the other sensory receptors. Our brain then tells us what it thinks is the appropriate behavioral and/or physiological response to actual or perceived stressors. The brain has its own set of stressors – glucocorticoids and catecholamines are the two main fight-or-flight stress response hormones, but there are also pro- and anti-inflammatory cytokines along with the parasympathetic nervous system.

While we occasionally may need the catecholamines for those occasional times of a fright – increased heart rate and blood pressure – to help us cope with a situation, chronic elevation of our heart rate and blood pressure will produce wear and tear on our cardiovascular system resulting, eventually, in heart attack or stroke. The active process by which the body responds to daily events and maintains homeostasis is called allostasis. Allostasis literally means “achieving stability through change” and is not intended to replace “homeostasis.” There is now a term “allostatic load or overload” to refer to the wear and tear that results from either too much stress or from inefficient management of allostasis, e.g., not turning off the response when it is no longer needed. Allostatic overload refers to the chronic behavior, such as poor eating patterns, whereas chronic stress has other references that could come from situations outside of your own behavior.

The common experience of being “stressed out” has as its core the elevation of some of the key systems that lead to allostatic overload – e.g., cortisol, sympathetic activity, and pro-inflammatory cytokines, with a decline in parasympathetic activity. Nowhere is this better illustrated than for sleep deprivation, which is a frequent result of being “stressed out”. Sleep deprivation produces an allostatic overload that can have harmful consequences (McEwen, 2006; McEwen, 2007). The effects include elevated evening cortisol, insulin, and blood glucose, elevated blood pressure, reduced parasympathetic activity, and elevated levels of proinflammatory cytokines, as well as the gut hormone, ghrelin, which increases appetite. Hunger for comfort foods and increased caloric intake are one result, along with depressed mood and cognitive impairment (Dallman, 2003;McEwen, 2006). In contrast to these potentially dysfunctional consequences, the same mediators are involved in the natural world in adaptation to environmental changes (McEwen and Wingfield, 2003).

The brain is the key organ of the stress response because it determines what is threatening and, therefore, potentially stressful, and also controls the behavioral and physiological responses, and resulting lifestyle, as I pointed out earlier, which are as important to development of allostatic load and overload as the stressful experiences themselves. Many other things can affect this perception – experiences within our early upbringing, genes and epigentics, different alleles in genetics – are among the environmental triggers.

One of the ways that stress hormones regulate function within the brain is by changing the structure of neurons. The hippocampus is one of the most sensitive and pliable regions of the brain, and is also very important in cognitive function. Within the hippocampus, the input from the entorhinal cortex to the dentate gyrus has complicated consequences by the connections between the dentate gyrus and the CA3 pyramidal neurons. The dentate gyrus-CA3 system is believed to play a role in the memory of sequences of events, although long-term storage of memory occurs in other brain regions, too. The dentate gyrus-CA3 system is balanced in its function and is susceptible to damage, there is also adaptive structural plasticity, in that new neurons continue to be produced in the dentate gyrus throughout adult life, and CA3 pyramidal cells undergo a reversible remodeling of their dendrites in conditions such as hibernation and chronic stress (Popov et al., 1992; Popov and Bocharova, 1992; McEwen, 1999). The role of this plasticity may be to protect against permanent damage. As a result, the hippocampus undergoes a number of adaptive changes in response to acute and chronic stress.

Adrenal steroids are important buffers of remodeling of hippocampal neurons during repeated stress, and adrenal steroids can also cause remodeling in the absence of an external stressor. The role of adrenal steroids involve many interactions with neurochemical systems in the hippocampus, including serotonin, GABA, and excitatory amino acids (McEwen, 1999; McEwen and Chattarji, 2004). Probably the most important interactions are those with excitatory amino acids such as glutamate. Excitatory amino acids released by the fiber pathway play a key role in the remodeling of the CA3 region of the hippocampus, and regulation of glutamate release by adrenal steroids may play an important role (McEwen, 1999).

Repeated stress also causes changes in other brain regions such as the prefrontal cortex and amygdala. Repeated stress causes dendritic shortening in medial prefrontal cortex (Sousa et al., 2000; Wellman, 2001; Vyas et al., 2002; Kreibich and Blendy, 2004; Cook and Wellman, 2004; Radley et al., 2004; Brown et al., 2005; Radley et al., 2005) but produces dendritic growth in neurons in amygdala (Vyas et al., 2002), as well as in orbitofrontal cortex (Liston et al., In Press). Along with many other brain regions, the amygdala and prefrontal cortex also contain adrenal steroid receptors; however, the role of adrenal steroids, excitatory amino acids, and other mediators has not yet been studied in these brain regions. Nevertheless, in the amygdala, there is some evidence regarding mechanism, in that tissue plasminogen activator (tPA) is required for acute stress to activate not only indices of structural plasticity but also to enhance anxiety (Melchor et al., 2003). These effects occur in the medial and central amygdala and not in basolateral amygdala, and the release of CRH acting via CRH1 receptors appears to be responsible (Matys et al., 2004).

