Summary and Key Points
- Nutrient deficiencies can result from insufficient intake, impaired digestion or absorption, problems with transport, impaired assimilation and states of over-utilization.
- It takes a methodical approach to assess the root causes behind a nutrient deficiency in order to apply the most effective therapy to rectify it. Supplementation is not always the optimal or correct solution.
- While insufficient intake is the most common reason for developing a nutrient deficiency, there are other causes that will not be solved simply by providing more of a nutrient either through a supplement or food.
- Maldigestion which involves the insufficient processing of nutrient-containing foods and malabsorption which involves the impaired absorption of digested foodstuffs are common mechanisms for developing nutrient deficiencies outside of insufficient intake.
- Disrupted or impaired transportation of certain nutrients can lead to functional nutrient deficiencies even when intake, digestion and absorption are optimal.
- Chronic inflammation, pregnancy, periods of growth or tissue repair, nutrient deficiencies, drug or supplement use, acute illness, genetic variations are examples of mechanisms that can lead to nutrient deficiencies via “overutilization.”
- AIP is a nutrient-dense elimination diet that includes certain nutrient-dense foods, but also excludes other nutrient-dense options. This must be taken into account in order to avoid inadvertent nutritional deficiencies.
- Removing foods as part of AIP that are contributing as allergens, disrupting the integrity of the gut lining, disturbing the ecosystem of the gut microbiome, disturbing normal digestive function, non-specifically contributing to a state of chronic inflammation or otherwise displacing more nutrient-dense foods are all mechanisms by which AIP can directly and indirectly address nutrient deficiencies.
- Early evidence from the AIP Hashimoto’s study appears to indicate that organ meat, as part of the elimination phase of AIP, should be considered an essential food and not simply a bonus option to provide “supplemental” nutrients.
Before we get into the meat of today’s post, you may find this short glossary of terms helpful to understand some of our main points.
CLICK TO EXPAND // Glossary of terms used in this article
Science Corner: Glossary
Atom: the smallest identifiable unit of matter containing the properties unique to one chemical element. An atom is a unique arrangement of protons, electrons and/or neutrons (e.g. an oxygen atom would be identified as an atom that contains 8 protons).
(Chemical) element: an entirely pure substance, a collection of atoms having the same number of protons (e.g. oxygen, carbon, nitrogen).
Molecule or compound: a combination and specific arrangement of atoms (e.g. water or H2O, which is a combination of the elements hydrogen and oxygen. You can also think of it as a molecule containing two atoms of hydrogen and one atom of oxygen, hence the name H2O.).
Nutrient: any substance or component that is utilized by an organism in order to survive, grow or reproduce.
Nutrients can be classified into two categories macronutrients and micronutrients. The primary macronutrients are protein, fat and carbohydrate. Each macronutrient consists of a specific arrangement of essential components. Think of it as a collection of smaller building blocks.
- Proteins: chains of amino acids
- Carbohydrates: specific combinations of sugars such as glucose and galactose
- Fats: specific combinations of carbon and hydrogen atoms, also known as hydrocarbons
Micronutrients can be broken down into three main categories: vitamins, minerals and phytonutrients.
- Vitamins: (generally speaking) complex molecules (combinations of atoms) that perform various vital functions to the existence of an organism (e.g. vitamin B12).
- Minerals: singular elements (atoms) that can make up vitamins as well as interact with other vitamins, enzymes or molecules to carry out very specific functions for the organism (e.g. magnesium).
- Phytonutrients: an incredibly complex array of plant based compounds including flavonoids and carotenoids that exert innumerable effects in the human organism, often in concert with macro and micronutrients.
Please feel free to refer back to this glossary of terms and definitions while also utilizing the supplied visual representations to help you become a nutrient expert!
Am I Getting Enough Nutrients on AIP?!
Most people’s first response to this question would be an emphatic YES! AIP also known as the Paleo Autoimmune Protocol, as outlined by many of the experts in this field including Sarah Ballantyne, PhD, is one of the most nutrient-dense diets that one can consume. In relative terms, one can also agree that when AIP is compared to other dietary templates such as the Standard American Diet (SAD) or a vegan diet that the total nutrient density of AIP is significantly higher than the nutrient density of most other dietary patterns.
So I am eating AIP, everything is good, right? Well, let’s hold on just one second.
AIP in its strictest terms is a nutrient-dense elimination diet designed to include some of the most nutrient dense foods such as dark leafy greens and organ meats, while eliminating foods that could potentially exacerbate immune dysregulation, disturb or impair digestion of certain nutrients or disturb the vital ecosystem we now know as the gut microbiota.
Any form of an elimination diet, however, whether it is AIP, a ketogenic diet, a vegan or plant-based diet, a carnivore diet, etc. is potentially removing certain macro or micronutrients that serve essential roles in the body and one must be cautious and calculated to avoid permanently eliminating foods that may serve as one of the only reliable sources of a given nutrient.
While the insufficient intake of a nutrient is the most common reason for becoming deficient in that nutrient, we must consider the entire sequence from consumption of the nutrient to its actual utilization in order to fully answer the question, “Am I getting enough?”.
Here is a brief and simplified outline of the functional nutritional sequence.
We can see from this outline that ingesting or eating a nutrient is really only just the first step in the process by which that nutrient gets to the location necessary to carry out its desired function. Issues with digestion/absorption, transportation, assimilation and utilization can all lead to the same outcome of impaired functioning due to a “nutrient deficiency.”
That begs the question: If I develop or already have a nutrient deficiency, how will I know which step is causing the problem?
Good question, let’s break this down step by step.
