Desulfovibrio and Parkinson’s: Misleading Connection?


I’m not entirely sure who my audience is on this one, but a reader recently forwarded an article suggesting that Parkinson’s disease could (potentially) be preventable, citing scientists’ discovery that a specific strain of gut bacteria, Desulfovibrio, may be a primary cause. It’s a fascinating idea, and it definitely got my inner Health Science Nerd activated. However, after some critical reflection, I feel compelled to share a few thoughts on the matter because things may not be as they seem. Again, these are just a few thoughts, and this is not meant to be some kind of journal entry. That said…

The article seems to imply that identifying and removing these bacteria could potentially prevent the disease. The actual study, published in Frontiers in Cellular and Infection Microbiology provided some interesting, albeit unconvincing results. A related study published in CNS Neuroscience & Therapeutics, is a little more responsible, but even that delves into potential treatment options that can alter the microbiome permanently without really addressing important underlying factors. Regardless, I think we should all look very carefully before we leap. I believe there is a much bigger issue to contend with.

While I agree that Parkinson’s is likely preventable in some cases and treatable in most others, I feel compelled to emphatically state that it’s crucial to approach these findings with extreme caution. While intriguing, the intricacies of cause and effect demand that we examine this issue (and finding) more critically. This is to say that, like most things related to health, things may not be as they appear on the surface. Remember that nature is complex and always has a few tricks up her sleeve. Similarly, we must always remember that treating only a symptom or a minor element will likely not solve the underlying problem. In fact, doing so can make things significantly worse.

Let’s start with a simple question. Is Desulfovibrio (or any other bacteria) truly the root cause of Parkinson’s disease or merely a part of the broader breakdown leading to the condition? I am afraid I must appeal to Occam’s Razor on this one. Consider the following as nothing more than an exploration of this question.

Is It Hidden In Plain Sight?

Parkinson’s, a progressive neurological disorder affecting around 500,000 people in the US, prompts the question: What commonalities exist among those affected? This is a question that has been asked for many years. Potential answers are numerous, but the underlying assumptions may have been flawed. However, Professor Per Saris from the University of Helsinki suggests that specific Desulfovibrio strains are likely culprits, with environmental exposure being a primary cause, as opposed to individual genetics. While it is an interesting hypothesis and might even be partially true, I’m unsure about the ultimate conclusion.

At face value, it seems easy to point the finger at something like Desulfovibrio. Indeed, it is a great place to look, and the evidence is compelling. After all, Desulfovibrio has a long history of potential negatives to consider. However, even if that is somewhat accurate, logic (and cause and effect) dictates that it simply cannot be the whole story. So, what is? Unfortunately, at least according to the vast majority of the literature that I have examined on the topic, the seemingly obvious clues are being ignored or, at the very least, grossly underappreciated.

To begin with, despite current perceptions on the matter, it is essential to understand that Desulfovibrio is not an inherently harmful bacteria. Hence, we should be very careful not to infer that it is. Instead, we should see it as nothing more than gram-negative sulfate-reducing bacteria. I’ll explain in a minute, but just know that framing it this way allows us to reduce our biases (especially confirmation bias) by seeing it as nothing more than a small part of a bigger picture while likely playing a few very specific and important roles. After all, nature seems to have a plan. Of course, if that is true, rather than being the sole cause of any disorder, it is likely more of a crucial indicator pointing to an even better answer. After all, these bacteria are found in healthy hosts. Therefore, I would suggest that other clues are there if we are willing to see them.