Although there is very little evidence regarding the effects of ordinary life stressors on brain structure, there are indications from functional imaging of individuals undergoing ordinary stressors, such as counting backwards that there are lasting changes in neural activity (Wang et al., 2005). Another study, using voxel-based morphometry, has uncovered a relationship between shrinkage of grey matter volume in the hippocampus and orbitofrontal cortex and prospective reports of chronic life stress over a 20 year period (Gianaros et al., 2007).

Another important factor in hippocampal volume and function is glucose regulation. Outright Type 2 diabetes and poor glucose control as measured by glycosylated hemoglobin is associated with reduced hippocampal volume (Gold et al., 2007). Furthermore, poor glucose regulation is associated with smaller hippocampal volume and poorer memory function in individuals in their 60’s and 70’s who have “mild cognitive impairment” (Convit et al., 2003), and both mild cognitive impairment and Type 2, as well as Type 1, diabetes are recognized as risk factors for dementia (Ott et al., 1996; de Leon et al., 2001; Haan, 2006).

Having a positive outlook on life and good self-esteem appear to have long-lasting health consequences (Pressman and Cohen, 2005), and good social support is also a positive influence on the measures of allostatic load (Seeman et al., 2002). Positive affect, assessed by combining momentary experiences throughout a working or vacation day, was found to be associated with lower cortisol production and higher heart rate variability (showing higher parasympathetic activity), as well as a lower fibrinogen response to a mental stress test (Steptoe et al., 2005).

I have given you some scientific information to back up some basic principles. A major goal should be to try to improve sleep quality and quantity, to have good social support and a positive outlook on life, to have a positive self-esteem, to maintain a healthy diet, to avoid smoking, and to engage in regular moderate physical activity. Concerning physical activity, it is not necessary to become an extreme athlete, and seemingly any amount of moderate physical activity helps (Bernadet, 1995; Rovio et al., 2005).

Foundations, foundations, foundations.

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
July 3rd, 2016 

“Metabolic Healing 23 and Me Test Interpretation”

You upload your 23 and Me raw data and it generates a 38-page report with explanations.

I highly recommend that you test your own genetics here:

US Residents: http://www.23andme.com/drloscalzo

Canadian Residents: https://www.23andme.com/en-ca/

Then run this report.

http://www.23andme.com/drloscalzoTestInterpretation

You can also run the free genetics genie.org methylation and detox reports and use my cheat sheets to help with interpretation.

Genetics – Detox Interpretation

Genetics – Methylation Interpretation

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
June 26th, 2016 

Loss of delta-6-desaturase activity as a key factor in aging

I came across some interesting research regarding delta-6-desaturase (D6D), the enzyme responsible for elongating the short-chain essential fatty acids, linoleic acid and alpha linolenic acid, into the long-chain EPA, DHA, GLA, and DGLA.

We’ve known for a long time that deficiencies of B vitamins, magnesium, vitamin C, zinc, and other nutrients can slow down this conversion.

This article by Dr. David Horrobin attributes D6D deficiency to more rapid aging.

According to Dr. Horrobin, with aging, delta-6-desaturase (D6D) levels have been found to fall rapidly in the testes and more slowly in the liver in aging rats.

Factors which inhibit D6D activity are diabetes, alcohol, and radiation – all of which may be associated with accelerated aging.

In meat eaters or omnivores, since arachidonic acid is acquired from food, the main consequences of D6D loss will be deficiencies of GLA, dihomogammalinolenic acid (DGLA), and prostaglandin (PG) E1. PGE1 activates T lymphocytes, inhibits smooth muscle proliferation and thrombosis, is important in gonadal function, and raises cyclic AMP levels in many tissues.

Moderate food restriction raises D6D activity by 300%. Food restriction is the only activity that consistently contributes to slowed aging.

Other factors important in regulating D6D and the conversion of GLA to PGE1 are:

• Zinc
• Vitamin B6
• Vitamin C
• Melatonin
• Possibly vitamin B3

If you are a little cloudy on D6D and all its functions and inhibitors, please review the Macronutrients module for details.

http://www.ncbi.nlm.nih.gov/pubmed/6270521   

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
June 5th, 2016 

Aromatase, 5 Alpha Reductase, and Hair Loss

Maybe these words seem like gibberish to you now, but they will be clear as you progress through the course work.

I had an interesting situation come up recently and would love to share. It’s a work in progress so I can keep you posted.

A client with a history of thyroidectomy due to cancer complains of episodic periods of hair loss (among many other complaints; just this one hits women where it hurts most, LOL).