1. Intake or Ingestion
The first step, as I mentioned before, is assessing and rectifying intake. If you are not consuming an essential nutrient, which can be defined as any nutrient that cannot be produced by the body or by other constituents of the human organism (think: our “gut bugs”) to meet physiological demands, then you will certainly become deficient.
Now, you may be asking: What are the essential nutrients?
I do not have time to get into a more nuanced discussion of this topic, but below for those interested, you will find the most agreed upon list of these essential nutrients as organized by the previously described categories of macro- and micronutrients.
CLICK TO EXPAND // A breakdown of essential nutrients
Science Corner: Essential Nutrients
- Amino acids (9 in total): phenylalanine, valine, threonine, tryptophan, methionine, leucine, Isoleucine, lysine, histidine
- Polyunsaturated fats (2 in total):
- Alpha linolenic (ALA), an omega 3 fat
- Linoleic acid, an omega 6 fat
- Polyunsaturated fats (2 in total):
- Vitamins (13 in total):
- B vitamins: B1, B2, B3, B5, B6, B7, folate (B9), B12
- Fat-soluble vitamins: A, D, E, K
- Vitamin C
- Minerals (18 in total): oxygen, hydrogen, carbon and nitrogen (we don’t typically think of these because they are so ubiquitous), potassium, chlorine, sodium, calcium, phosphorous, magnesium, iron, zinc, copper, iodine, chromium, molybdenum, selenium, cobalt
To the best of our understanding these essential nutrients (9 amino acids, 2 fatty acids, 13 vitamins, and 18 minerals) are the minimum our body needs in order to survive and reproduce. How much of each and the situations when other nutrients may become “conditionally” essential is still very much debated, but, as previously mentioned, I do not have the time to get into this area today.
But, back to our question. You may be saying, “I am following the AIP elimination template, I am including more dark leafy greens, animal foods and even managed to try organ meat once this month, surely I am covered?”
We still aren’t so sure.
Over the past 5 months, I have been conducting a research study with Angie and Mickey examining the effects of AIP in those with Hashimoto’s disease. While we are just beginning our formal data analysis, a few potentially concerning trends or patterns have emerged. While I cannot go into specific detail as we have yet to publish our findings, there is some indication that the removal of certain non-AIP foods without the concurrent inclusion of key nutrient dense foods on a regular basis can lead to functional deficiencies.
Organ meats are the most nutrient-dense food across the board on AIP, however, it is very easy to not include them given their relatively poor palatability. It is also easy to rationalize that the regular inclusion of organ meats is simply a bonus, not mandatory or essential when consuming the elimination template of AIP. However, early indications from the study point to the possibility that organ meats are not a bonus, but an essential component.
When we look at the nutrient dense foods eliminated during the initial phase of AIP (legumes, nuts, seeds, eggs and dairy) one quickly is removing some of the top sources of vitamin K, folate, copper, magnesium, and choline just to name a few nutrients.
Organ meat contains all of these nutrients, often times in staggeringly sufficient amounts. In practical terms, organ meat is nature’s multivitamin, sitting alongside bee pollen as two of my go to nutrient dense natural food “vitamins.”
AIP is an incredible dietary template and clinical tool that I have seen change lives, but we must be vigilant and evolve our approach as we gain a better understanding of what is occurring in the body as a result of eating in this manner. We’ve covered a lot of ground here in this first section, and we will address more of the therapeutic approach to addressing deficiencies related to intake later in the article.
For now, let’s move on down the GI tract to the next step in the functional nutrition sequence.
The macro- and micronutrients described previously in this article are all digested and absorbed in fascinatingly complex ways that would take much too long to describe as part of this article, but the quick summary of this collective process can be thought of like this:
Most nutrients are digested or processed from larger foodstuffs or constituent molecules via specialized digestive enzymes and stomach acid. The digested nutrients are then absorbed via specialized transporters, channels or carrying molecules within the small intestine — the first segment of intestine after the stomach or in the large intestine. In most cases the larger macronutrients such as proteins, carbs and fats must be broken down by various but specific enzymes to smaller constituent groups (e.g. amino acids and glucose) in order to be absorbed. There is significant “redundancy” in the form of many enzymes and transporters as well as an incredibly large surface area in the small intestine in order to facilitate the optimal digestion and absorption of these nutrients. Despite this redundancy, however, one’s capacity or ability to digest and absorb the nutrients can be impaired for a number of reasons.
Here are a few quick examples.
- In active celiac disease, the normal “villous” structure of the small intestine that provides the incredibly large surface area in which to interact and absorb the incoming nutrients is “flattened” as a result of an inflammatory immune response. This “flattening” leads to significantly impaired absorption of key nutrients. One of the most commonly understood deficiencies that occurs primarily because of this impaired absorption is iron. It is so common that it is recommended that anyone newly diagnosed with iron deficiency or iron deficiency anemia be screened for celiac disease! This is an an example of a deficiency caused by an intrinsic issue with absorption as compared to an issue with the digestion of the nutrient (we will see this shortly).
- B12 deficiency can occur because of any number of issues at all 5 steps of the functional nutritional sequence, but for now, let’s see how B12 deficiency can occur because of issues with absorption. Individuals with Crohn’s disease affecting the terminal ileum (the last segment of the large intestine where B12 is absorbed) are known to have higher rates of B12 deficiency and are at a higher risk for becoming deficient. Interestingly, individuals with ulcerative colitis, which does not directly affect the terminal ileum or small intestine, have also been found to have higher rates of B12 deficiency due to microscopic and non-specific inflammatory responses affecting the small intestine and terminal ileum. Both of these examples in IBD showcase how intrinsic issues with absorption can ultimately lead to nutrient deficiencies even if someone is consuming “enough” of the nutrient in question.