Perhaps we should focus on stealth and long-standing deficiencies and contributing behaviors for a moment. In this case, it seems to me that the signs are pointing to something related to sulfur status – of which we need a constant supply, but we rarely get. Consider the logic. The presence of sulfate-reducing bacteria can influence sulfate availability in the gut (and body), impacting the absorption of essential sulfur-containing compounds vital for amino acid synthesis and coenzyme function. Of course, sulfate availability can also affect the absorption of certain vitamins, especially thiamine (vitamin B1), which plays a big role in neurotransmitter synthesis and nerve cell function, and biotin (vitamin B7), which is important for many things, but here, myelin formation. Of course, both vitamins are important for energy metabolism and other biochemical reactions in the body and brain. Holistically, if we see an abundance of sulfate-reducing bacteria, we must acknowledge the potential for a variety of deficiencies, including sulfur deficiency specifically, and appreciate that certain conditions come with such deficiencies. The key is in the contrast.

Just a bit of digging might tell the tale. As it turns out, sulfur deficiency is linked to a variety of health issues, but this includes things like depression and other neurological conditions. It seems to me that the (ultimate) critical connection here might be the impact on glutathione, a sulfur compound crucial for brain health. However, going down this road, we must understand that deficiencies in precursor sulfur amino acids compromise glutathione synthesis, which is linked to neurodegenerative diseases like Parkinson’s.

Unfortunately, very few in the research community seem to be exploring this to any significant degree. Perhaps this has to do with the difficulty of being able to directly influence glutathione levels, an ignorance of the importance of sulfur, or a misconception regarding its toxicity. Regardless, I believe this avoidance is a mistake because there is plenty of evidence suggesting that sulfur-rich foods can help prevent age-related neurological diseases. Perhaps this insight alludes to issues related to our ability to properly digest and absorb the necessary nutrients. Of course, this makes a lot of sense when we consider the rising number of neurological diseases that seemingly align with the alarming rise of people dealing with intestinal issues.

Here’s another point to consider. Parkinson’s disease is frequently correlated with a decline in nutrition status. For example, deficiencies in vitamin B12 have been implicated in both Alzheimer’s and Parkinson’s diseases. However, when considering what I have mentioned thus far, we must admit that a strong theme is emerging, but intestinal bacteria is only a part of that theme.

Holistically, the association can be narrowed to a fairly straightforward relationship—the intake of animal products abundant in methionine and cysteine, which also happen to be crucial sulfur-containing amino acids necessary for the creation of glutathione. Remember that the availability of precursor amino acids, especially cysteine, is crucial for maintaining optimal glutathione levels. Of course, this connection gains even more credence when considering related conditions and indicators, such as the dysregulation of cysteine metabolism observed in numerous neurodegenerative conditions and throughout the aging process.

Of course, the further you go down this road, the stronger the theme becomes. In essence, the “simple complexity” suggests that perhaps the actual problem in diseases like Parkinson’s might be related more to sulfur or glutathione status (or a similar or related factor) than a particular strain of bacteria. If true, the bacteria are likely illuminating the road to this discovery as they merely play a role in the breakdown that led to the disease. However, this insight also provides a warning that treating only the bacteria and not addressing the underlying cause might create bigger problems. I’ll discuss this in a little more detail shortly, but remember that you cannot truly solve a problem that has not been properly identified.

Of course, while the preceding might otherwise support the idea that reducing or eliminating Desulfovibrio might be beneficial or that Desulfovibrio might potentially contribute to Parkinson’s via depletion of essential nutrients, we must seek contrasting information to ensure that big mistakes are not being made. Again, the key is in the contrast, and cause and effect says it all.

As it turns out, Desulfovibrio might also be a beneficial acetic acid producer and might play a vital role in intestinal integrity via mechanisms related to microbial diversity that we still do not fully understand. The evidence for this idea is mounting. Of course, this also might suggest that instead of being something bad, it has simply been given room to thrive. Hence, even considering its reduction should raise concerns about possible unintended consequences. For example, eliminating this bacterium could potentially disrupt microbial metabolite profiles, metabolic pathways, and host responses, potentially leading to changes in energy metabolism and nutrient absorption.