She notes that it happens when her iron gets low. Makes sense. I find that she has a terrible T4 to T3 ratio – poor conversion. She’s been in Synthroid only and has been reluctant to consider T3 until recently.

Both T3 and iron deficiencies can lead to hair loss. But she wants me to solve the hair loss dilemma without having to take T3 (urg… how?).

Well, back in February, she started an episode that’s continued (with a few ebbs and flows), and she is very concerned. Of course, we play detective to see what else has changed (besides long history of stress due to special needs kids and an abuse as a child).

Back then, she started acupuncture and chaste tree, along with some B-vitamins, so she is suspicious of all of these. She told me that when she stopped chaste tree, her hair loss situation improved; when she started chaste tree, it got worse. I was intrigued by this.

Chaste tree helps to improve estrogen progesterone ratio by stimulating progesterone and inhibiting aramotase, the enzyme that converts testosterone to estrogen. Hmmmm… most chaste tree research reports chaste tree improves hair loss, so because I am curious (key word, and one you need to value — get curious when things don’t line up), I decided to do some research.

In rare cases, the aromatase inhibitors backfire and the extra testosterone gets converted to DHT, a “dangerous in excess” testosterone metabolite. DHT is the type of testosterone responsible for triggering male pattern baldness in susceptible men. Ahhh… getting

somewhere.

So, if this is what’s happening, why? (Get curious again.) The enzyme that converts testosterone to DHT is 5 alpha reductase; that enzyme is inhibited by zinc, saw palmetto, GLA, and other things.

Now it’s making sense.

Her alkaline phosphatase has been very low for a long time. She is taking zinc, but not enough (due to fear of excess!!)

So I convinced her to increase her zinc, and we are going to do a DUTCH test to see what is going on before trying other approaches.

The point of this story is that you are being given the tools to understand the biochemistry and physiology well enough to ask curious questions then explore and find novel solutions to complex problems.

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
May 22th, 2016 

Iron Storage Disorders

The storage form of iron is called ferritin, which get stored in the liver.

Normal serum iron and low ferritin is one of the early indicators of iron deficiency anemia.

But what does it mean when iron is low or low normal and ferritin is high?

There are a number of possibilities. This article explores one: inflammation.

It seems that inflammation increases the storage of iron as ferritin in order to “hide” the iron from potentially harmful microorganisms, which could thrive in its presence.

Read more HERE: http://www.irondisorders.org/anemia-of-chronic-disease

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
May 8th, 2016 

The Power of Why

Today’s pearl is short and sweet; it was inspired by Jane Guyette.

When someone presents with a symptom or set of symptoms, and it points to an imbalance in one part or another, always ask, why is this malfunction occurring?

You are learning ways to assess the symptoms and map them to specific imbalances and body systems. And it’s always important to just keep asking why until you get to the root.

Why are the ovaries not producing enough progesterone in relation to estrogen? Is there an exogenous source of estrogen? Why is the pituitary malfunctioning? Is there a tumor? Was there a head injury? When you ask enough why questions, you are more likely to get to the root.

I will go into more depth at the NEPT Retreat when we can role play.

The Bottom Line: Keep asking why and that will prompt questions for the client that may get at aspects of their history that they hadn’t mentioned before and can help you put the puzzle pieces together.

Band-aids are a great tool, as long as you find and correct the source of the bleeding.

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
May 1st, 2016 

Autoimmunity and Insulin Resistance

At the end of May, I’ll be doing a talk at the Canadian Holistic Health Association’s annual meeting. The talk is on Autoimmunity and Insulin Resistance.

I’ve collected a few articles that might be of interest.

Usually we just think about type 1 diabetes as autoimmune; however, recent studies suggest an autoimmune connection with type 2 diabetes as well.

Here are a couple of articles.

1. http://www.ncbi.nlm.nih.gov/pubmed/18556968  Zhou P, Ten S, Sinha S, Ramchandani N, Vogiatzi M, Maclaren N. Insulin receptor autoimmunity and insulin resistance. J Pediatr Endocrinol Metab. 2008 Apr;21(4):369-75.
2. http://www.drsharma.ca/obesity-is-type-2-diabetes-and-autoimmune-disease
3. https://www.nahypothyroidism.org/insulin-resistance-can-trigger-hashimotos-disease/
4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543968/
5. https://med.stanford.edu/news/all-news/2011/04/type-2-diabetes-linked-to-autoimmune-reaction-in-study.html

Edmonton, Alberta: Winer DA, Winer S, Shen L, Wadia PP, Yantha J, Paltser G, Tsui H, Wu P, Davidson MG, Alonso MN, Leong HX, Glassford A, Caimol M, Kenkel JA, Tedder TF, McLaughlin T, Miklos DB, Dosch HM, & Engleman EG (2011). B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies. Nature medicine PMID: 21499269′.