- Pancreatic insufficiency or an inability to secrete sufficient pancreatic enzymes into the gastrointestinal tract is a primary mechanism of maldigestion that can lead to numerous nutrient deficiencies including protein, essential fatty acids and fat soluble vitamins. While pancreatic insufficiency is commonly understood to occur with cystic fibrosis (a genetically based disease) as well as in chronic alcoholism, research is beginning to show that individuals outside of these disease states also are showing clinical evidence of pancreatic insufficiency. A 2009 study by Leeds, et al found that approximately 6% of individuals with IBS-D or diarrhea predominant IBS were found to have evidence of pancreatic insufficiency as measured by fecal elastase (8). These authors conclude and highlight the need to assess for potential pancreatic insufficiency and the likely co-occurring fat soluble vitamin nutrient deficiencies in those presenting with IBS-D.
While these examples highlight nutrient deficiencies that can occur secondary to malabsorption or maldigestion in individuals with three specific autoimmune conditions as well as the broader label of IBS-D, I also want to briefly highlight another condition that is not strictly autoimmune in nature, but affects a number of individuals with autoimmune disease.
Small Intestinal Bacterial Overgrowth or SIBO is precisely what the name suggests, an overgrowth of gut bacteria in the small intestine.
CLICK TO EXPAND // More about SIBO
Science Corner: Small Intestinal Bacterial Overgrowth (SIBO)
In the strictest sense, is defined as an overgrowth of bacteria, specifically >10^5-10^6 organisms per mL of aspirated (biopsied) small intestinal fluid. The normal small intestine has approximately 10^3 organism per mL of small intestinal fluid, so we can see there is a significant difference between 1000 organisms per mL of fluid in healthy individuals versus 100,000 or even 1,000,000 per mL in those with bacterial overgrowth.
Practically speaking, very few individuals are actually diagnosed with SIBO by sampling fluid from the small intestine as this is an invasive and costly procedure, but I want to provide you with this information as the strictest gold standard definition of this condition, while also providing the caveat that this condition is most commonly diagnosed using a surrogate laboratory technique known as breath testing. With breath testing, individuals consume a solution of substrate that is commonly utilized in normal bacterial metabolism, and we then measure the end product of this metabolic process: either hydrogen or methane gas.
The individual collects breath samples at various time points, and we can estimate (utilizing an understanding of the normal transit time for the testing substance), whether or not there is an overgrowth of bacteria in the small intestine. More concretely said, if we notice an elevation in the exhaled hydrogen at a time point that corresponds to when the consumed substance should be in the small intestine, we are suspicious that there may be an overgrowth of bacteria. If we notice an elevation in the exhaled hydrogen at a time point that corresponds to when the consumed substance is normally in the large intestine (after the small intestine), then we would not suspect SIBO.
SIBO is emerging as an incredibly diverse and complex pathology that can manifest in numerous symptoms including gas and bloating, to diarrhea and malabsorption. While we would suspect clinically obvious diarrhea to potentially lead to nutrient deficiencies secondary to impaired absorption, we are also starting to see that specific types of bacterial overgrowth not typically manifesting clinically as classical diarrhea can lead to nutrient deficiencies via other maldigestive/malabsorptive mechanisms. Some types of gram negative coliform bacteria (normally in the large intestine) can actually produce certain toxins that damage the lining of the small intestine and disrupt otherwise normal absorptive function (2). Others still have been shown to deconjugate bile acids, necessary molecules for the absorption of fat and the associated fat soluble vitamins.
I share all of this not to scare anyone with SIBO or send everyone to the physician to get a breath test, but simply to increase awareness. Clinically and anecdotally I have observed patients with SIBO and small intestinal inflammation requiring greater amounts of B vitamins and fat-soluble vitamins to overcome nutritional deficiencies, or show predominantly B vitamin and fat-soluble vitamin deficiencies upon nutritional/organic acid testing.
To be clear, only some individuals with SIBO will have issues with malabsorption/maldigestion or early fermentation that result in a meaningful nutritional deficiency, but I have seen it enough clinically that I am very methodical and thorough with my patients when it comes to nutritional intake or supplementation in these cases.
The next step in most cases after absorption of a given nutrient is transportation to various cells, tissues or organs of the body. There are numerous routes of transportation depending on the nutrient in question. I will provide some clinical examples of where the transportation system breaks down resulting in nutrient deficiencies.
As I mentioned earlier with regards to celiac disease, one can become iron deficient simply due to poor absorption which results from blunting or damage to the villi in the small intestine housing the machinery for absorbing iron. While this is certainly one common way for becoming iron deficient, there is another equally, if not more common way for becoming functionally iron deficient.
Once absorbed into the cells lining the intestine, the body must “decide” the fate of iron. Typically, in iron depleted states, the iron will be pushed down the “iron utilization” pathway. In iron replete states, the iron will be pushed down the iron “storage” pathway where it will bind to a large molecule called ferritin. Iron stored in ferritin is functionally inaccessible to other cells and tissues. Why is this a problem?
CLICK TO EXPAND // More about iron transportation
Science Corner: Iron Transportation
Iron is required for synthesis of heme, an essential molecule used to make hemoglobin (the oxygen-carrying structure in red blood cells) and other heme-containing proteins such as cytochrome C (a protein structure in the electron transport chain essential for making the energy currency of the body, ATP). Typically ferritin remains in the enterocyte, and thus, iron is not transported into the blood plasma as it would be if bound instead to the transport molecule transferrin. From the enterocyte, ferritin can be excreted out of the body when the enterocyte “dies” and is shed in the lumen of the intestine and excreted in waste.