Moreover, and arguably the most important consideration, is that the absence of Desulfovibrio may impact microbial diversity, which can negatively impact gut barrier integrity, increasing the risk of inflammatory conditions and further hindering digestion and absorption. In turn, if we try to eliminate Desulfovibrio, we might exacerbate nutrient deficiencies, ultimately exacerbating the issue we are trying to treat. Let me be clear that I am not suggesting that this idea is a proven fact. Instead, I’m saying that this information seems to suggest that it is a very real possibility that should be explored.

Nonetheless, if my theory about nutrition status is even close to correct, we should be able to find some additional clues to support the theory. As it turns out, those clues are there. For starters, we know that the incidence of Parkinson’s is on the rise. Of course, gastrointestinal issues are on the rise as well. Moreover, we know that nutrient deficiencies are on the rise, too, especially in children. Should these potential connections not be explored?

Of course, some of the more well-known and common deficiencies related to this condition include things like Vitamin B12, iron, Vitamin A, Vitamin D, Calcium, Magnesium, and iodine. So, consider the best food sources of these essentials and then compare that list with our best sources of sulfur-containing amino acids. They match. Then, simply compare that finding with the Standard American Diet. There seems to be a stark mismatch between need and received. Of course, much of this problem is rooted in terrible misconceptions about what a healthy diet entails.

This is a vastly underappreciated and understudied association. Nonetheless, it makes a lot of sense when you think about it. However, in the spirit of cause and effect, we have to walk it back to the literal root.

There is a growing awareness of sulfur depletion in our soil and its connection to potential deficiencies in the plants and animals we consume. Logically, if our food is sulfur deficient, then we might be as well. If that is true, such deficiencies would probably be widespread and create all sorts of problems related to this topic.

Well, that appears to be the case. In fact, MIT Senior Research Scientist Stephanie Seneff has repeatedly emphasized sulfate deficiency as a widespread and overlooked nutritional issue in humans. More importantly, she associates this deficiency with a variety of health conditions, including progressive neurological disorders. Of course, that is just one example. There is actually quite a bit of literature on the essentiality of sulfur and the impact of what happens when we do not get enough, specifically regarding the drop of cysteine and glutathione, which, of course, impacts neurological health. The connections here are alarming, but they might also provide crucial insight into why we are now beginning to see a dramatic rise in Parkinson’s in younger people.

I think my theory holds at least enough water to warrant further investigation. Regardless, I agree that Desulfovibrio’s role in Parkinson’s warrants further research as well, but I also think the focus should extend well beyond. Instead, at least on this one, we should dig deeper – until we hit the bedrock.

In the interim, we must understand that prevention is key. It can take years for deficiencies to manifest and, sometimes, years to correct. Hence, a more responsible approach might involve simply doing a better job of honing our understanding of a more physiologically sound diet, improving nutritional status overall, and enhancing microbial performance to ensure optimal absorption of vital brain-nourishing nutrients, including sulfur.

With that said, I’ll concede to the importance of prebiotics, probiotics, and FMTs where necessary. Having a healthy and balanced microbiome is critical for nutrient absorption and overall health, and these options encourage natural processes. However, we must note the underlying behaviors that led to this problem in the first place. Of course, that also suggests that we should be very careful about throwing a bunch of antibiotics at a problem that is not yet fully understood. Especially when we are not entirely sure about the full scope of the various factors involved.

Now, while I do not have all the answers to this particular issue, I do think it is important to remember that the complex nature of health issues demands a truly holistic perspective. Oversimplifying complex processes in the human body can be dangerous and typically leads to unintended consequences. Thus, a meticulous and comprehensive examination is essential before going all-in on potentially hazardous medical interventions, especially those involving the microbiome or the brain. In the spirit of that thought, and for those who are interested in continuing this exploration, I will continue and provide a deeper dive into this potential.

A Deeper Dive: What Are We Missing?