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
April 24th, 2016 

Latent Autoimmune Disease in Adults

I will be speaking for the Canadian Holistic Nutrition Society in May. The conference is focused on autoimmune diseases. I am talking on the little-talked-about connection between insulin resistance and autoimmune disease and discussing an autoimmune diabetes that comes on in adulthood called LADA – Latent Autoimmune Disease in Adults.

I discuss LADA in the blood sugar module, IRSPT: Insulin Resistance Solution Practitioner Training, and there I list the blood tests that help detect it.

LADA is often misdiagnosed as type 2 diabetes. A few things tip you off to look again, and I’ve developed my own protocol for assessment.

Here are some differentiating factors to help you recognize the difference between LADA and insulin resistance/metabolic syndrome/type 2 diabetes:

1. Fat distribution: LADA people are often thinner than the classic type 2 diabetic. Type 2 diabetics are usually overweight with fat distribution around the middle. LADA people are often lean.
2. Fasting insulin: Type 2 diabetics usually have high fasting insulin; LADA have low.
3. Postprandial insulin (after meals): Type 2 diabetics usually have a big spike in insulin levels after meals; LADA people often have very little.
4. Response to oral blood sugar lowering medications: Type 2 diabetics usually respond well. At least initially, LADA people often need multiple medications and, after a short while, tend to not do so well thus are often put on insulin.

These are some of the common differentiators. If you suspect LADA, there are a few blood tests you can do to confirm.

Often, I do the fasting and postprandial insulin measures to determine if their pancreas is making too much or too little insulin.

If the fasting and postprandial insulin are both low, I then need to differentiate between type 2 diabetes that’s resulted in pancreatic failure from excess insulin production, or LADA where the pancreas is under autoimmune attack.

The tests for LADA are:

• anti islet cell antibodies
• anti insulin antibodies
• GAD antibodies (glutamic acid decarboxylase, an enzyme that converts glutamic acid to GABA, and is produced by the pancreas)
• c-peptide which is an indicator of insulin production

The full panel runs over $500, so if budget is a consideration and the client doesn’t have insurance coverage, I often start with one of the antibodies and explain that they may need to go back and get tested again if the test is negative.

The bottom line: Keep your eyes and ears open, ask the right questions, and when someone comes in who’s relatively lean, says they are on multiple medications, their blood sugar is still not controlled, and the doctor is suggesting insulin — think “LADA”.

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
April 17th, 2016 

Skin Issues – Root Causes

If you have someone suffering from recurrent skin issues — eczema, psoriasis, dry skin, pitching rashes, and more — look deep.

Fatty acid imbalance, gluten intolerance, liver congestion and stagnation, and impaired digestion can all lead to skin problems.

Supplementation with fatty acids and an herb called yellow dock can help.

Please post to the Facebook group any successful interventions you’ve had in dealing with skin issues.

Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl
April 10th, 2016 

Think Functionally

It’s really tempting to start to grasp for protocols for symptoms and diagnosed conditions that your clients present with. After all, you want to serve them and find solutions.

I still hear a lot of, “What should I do for this or that condition,” as if it’s the condition that we are supporting, not the client.

We’ve been trained to think that way. Conventional medicine thinks that way. We mostly grew up in a conventional medicine model (except for a few lucky ones among us whose parents were ahead of their time).

Indeed, I do give you done-for-you “protocols” for many “conditions”. But in reality, those protocols are reminders about the condition, the questions to ask your client, and the thought process.

So when a new client presents, I want you to get into the mode if thinking about the person, not the symptoms.

What do the symptoms indicate? What body systems may be at the root cause of the imbalance? What foundational diet and lifestyle areas are out of balance? What was the set of events that led up to the person experiencing the set of complaints?

All of these are important questions to ask, and indeed 90% of the answers come from taking an excellent history. Yet many practitioners tend to skip over the history taking so they can jump into fixing.

Remember: your job is not to fix anyone.

Your job is to determine what’s in the way of your client’s inner healer – what’s keeping her or him from doing their job? Ask and you shall receive.

Ask the right questions to the client and also do the labs and other documentation they provide. When you can put it all together and make sense of it, that’s when you are on a path that will lead them to true healing.

I am excited to be in the process of revitalizing the Master Health Tracker spreadsheet to contain forms you can use to map out your client’s history and interventions. It’s so valuable to be able to always keep their health picture close at hand without having to memorize their findings.

It will be presented at the retreat for sure, and hopefully before.

If you haven’t completed Modules 5 and 7, History Taking and Physical Exam, dive right in as soon as they are open to you. If you have, I suggest you review.

The new Master Health Tracker will give you a place to consolidate and analyze client information and refer back to it easily. I struggled for years with paper forms and a variety of online documents, word files etc. I find the Master Tracker the easiest way to keep it all in one place!