Besides being used for normal “storage”, ferritin is also known as an acute phase reactant. In times of acute stress, such as infection or in an acute inflammatory state, ferritin, amongst many other proteins and molecules, is increased. As an adaptive, protective mechanism, iron is essentially sequestered into the storage form ferritin, so that potential microbes such as bacteria cannot utilize it for growth and replication. In the short term, this is a very helpful immune response that may help humans suppress the pathogen by limiting its potential to grow and spread, and ultimately recover back to a normal balanced state.
Unfortunately, this acute phase reaction to a potential bacteria is also triggered by stimuli other than bacteria. Actually, in most cases, an acute phase or inflammatory response is triggered by something other than bacteria and persists much longer than a bacterial infection. Low levels of chronic inflammation will upregulate this pathway so that the body is essentially always in iron storage mode, so little to no iron goes to iron transport and utilization.
Even if iron is absorbed and present in the body, it may not be transported to the cells that utilize it in the production of hemoglobin or cytochrome C so it is like the body doesn’t have any iron! Ferritin, our storage molecule, becomes very active in states of perceived infection and inflammation such that low levels of chronic inflammation may be “tricking” the body into storing iron instead of transporting it to be functionally used.
This process whereby iron is transported into “storage” iron and not “functional” iron is essentially the process behind anemia of chronic disease or anemia of chronic inflammation.
The process of absorbing vitamin B12 is fairly intricate and complex, but it is important to understand as deficits in transport can often be the source of the deficiency and not intake or even absorption. While I list transportation after intake and absorption in our functional nutrition sequence, the key transportation step for B12 actually occurs before absorption in the small intestine.
B12 is a vitamin that requires a special transport protein called Intrinsic Factor (or IF for short). IF must bind to B12 in the small intestine and transport it to the gut lining in order for it to be absorbed. I bet you can already see where the breakdown is going to occur?
In conditions that could deplete the levels of IF such an an autoimmune gastritis, also known gut autoimmunity, there is not enough IF to bind and transport B12 so an individual will slowly become deficient despite consuming B12 (hence, the name pernicious anemia).
CLICK TO EXPAND // More about B12 absorption
Science Corner: B12 Absorption
As mentioned before, the absorption of B12 is rather complex. A simple summary of the entire sequence involves these steps.
- Ingestion of food-bound B12
- Release of B12 after digestion of food components by HCl and other enzymes
- Binding to Salivary R protein, a protein released initially in saliva and present in the gastric juices (I think of this almost as a protective step)
- Cleavage of the B12/R protein complex by pancreatic enzymes such as trypsin
- Binding of B12 to IF that was initially released from parietal cells in the stomach
- Absorption of the B12/IF complex in the lower small intestine.
Assimilation can be thought of in many ways. One can think of assimilation as simply another term for absorption of a nutrient in the gut, but I like to think of assimilation as the incorporation of a nutrient into a cell so that it can then be utilized. For some nutrients, (or at least certain aspects of a nutrient’s role in the body), the steps of assimilation and utilization become merged.
Good examples of this phenomenon involve nutrients that perform structural roles such as cholesterol and omega 3 fatty acids. While both of these fats serve other roles as energy producing molecules and precursor molecules to make other compounds, they both can, upon assimilation, be utilized in the dynamic cell membranes of all of our cells.
Perhaps the nutrient that has received the most study, however, for its issues with dysregulated assimilation is glucose or blood sugar.
After absorbing glucose from the gut into the bloodstream, we must then transport it into cells where it can then be taken to the specialized organelle, the mitochondria, and utilized to produce ATP — the energy currency of the body!
There are numerous ways glucose can get into the cell, but the primary ways involves another protein known as insulin acting as a second signal to actually get the glucose inside the cell.
While the entire process is significantly more complex, essentially what must occur is insulin must bind to its own receptor- kind of like a lock and key to initiate a cascade of changes that allows glucose to be brought into the cell.
If there is no insulin or insulin is not able to produce the signal required to allow glucose inside the cell, the glucose remains in the bloodstream (outside of the cell) where it cannot be utilized for energy.
CLICK TO EXPAND // More about insulin
Science Corner: More About Insulin
In type 1 diabetes, there is an autoimmune response that damages and destroys the cells responsible for producing insulin, essentially creating an insulin deficient state. Without insulin to accompany the glucose, the individual cannot bring glucose into the cell for energy. Most individuals when first diagnosed are in a relative state of starvation, breaking down lean tissue, losing weight and producing high amounts of ketone bodies, an alternative fuel source when glucose cannot be used.
When you measure the blood level of glucose, however, in these individuals it is often in the 400-600s (normal is around 90), a perfect example of how a nutrient can be ingested, digested, absorbed, transported in the blood but not assimilated into a cell to be used.
In type 2 diabetes, individuals have insulin, and oftentimes too much insulin, but the cell is not responding to the signal. This phenomenon is what we refer to as hormonal resistance or more specifically insulin resistance as the cell is resistant to the insulin signal.
There are many reasons why this can occur. In the normal physiologic state of pregnancy, the mother actually becomes slightly insulin resistant due to hormones produced by the placenta (think: the fetus wants the blood sugar). One also can become insulin resistant after exercise or consumption of certain fruits or vegetables as these stimuli have actually increased the oxidative load on the cell. If the cell perceives there is too high an oxidative burden inside of it (think reactive oxygen or reactive nitrogen species), it may choose to not let any more glucose inside until the normal byproducts of breaking down glucose for energy or oxidative species are converted by our own antioxidant defense enzymes into less harmful compounds.
Think of it as the cell needs more time to handle the oxidative compounds created by the exercise or fruit or vegetable consumption prior to letting more glucose inside to start the process over. These changes are transient and resolve quickly in normal individuals, however, in individuals with consistent caloric excess or overwhelmed antioxidant defenses, one can become insulin resistant and not resolve these transient changes.