For years, Desulfovibrio bacteria were associated with negative effects in the gut due to their involvement in reducing sulfate to hydrogen sulfide (gas). Without clear or full evidence, elevated hydrogen sulfide levels were often linked to various gastrointestinal issues, such as inflammation and damage to the intestinal lining. Despite being a completely normal byproduct of microbial activity in the gut and sometimes a clue into gastrointestinal improvement, this perception has led many to see Desulfovibrio bacteria in a negative light. However, our understanding of these bacteria, along with their role, has evolved in recent years, emphasizing the importance and dynamic nature of microbiota research.

Desulfovibrio is now being recognized as a “ubiquitous commensal bacteria” in the human gastrointestinal tract. While I concede that limited knowledge exists about the relationship between Desulfovibrio and host health, what we have discovered thus far is quite telling. For example, an analysis of data from the Guangdong Gut Microbiome Project revealed that Desulfovibrio (piger) is a prevalent Desulfovibrio species and is positively linked with bacterial community diversity. Interestingly, the relative abundance of Desulfovibrio exhibited positive correlations with beneficial genera and negative associations with harmful ones. Moreover, Desulfovibrio abundance was negatively correlated with body mass index, waist size, triglyceride levels, and uric acid levels, indicating a potential association with healthy hosts in specific human populations.

There are similar studies using different strains of Desulfovibrio. Regardless, and at the very least, these facts should give us pause. What else have we missed? Probably quite a bit. Now, while I concede that further research is needed, we must also admit that these insights suggest that perhaps we may have missed the mark regarding our initial assumptions or interpretations. I believe this is especially true regarding connections to neurological disorders.

DROP DOWN to examine some info about the interplay of sulfur, methionine, and cysteine.

***** Important Context *****

Remember that sulfur is critically important. However, its importance is often masked by complexity and misconceptions. To begin with, methionine is considered an “essential” amino acid, and cysteine is considered to be a “non-essential” or “semi-essential” amino acid. However, these titles are entirely misleading. Both are critically “essential,” but both also require a solid foundation to work from.

Cysteine, a sulfur-containing amino acid that is vital for protein synthesis and various biological processes, plays a crucial role in our antioxidant defenses, detoxification, and the overall structure of proteins like collagen and keratin. The fact that it is an essential precursor to glutathione, our ‘master molecule’ antioxidant, only adds to the debate here. Regardless, we have to remember that cysteine is synthesized from methionine, which is another sulfur-containing amino acid that we have to consume. And to be clear, methionine is vital for normal growth and development. 

Now, our bodies seem to find that each part of this process is rather important. In fact, approximately half of the methionine requirement in the diet is allocated to cysteine production alone. Another decent portion of that methionine serves as a building block for proteins or is used as a precursor to key molecules like succinyl-CoA, homocysteine, and creatine. Recent research has even found that methionine also plays a regulatory role in metabolic processes, the innate immune system, and, more importantly, digestive functioning. In other words, it’s pretty important, and a deficiency seems to be involved in many of the nation’s leading chronic diseases. That is a massive clue!

The point here is that the vast majority of it gets used up pretty quickly. Now, considering that your body doesn’t make methionine and is going to use what it can get to make important things, such as cysteine, that also means that we are looking at a slew of potential problems for those who don’t get enough in the first place. Therefore, if someone subscribes to a misguided diet and limits or excludes foods rich in sulfur and methionine, these necessary and complex systems begin to break down as people begin to operate in deficiency.

Understand that a deficiency in methionine-rich foods implies a potential shortfall in cysteine production, affecting immune function, glutathione synthesis, and protein synthesis, leading to severe health issues, including neurological problems. Cause and effect! But all of that is somewhat irrelevant if the sulfur supply is limited to begin with. Sulfur deficiency introduces a cascade of detrimental effects, particularly because of the restriction or lack of availability of quality cysteine and methionine. This limitation has profound repercussions on various metabolic processes, potentially exacerbating the manifestation of unpleasant symptoms already experienced and elevating the risk of chronic diseases in general.  