Think of it as insulin knocking on the door with glucose nearby, but the cell does not open the door to let glucose in. No assimilation, no utilization. This description is essentially what is underlying diabetes, now one of the most common and still vastly under-diagnosed conditions in Americans today.
While many of us likely know a friend or loved one with diabetes, there are hundreds of thousands more individuals with what we would call “pre-diabetes” or “insulin resistance”: the early metabolic signs that glucose is not being assimilated and utilized properly and that insulin is not able to do many of its other important signaling roles as well.
Many individuals with insulin resistance are not obese and otherwise do not know that the amount or type of food they are consuming could be contributing to the problem.
I share all of this, once again, not to scare anyone into getting your blood sugar levels checked, but to simply raise awareness about this relative functional “deficiency” that can and often does occur in a state of excess intake.
There is no way I could include every possible example of impaired utilization or over-utilization as mechanisms for the development of nutrient deficiencies, so I simply want to point out some of the bigger culprits and illustrate how important it is to appreciate the multi-dimensional, complex systems at play in the human organism.
The most common cause of “over-utilization” of a nutrient is a state of chronic inflammation. Inflammation, as I described in my first article for Autoimmune Wellness (Is Baking Soda an Effective Treatment for Autoimmune Disease?) is not some “evil monster” but a coordinated cellular response. In order to carry out a proper inflammatory response, you need the raw materials to make immune cells and the compounds they secrete as part of the response.
You see that this is a very energetically demanding process requiring both energy in the form of ATP and nutrients to continue to make cells and their secreted substances. In states of inflammation and tissue repair, the macronutrient protein becomes one of the most critical nutrients necessary to make more and more immune cells. It is commonly understood that individuals hospitalized in the intensive care unit (ICU) or patients following surgery require higher amounts of protein given the demands of the body’s inflammatory (healing) response.
Additional nutrients including B vitamins necessary for energy production also can become deficient without a concomitant increase in intake during such times. While most of us will be lucky enough to avoid hospitalization in the ICU, we are coming to see that even small levels of chronic inflammation can create, over the long term, an increased need for key nutrients such as numerous B vitamins and protein.
What is more troublesome, however, is when we begin to see the effects of chronic inflammation intersect with the other possible causes of nutritional deficiencies. In the case of active inflammatory bowel disease, one can get into a vicious cycle of maldigestion, malabsorption, impaired transportation and over-utilization all contributing to impaired nutrient status. Given the impairments at multiple levels of the functional nutritional sequence, one can become rapidly deficient with supplementation alone providing very little meaningful support.
I make this point to highlight the importance of our next section as one must correctly identify the steps of the nutritional sequences that are compromised and apply the appropriate therapeutic modality or modalities.
Diagnostic and Treatment Approaches to Nutrient Deficiencies
There are 3 critical steps to addressing nutritional deficiencies. The first is actually identifying the nutrient deficiency itself. The second is determining the impaired functional level(s) (a.k.a. the reason) primarily leading to the deficiency in question. Third is applying an appropriate treatment given the identified deficiency and level of impairment. As you will see in the upcoming section, it is not as simple as measuring a blood level of a certain nutrient and giving you a supplemental amount of the deficient nutrient.
Here is a breakdown of my methodical approach:
Deficiencies with intake can be identified by methodical questionnaires and food diaries. Apps such as Cronometer are revolutionizing how one can track nutritional intake and assess macro and micronutrient intake. I am commonly utilizing this application to determine adequate nutrient intake in my patients. Simply recording food intake over a 1-3 day period and inputting it into Cronometer can provide a fairly accurate assessment of whether or not one is meeting baseline needs (independent of other factors such as impaired digestion/absorption, over-utilization, etc.)
The obvious first step to address identified insufficiencies in intake is to include more foods containing the nutrient in question. Supplementation of nutrients via a supplement can also be used to rectify deficiencies related to intake, but this is my second option as usually any non-food-based supplement lacks the myriad components or nutrients found in the foods containing the nutrient in question. If available I will use “food-based” supplements to address deficiencies such as cod liver oil, bee pollen, desiccated liver capsules, kelp flakes, etc.
What I see very commonly, however, is that individuals try to address nutrient deficiencies related to issues with malabsorption/maldigestion or over-utilization as if they are issues of intake or ingestion. This is an incredibly important point as we can often waste time, money and even cause potential harm by attempting to take a supplemental nutrient at higher and higher doses when the issue was never really intake to begin with and would resolve by addressing an issue with digestion, absorption or over-utilization.
2. Digestion and Absorption
Within the field of functional medicine, there are myriad of fairly simple tests that can be used to assess issues with maldigestion or malabsorption. While one can certainly perform blood testing to identify a nutrient deficiency such as vitamin A of B12, when it comes to issues with maldigestion or malabsorption, I am commonly identifying these issues first through a combination of clinical history and diagnostic testing, then making the clinical judgement to test for various nutrients that could be deficient or simply assuming based on evidence-based practice that someone with such issues is almost certainly deficient.
An example of this sequence could involve performing a stool test that quantitatively and/or qualitatively assesses the amount of fat in the stool (an indirect assessment of how much fat is digested and absorbed). If the stool is noted to be overly “fatty,” then an individual is likely deficient in key essential fatty acids as well as the associated fat soluble vitamins.
Another marker known as a pancreatic elastase is a very reliable marker to assess for pancreatic insufficiency. Low levels of pancreatic elastase in the stool indicate pancreatic insufficiency and likely have lead to multiple deficiencies including the fat soluble vitamins. Testing for SIBO, as mentioned previously in the article, via breath testing can be a helpful tool to assess one’s risk for B vitamin and fat soluble vitamin deficiency via maldigestion or malabsorption. A test known as a D-Xylose test is a gold standard test for assessing intrinsic deficits in absorption.
Intestinal permeability tests such as the lactulose/mannitol test can also indirectly assess the likelihood of maldigestion and malabsorption which would place an individual at risk for nutrient deficiencies. There are numerous other tests that can be performed within the domain of digestion/absorption, but I simply wanted to stress the importance of identifying such deficits and understanding the likely downstream nutritional deficiencies that could occur secondary to gastrointestinal issues.
Common techniques to improve digestion and absorption include the use of supplementary stomach acid (HCl) as well as digestive or pancreatic enzymes. What is often overlooked, however, is the removal of certain foods that could be contributing to poor digestion or absorption of certain nutrients. While removing gluten in the case of celiac disease is the most obvious example of this phenomenon, grains, dairy, soy, legumes and nuts are all examples of AIP eliminated foods that could be contributing directly and indirectly to impaired digestion or absorption of key nutrients.
The autonomic nervous system which includes the sympathetic “fight or flight” and parasympathetic “rest and digest” branches plays a very important role in digestion. As the names suggest, signaling by the parasympathetic or “rest and digest” branch of the nervous system is essential for secretory function of key components needed to properly digest and absorb nutrients. The sympathetic or “fight or flight” branch, generally speaking, will decrease the motor signals promoting gut motility and also diminish the response of various secreted compounds that would otherwise promote digestion and absorption. These scientific explanations are simply a more complicated way to say that eating while calm and relaxed will improve digestion and absorption of the food you eat, and engaging in a regular stress reduction practice such as meditation or listening to music may be essential for addressing a nutrient deficiency.
In addition to these steps, correcting SIBO via a low-FODMAP diet, probiotics and/or herbal antimicrobials, decreasing the inflammatory burden present in active IBD either through diet, supplements or prescription medications, and restoring optimal motility through diet, hydration, herbs, supplementation or prescription medication are all concrete examples of directly addressing disturbances in digestion or absorption leading to clinically significant nutritional deficiencies. While one can certainly utilize sublingual supplements in certain situations to circumvent the primary issues of impaired digestion and absorption, one must also actively correct the primary digestive or absorption issue during the period of supplementation to truly undress the root causes.
I will provide two examples for diagnosing nutritional deficiencies related to transport in connection with the previously mentioned nutrients iron and B12 from the earlier section.
Assessing iron status and a potential deficit in iron is a somewhat controversial topic, but starts with basic blood chemistry testing multiple iron parameters including iron (serum), TIBC, transferrin, and ferritin as well as hemoglobin. One may additionally want additional information such as plasma copper and zinc, Ceruloplasmin, and magnesium (serum or RBC). If you are concerned about the possibility of a deficiency or iron, it is critical to find an experienced provider who can work with you to perform and interpret this bloodwork. An elevated ferritin alone or a low hemoglobin level cannot adequately determine if you have an iron deficiency.
Assessing B12 status usually involves a series of blood tests. Serum B12 levels can be helpful to determine if there is a profound deficiency, however, serum B12, while a very specific test for B12 deficiency, is not as sensitive as other tests and may miss a borderline deficiency or an issue with utilization — we will talk more about B12 deficiency testing and treatment in the utilization section.
When it comes to issues with transport, some individuals can become B12 deficient because of a lack of Intrinsic Factor (IF), the transporting and chaperone protein that must bind B12 in order to be absorbed. In autoimmune gastritis, the immune system begins “attacking” the gastric (stomach) parietal cells that produce IF. No parietal cells equals no IF, no IF means no transport and absorption of B12. In situations where intake, digestion/absorption and utilization issues have been addressed, but a person persists with B12 deficiency, it is critical to test for autoimmune gastritis via anti-parietal cell antibodies as this could be the root cause behind low B12.
While decreasing sources of chronic inflammation can be an example of a way to improve a nutrient deficiency caused by all of the root steps outlined in this article, it is the primary way to address issues with transport as outlined with the specific example for iron deficiency related to anemia of chronic disease.
In the case of B12 deficiency related to autoimmune gastritis, it appears that B12 injections may both circumvent the impaired transport and absorption of B12-IF, and also decrease the anti-parietal cell antibodies — the autoimmune response itself (9). Sublingual B12 can be an alternative as well to increase serum B12 levels, but does not appear to have the same lowering effect for anti parietal cell antibodies. Oral supplementation may potentially exacerbate the autoimmune response and does not appear to be a viable or efficacious treatment.
Additional examples and therapies for optimizing transport include addressing the function of one’s liver and gallbladder. These organs are essential for producing and releasing bile acids into the digestive tract and maintaining the normal circulation of these compounds. Without sufficient biles acids and intact re-circulation of these compounds, one may suffer significant malabsorption of fats including the essential fat soluble vitamins A, D, E, K. While this example could also fall under the maldigestion/malabsorption category, I like to think of the production, secretion and circulation of bile acids as a transport issue. Ways to address impaired bile acid secretion and re-circulation include taking supplementary bile with pancreatic enzymes, ensuring adequate ingestion of choline, consuming fermented foods or taking certain strains of probiotics.
In sticking to the example of impaired assimilation of blood sugar into cells related to insulin resistance, I wanted to provide some basic tests that can be performed to assess one’s sugar control — essentially your capacity to assimilate glucose.