So, while the intricacies of this chain of events are seemingly complex, the result is rather simple. Neglecting essential nutrients from sources aligned with our physiology results in consequences that are both highly detrimental and, unfortunately, quite predictable. Of course, when our food is sulfur deficient, the prospect of reaching sufficiency becomes problematic. On-going supplementation is likely necessary because deficiency creates problems up and down the chain. Unfortunately, the long-term impacts are often simply ignored, and they are extremely hard to study. Therefore, we must use logic and reason as our guide until such time that appropriate guides and tests can be established.

This intricate process requires us to examine the interconnections among sulfur compounds, glutathione synthesis, neurological diseases, nutrition status, and the pivotal role played by gut microbiome bacteria (to name a few). Clearly, each of these elements will not be covered at length in this article. Nonetheless, we can start with what we know and examine what the clues point to. For example, we know that glutathione holds critical importance for various physiological functions. Conversely, a deficiency in sulfur amino acids jeopardizes the synthesis of glutathione, which is critically linked to neurological conditions and overall health status. Specifically, the impairment of glutathione function is a significant factor associated with the loss of neurons during the aging process and in afflictions like Huntington’s disease, Parkinson’s disease, stroke, and Alzheimer’s disease.

I should probably clarify this process. While the body synthesizes glutathione, cysteine is a limiting factor in glutathione synthesis. That means you have to have enough cysteine to get enough glutathione. Similarly, you need enough methionine to get enough cysteine. However, other factors, such as aging, chronic diseases, and environmental stressors, can also negatively impact its production. So, we must always assume that we are running on a glutathione deficiency.

Of course, that also means that dietary and lifestyle measures likely play a significant role in supporting glutathione levels. However, here is a bit of a twist. As it turns out, these same factors can affect the abundance and prevalence of Desulfovibrio in the gut, which can also hinder overall microbial diversity, which ultimately impacts the absorption of vital nutrients, which can create the deficiencies typically linked with these conditions.

A correlation between diminished nutrition status and the prevalence of other neurological disorders is rather clear, albeit ignored in many settings. However, in many ways, these connections underscore the dangers of dietary misconceptions and extreme diets, the importance of improving the health and diversity of our microbiome, and choosing dietary sources that are rich in sulfur-containing amino acids (while also omitting anti-nutrient sources where possible). As demonstrated, these vital nutrients appear to be limited in the diets of many, and many dietary options rich in these nutrients appear to be falling out of favor due to various pressures – hence, the increasing problem.

Remember that the reduction or elimination of specific foods triggers a cascade of potential issues affecting protein structure, enzyme function, and the body’s detoxification capabilities. However, this happens over time. What you need to know is that many neurological diseases also include issues related to protein structure, enzyme function, and various biological processes. In fact, this might explain many of the chronic diseases we currently face.

The point is that if we are going to point the finger at Desulfovibrio bacteria, I think it is wise to note its role in the gut microbiome, acknowledging its association with sulfate reduction while also emphasizing its potential positive contributions, such as its potential role in acetic acid production, weight loss facilitation, and pathogen control. Hence, I believe that, while compelling, the Desulfovibrio clue does little more than suggest a potential dietary or behavioral connection to neurological diseases that may be found or potentially rooted in sulfate status or the status of some related compound(s).

Of course, there is another twist to consider. We should probably remember that while a lack of microbial diversity can lead to neurological conditions, these neurological conditions might also influence the gut microbiome, demonstrating a dynamic relationship that goes well beyond Desulfovibrio alone. In fact, when we think of it that way, we should probably take some time to ponder which one is truly the cause.

DROP DOWN to see more clues provided by Alzheimer’s

***** Some Additional Clues *****

While we are at it, I’d like to present another aspect that suggests the presence of a significant connection between sulfur deficiency and neurodegenerative diseases, a connection that may be more substantial than our current understanding acknowledges. Indeed, neurodegenerative diseases are complex, with various contributing factors. I don’t mean to oversimplify, but here is something else to consider. As I have alluded to, it’s at least plausible that nutrient deficiencies, specifically sulfur deficiency, play a crucial role.