Using a blood sugar meter to measure fasting blood sugar in the AM is a very simple test that can be done at home. Ideal fasting blood sugars range from 70-95 mg/dL. Anything above 100 should make you concerned for impaired assimilation. Insufficient sleep, stress, late meals, excessive carbohydrate intake are all possible reasons for elevated fasting blood sugar. Additionally, one can consider testing blood sugar after meals. Called post prandial blood sugar, assessing your blood sugar 1-2 hours after a meal can given you an idea of how well your body is assimilation glucose after ingestion. Ideal ranges for 1 hour and 2 hour blood sugars are <135 and <115 mg/dL respectively.
Alternatively one can measure hemoglobin a1c, which gives an indication of the average blood sugar over approximately 3 months. In conjunction with a fasting morning blood sugar, and a post prandial blood sugar, these three markers can provide a good picture of one’s blood sugar control and capacity to assimilate glucose. Fasting insulin is another test that can be used to assess blood sugar assimilation.
In regards to assessing the assimilation of other essential nutrients such as essential fatty acids and magnesium, some clinicians are utilizing specialized testing to look at the amount of such nutrients in red blood cells (RBCs). Rather than simply looking at what is in the serum which contains many cell types all within an aqueous solution, testing for nutrients inside of the cell (in this case RBCs) gives an indication to the actual uptake or assimilation of nutrients into the functional cellular unit. Testing for the various amounts of essential fatty acids in RBCs including the omega-3 fats alpha linolenic and EPA and DHA has been used to assess cardiovascular risk — lower EPA/DHA levels in the RBC has been associated with high risk for heart attacks and strokes (10). There is some evidence, at least in mice, that following the consumption of omega-3 fats, RBC levels of DHA and EPA increased and were correlated to the levels of these fats in other organs such as heart, muscle, lung and adipose tissue (11). There are many labs currently performing red blood cell analysis of the essential fatty acids, so ask your doctor or functional medicine provider if this test would be right for you.
Treatment for addressing impaired assimilation of glucose or insulin resistance is not as simple as simply removing carbohydrates. While a low-carb and ketogenic diet can certainly address some issues of insulin resistance, one must once again look at all the potential root causes: poor sleep, excessive stress, over/under activity, poor meal timing, certain pharmaceutical drugs and even the improper use of some supplements. Working with a health coach, nutritional therapy practitioner and/or doctor can help you to identify the root causes and implement dietary and lifestyle strategies to support improve glucose assimilation.
Some examples of foods and supplements than can be used to help including cinnamon, chromium, berberine, alpha-lipoic acid, and probiotics to name a few, but please be sure to work with a qualified provider to utilize the proper amounts and dosages of such herbs or supplements.
One area of expanding and fascinating research involves the role of the gut microbiome to determine one’s blood sugar responses to certain foods. A 2015 study from Zeevi et. al showed the ability of researchers to create a reliable algorithm that could actually predict an individual’s personal response to certain carbohydrates and foods (12). A recent follow up to this study published by Mendez-Suarez et. al. continue to shed light on this fascinating inter-person variability of glucose responses to certain foods (13). Specifically the authors were able to create an accurate predictive model for someone’s glucose response to a specific food using a stool test (aka a picture of their gut microbiome). For comparison, the model created to predict someone’s glucose response simply based on the calorie or carbohydrate content was only about half as accurate! This is emerging proof that the health of your gut microbiome may play a larger factor to your blood sugar assimilation than the food itself!
This section deserves an entire blog post in an of itself, so I will simply outline the key maxim for identifying a nutritional deficiency based on a utilization (“over-utilization”): find the root cause.
It is probably obvious that any source of chronic inflammation as I have described earlier is going to only exacerbate cellular processes, either pushing your metabolism into less efficient pathways and utilizing more nutrients to carry out such processes. Insulin resistance, excessive oxidative stress, tissue build up and breakdown are major offenders when it comes to processes contributing to nutrient over-utilization. Listed below are some of the other common sources of “over-utilization.”
- Pharmaceutical drug use (e.g. metformin and B12)
- Wound healing
- Supplementation (e.g. brain chain amino acids and B1, B2, B3, B5, lipoic acid)
- Genetic mutations (SNPS) (e.g. MTHFR and glycine, folate)
As you can see, some of these states are not necessarily “good” or “bad” they are simply situations that require both additional caloric intake as well as additional nutritional consumption. Athletes can be very prone to nutritional deficiency even in the setting of sufficient extra caloric consumption if the extra caloric consumption is nutrient-poor food.
Working with a functional medicine doctor to assess for potential deficiencies related to blocks in a nutrient’s utilization or its over-utilization can be a critical step to identifying and addressing deficiencies not caused by deficits in the other steps of the functional nutritional sequence.
A couple quick examples of tests that can be performed to identify such utilization deficiencies include organic acid (nutritional) testing as specific blood chemistry testing. In the case of B12, one may perform a serum B12 blood test and find the level to be normal, only to discover that one’s methylmalonic acid (a more specific marker for the functional utilization of B12) is actually high. In this example, a high methylmalonic acid with a normal serum B12 indicates a B12 deficiency likely caused by poor utilization as B12 is necessary in cells to convert methylmalonic acid to a another organic acid metabolite.
My silly analogy to explain this more concretely is to think of B12 as a crossing guard and methylmalonic acid as “children leaving school” trying to cross the street to become “children going home.” When there aren’t enough crossing guards (B12) to get the “children leaving school” (methylmalonic acid) across the street to become “children going home” (a new organic acid metabolite), we get a build up of “children leaving school” (methylmalonic acid) on one side of the street. In this scenario, you could theoretically have enough crossing guards (B12) to do the job, but perhaps they are at a different school, inside of the school or otherwise not in the right place to perform the job (illustrating the idea of having “normal” blood levels of B12, but still being functionally deficient).