For example, a recent study suggests that screening for Alzheimer’s disease can be done with high accuracy by testing a person’s blood for phosphorylated tau (p-tau), a type of protein. The study focused on the biomarker p-tau217, which increases alongside other damaging proteins, beta-amyloid, and tau, in the brains of individuals with Alzheimer’s. The study found that a simple blood test was up to 96% accurate in detecting elevated levels of beta-amyloid and up to 97% accurate in identifying tau. However, if we think about that, we see a compelling and familiar connection.

While this finding presents a promising non-invasive method for early Alzheimer’s screening before symptoms manifest, which is absolutely fantastic, it also sets off alarm bells for me regarding what we have been talking about thus far. Unfortunately, only those who have dug into the nutritional aspect would have had a chance to see the same signs that I am seeing here. So, for this understanding, we need to focus on abnormal processes such as phosphorylation and misfolding.

As previously stated, sulfur is a crucial element for the synthesis of cysteine and methionine. Well, cysteine, in particular, is also important for the formation of disulfide bonds in proteins. However, if there’s a deficiency in quality cysteine due to sulfur deficiency, it might very well affect the proper folding and stability of proteins. Similarly, sulfur deficiency might compromise the antioxidant defense mechanisms, leading to increased oxidative stress and potential damage to proteins. Moreover, if there’s a deficiency, there is a really good chance that enzyme function could be compromised, affecting processes such as protein phosphorylation and dephosphorylation. So, of course, we would see an abundance of damaged proteins.

But wait – there’s more! We should probably look at something often overlooked in such conditions. The Standard American Diet consists of a lot of refined sugars and grains and usually a severe lack of sulfur. This mix contributes significantly to systemic and consistent inflammation in the body. After all, sulfur compounds have anti-inflammatory properties. Hence, a severe sulfur deficiency, along with increased sugar and grain consumption, will absolutely lead to increased inflammation. It so happens that chronic inflammation is also associated with neurodegenerative diseases. Of course, these inflammatory processes typically contribute to abnormal protein aggregation and misfolding, and the theme continues.

Of course, sulfur deficiency might also disrupt signaling cascades that regulate processes like protein phosphorylation. Dysregulation of these pathways can contribute to abnormal protein modifications. And to bring this all back to the point, we need to understand that methylation is crucial for various cellular processes, including DNA and protein methylation. Well, you probably guessed it: a sulfur deficiency might impact these processes as well, negatively impacting protein function and stability.

All this to say that while it may not be the entire answer, I have a very strong feeling that the role and impact of a long-standing sulfur deficiency is at least part of the equation. However, if I am right, the question then becomes, why don’t we know this for sure? Well, the truth is that testing for an accurate assessment of sulfur status is exceptionally challenging, primarily due to the diverse forms in which sulfur exists within the body and the dynamic nature of its distribution. This is the same reason why testing for glutathione can be misleading. Moreover, the body constantly mobilizes sulfur compounds, making it exceptionally difficult to obtain a precise, static measurement.

Granted, we can sometimes get close, but current methodologies involve expensive techniques that provide only indirect indicators of sulfur status. Hence, some are quick to suggest that it’s simply not worth the effort. Regardless, as of now, technological limitations impede the development of comprehensive tests that can offer real-time and precise insights into individual sulfur metabolism. Accordingly, studying much of what I have discussed thus far is exceptionally difficult.

Nevertheless, even in the face of these challenges, we can draw certain valuable insights to inform our choices. Recognizing the significance of sulfur (and quality animal products) in the body, particularly its role in mitigating neurodegenerative diseases, underscores its importance for overall health. Accordingly, and considering the widespread deficiency in sulfur among many individuals across this great nation, and especially considering its essential role in optimal health, it becomes prudent to take action long before the problems manifest. I recommend consulting with a nutritionally competent physician or researcher to explore whether sulfur supplementation or the incorporation of sulfur-rich foods aligns with individual needs. That said, it seems to me that taking proactive steps in this regard could benefit future brain health and overall well-being.