The essence of treatment is once again, match the therapy to the root cause. Generally speaking additional intake of the nutrient in question is almost always essential, however, one must also consider the context of intake. If you are needing more carotenoids such as beta carotene and you consume them as a supplement on an empty stomach or in a meal with no source of fat, you are likely compromising your ability to absorb the carotenoids and actually haven’t solved the problem. Some individuals will need to consume more protein to obtain more amino acids or more fat to obtain essential fatty acids and fat soluble vitamins, but if they are consumed with sub-optimal digestion or without supplemental digestive support in the forms of enzymes or bitters, one may once again be falsely assuming the increased intake has adequately compensated for the state of over-utilization.
There is much nuance to this approach and it is critical to assess all stages of the functional nutritional sequence, and to not only supply additional nutrients when necessary but to resolve (if possible) sources of chronic inflammation, oxidative stress, immune stimulation, tissue breakdown, etc., contributing to the increased need for a given nutrient than one would otherwise expect in a healthy individual in homeostatic balance.
If you have stuck with us for this nearly 9,000-word journey, I thank you and commend you for your dedication and willingness to share in this exploration together. This has been by no means an exhaustive look at identifying and treating nutrient deficiencies, however, I hope you can take away an understanding of the importance of the functional nutritional sequence, and you can methodically use this framework to identify and properly address nutrient deficiencies. I sometimes wish that such deficiencies could simply be rectified with increased intake or supplementation, but as we have seen together through this journey, this is not always the case.
AIP is emerging as a powerful tool to addressing chronic illness and we continue to gather more objective scientific evidence for its power to restore nutrient sufficiency and the health of the gut microbiome. We must not, however, as a collective community see its current iteration as a perfect solution and must apply our emerging understanding of its nutritional composition, the ways in which individuals practically adhere to the dietary template, and the biochemical and physiologic changes that occur as part of its consumption to make continued, further improvements so that debilitating autoimmunity and chronic disease can become a thing of the past.
- Ibbs S, Muhammed R. PTH-055 Vitamin b12 deficiency is common in children with ulcerative colitis as well as crohn’s disease Gut 2017;66:A233.
- Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterol Hepatol (N Y). 2007;3(2):112-22.
- Jia W, Xie G, Jia W. Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis. Nat Rev Gastroenterol Hepatol. 2017;15(2):111-128.
- Ramírez-Pérez O1, Cruz-Ramón V1, Chinchilla-López P1, Méndez-Sánchez N1. The Role of the Gut Microbiota in Bile Acid Metabolism. Ann Hepatol. 2017 Nov;16(Suppl. 1: s3-105.):s15-s20.
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- Cavalcoli F, Zilli A, Conte D, Massironi S. Micronutrient deficiencies in patients with chronic atrophic autoimmune gastritis: A review. World J Gastroenterol. 2017;23(4):563-572.
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- Sun A1, Chang JY1, Wang YP1, Cheng SJ1, Chen HM1, Chiang CP2. Effective vitamin B12 treatment can reduce serum antigastric parietal cell antibody titer in patients with oral mucosal disease. J Formos Med Assoc. 2016 Oct;115(10):837-844.
- Allaire J1, Harris WS2, Vors C1, Charest A1, Marin J1, Jackson KH3, Tchernof A4, Couture P5, Lamarche B6. Supplementation with high-dose docosahexaenoic acid increases the Omega-3 Index more than high-dose eicosapentaenoic acid. Prostaglandins Leukot Essent Fatty Acids. 2017 May;120:8-14.
- Fenton JI1, Gurzell EA2, Davidson EA2, Harris WS3. Red blood cell PUFAs reflect the phospholipid PUFA composition of major organs.Prostaglandins Leukot Essent Fatty Acids. 2016 Sep;112:12-23.
- Zeevi D1, Korem T1, Zmora N2, Israeli D3, Rothschild D1, Weinberger A1, Ben-Yacov O1, Lador D1, Avnit-Sagi T1, Lotan-Pompan M1, Suez J4, Mahdi JA4, Matot E1, Malka G1, Kosower N1, Rein M1, Zilberman-Schapira G4, Dohnalová L4, Pevsner-Fischer M4, Bikovsky R1, Halpern Z5, Elinav E6, Segal E7. Personalized Nutrition by Prediction of Glycemic Responses.Cell. 2015 Nov 19;163(5):1079-1094.
- Mendes-Soares H1,2, Raveh-Sadka T3, Azulay S3, Edens K1, Ben-Shlomo Y3, Cohen Y3, Ofek T3, Bachrach D3, Stevens J3, Colibaseanu D2, Segal L3, Kashyap P1,4, Nelson H1,2. Assessment of a Personalized Approach to Predicting Postprandial Glycemic Responses to Food Among Individuals Without Diabetes. JAMA Netw Open. 2019 Feb 1;2(2):e188102.
This is such a fantastic and comprehensive resource! Thank you for laying it out in such a clear and thorough way. Amazing.
[…] fact, the ladies over at Autoimmune Wellness believe that things like organ meats are necessary on AIP , not just […]
Hi both! Could I possibly ask, which of your cookbooks contain the most plant based + fish recipes? I’m currently vegetarian and have started on AIP and plan to work with a nutritionist in a week or two, but am aware that until then I might be a bit short on my nutrients and could do with meal ideas 🙂 So far my days look like: Banana smoothie with cocoyo, cassava wraps with guac and butternut squash & sage soup for dinner! I take b12 and iron spray supplements. SO – do you have a book that contains the least meat based recipes?
Hi Mali! AIP as a protocol is actually plant-based – check out my article here: https://autoimmunewellness.com/aip-is-a-plant-based-diet-protocol/
I would say all of the books contain a similar ratio – heavy on the veggies, with some nutrient-dense meats & seafood to round things out. You can’t go wrong with any of them! -M