A Few Closing Thoughts

Understand that I am merely presenting a theory. Or better said, a few clues that I think are greatly underappreciated. However, I think this idea holds enough merit to be considered a starting point for further investigation. Remember that it is crucial to exercise caution when establishing correlations and identifying causes, especially in medical scenarios. Getting back to the main point, we should remember that higher levels of Desulfovibrio might simply be a symptom rather than a cause or a contributing factor. With that in mind, perhaps it could be used as a test to help identify dysbiosis, sulfur deficiency, and the potential for neurological disease long before the disease takes hold.

I say that because logic dictates that, in many cases, an abundance of Desulfovibrio may be nothing more than a consequence of broader issues negatively affecting microbiome diversity, such as a diet rich in processed fats and sugars, which, again, also happens to be linked to an increased risk of nutritional deficiencies and neurological disease. Of course, that also means that, in at least some cases, the necessary and best treatments are both simple and currently underappreciated.

Applying this principle to the broader context, it is crucial to consider cause and effect and then address the underlying cause. At the same time, we must acknowledge that sometimes treatment requires addressing both cause and effect because a cascading cycle has presented itself. So, rather than prioritizing one over the other, sometimes the optimal approach is to address both (or multiple) aspects simultaneously. However, this presents a significant problem when you consider that the vast majority of practitioners are not effectively trained in nutrition or behavior-related diseases.

All this is to say that careful consideration of correlations, thorough investigation of test results, and a holistic understanding of contributing factors are essential in medical and research assessments. The interconnectedness of various elements in health underscores the importance of a comprehensive and balanced approach to treatment and the vitality of trying to avoid false attributions in general. We need options, and ignoring the difficult elements is unwise.

Again, I’m not entirely sure who my audience is here, and clearly, I cannot cover every aspect of this topic in one article. Nonetheless, I felt compelled to stress that we should be highly cautious moving forward. It is abundantly clear that we do not fully understand every nuance quite yet, and clearly, that has a lot to do with the fact that we are not considering all the variables. Similarly, a lot of that problem is rooted in the lack of interdisciplinary collaboration.

Still, it seems to me that if Desulfovibrio is a concern, rather than try to eliminate it, we must correct the behaviors that led to its proliferation and then attempt to balance it out with bacteria that naturally keep it in check, such as Firmicutes, Bacteroidetes, and Actinobacteria. By the way, a physiologically sound diet can usually achieve this with ease while also addressing the deficiency that typically accompanies such conditions. Of course, adhering to such a diet would require the abandonment of popular dietary misconceptions and recommendations, and sadly, that is something many, including the majority of health practitioners, are simply not prepared to do yet.

In closing, I will say that we should never stop searching for stronger clues regarding neurodegenerative disease (or any other health condition) because there are a lot of clues that point us in a very specific direction that is not currently being considered or appreciated. Again, interdisciplinary collaboration can help tremendously, and additional insights might be found by collaborating with a nutritionally competent epidemiologist or a Health Science professional. Either way, I think we are getting closer. Let’s keep up the good fight. We’ll get there!

If you enjoyed this article, you might also enjoy my article titled Feed the Mind to Feed the Body.

Dr. Robertson is a health researcher and educator, not a physician. The information provided here is not medical advice, a professional diagnosis, opinion, treatment, or service to you or any other individual. The information provided is for educational and anecdotal purposes only and is not a substitute for medical or professional care. You should not use the information in place of a visit, call consultation, or the advice of your physician or other healthcare providers. Dr. Robertson is not liable or responsible for any advice, course of treatment, diagnosis, or additional information, services, or product you obtain or utilize. IF YOU BELIEVE YOU HAVE A MEDICAL EMERGENCY, YOU SHOULD IMMEDIATELY CALL 911 OR YOUR PHYSICIAN.